PMID-sentid	Pub_year	Sent_text	comp_official_name	comp_offset	protein_name	organism	prot_offset
33232786-0	2021	TD-92, a novel erlotinib derivative, depletes tumor-associated macrophages in non-small cell lung cancer via down-regulation of CSF-1R and enhances the anti-tumor effects of anti-PD-1.	Erlotinib Hydrochloride	15-24	programmed cell death 1	Homo sapiens	179-183
33811537-2	2021	A clinical trial, SARC028, revealed that treatment with anti-PD-1 drugs was effective against UPS.	sarc028	18-25	programmed cell death 1	Homo sapiens	61-65
33940058-0	2021	An orally available PD-1/PD-L1 blocking peptide OPBP-1-loaded trimethyl chitosan hydrogel for cancer immunotherapy.	trimethyl chitosan	62-80	programmed cell death 1	Homo sapiens	20-24
33940058-7	2021	In conclusion, we discovered and optimized a PD-1/PD-L1 blocking peptide OPBP-1, viand subsequently loaded into a TMC based hydrogel oral delivery system, in order to maximally elevate the oral bioavailability of the peptide drug and effectively inhibited tumor growth.	tmc	114-117	programmed cell death 1	Homo sapiens	45-49
33972389-3	2021	Forty-three patients received combination therapy of programmed cell death protein 1 (PD-1) inhibitor with lenvatinib (ICI cohort 1), 108 patients received ICI-based therapy (ICI cohort 2) and 36 patients received non-ICI therapy (non-ICI cohort).	lenvatinib	107-117	programmed cell death 1	Homo sapiens	86-90
33972389-9	2021	CONCLUSIONS: The CNVs in plasma cfDNA could predict the clinical outcome of the combination therapy of PD-1 inhibitor with lenvatinib and other ICI-based therapies in hepatobiliary cancers.	lenvatinib	123-133	programmed cell death 1	Homo sapiens	103-107
33764509-7	2021	Tfh subsets including ICOS+PD-1+ and Ki-67+ Tfh were significantly increased, suggesting that the function of Tfh was enhanced in MPA although the total Tfh levels did not change significantly.	tfh	0-3	programmed cell death 1	Homo sapiens	27-31
33791214-2	2021	In this study, we aimed to assess the safety and efficacy of anlotinib, a novel multitarget tyrosine kinase inhibitor for VEGFR, platelet-derived growth receptor (PDGFR), and the stem cell-factor receptor (c-Kit), combined with anti-PD-1 treatment in patients with advanced NSCLC.	anlotinib	61-70	programmed cell death 1	Homo sapiens	233-237
33791214-14	2021	Conclusion: Anti-PD-1 treatment concomitant with anlotinib has tolerable toxicity and favorable antitumor activity in patients with previously treated advanced NSCLC.	anlotinib	49-58	programmed cell death 1	Homo sapiens	17-21
33804417-0	2021	Quantitative Dynamic 18F-FDG PET/CT in Survival Prediction of Metastatic Melanoma under PD-1 Inhibitors.	Fluorodeoxyglucose F18	21-28	programmed cell death 1	Homo sapiens	88-92
33232786-4	2021	In this study, we assessed whether a novel erlotinib derivative, TD-92, which possesses anti-tumor effects across several cancer cell lines, could enhance anti-PD-1 treatment.	Erlotinib Hydrochloride	43-52	programmed cell death 1	Homo sapiens	160-164
33232786-4	2021	In this study, we assessed whether a novel erlotinib derivative, TD-92, which possesses anti-tumor effects across several cancer cell lines, could enhance anti-PD-1 treatment.	td-92	65-70	programmed cell death 1	Homo sapiens	160-164
34822775-7	2022	Importantly, cancer patients with low plasma histamine levels had a more than tripled objective response rate to anti-PD-1 treatment compared with patients with high plasma histamine.	Histamine	45-54	programmed cell death 1	Homo sapiens	118-122
34710570-10	2022	CONCLUSION: We conclude that ceralasertib in combination with durvalumab has promising anti-tumor activity among patients with MM who have failed anti-PD1 therapy, and constitute a population with unmet needs.	ceralasertib	29-41	programmed cell death 1	Homo sapiens	151-154
34923342-3	2022	Interestingly, it has been shown that vitamin C is able to modulate the anti-cancer immune response and to help to overcome the resistance to immune checkpoints blockade (ICB) drugs such as cytotoxic T-lymphocyte antigen 4 (CLTA-4) and programmed cell death ligand 1 (PD-L1/PD-1) inhibitors.	Ascorbic Acid	38-47	programmed cell death 1	Homo sapiens	274-278
34753772-9	2022	These preclinical results reveal novel roles of tumor FGFR signaling in the regulation of cancer immunity through inhibition of the IFNgamma pathway, and the inhibitory activity of lenvatinib against FGFRs likely contributes to the enhanced antitumor activity of combination treatment comprising lenvatinib plus anti-PD-1 mAb.	lenvatinib	181-191	programmed cell death 1	Homo sapiens	317-321
34962580-7	2022	Median time to onset of heme-irAEs varies between patients but occurs earlier with CTLA-4 inhibitors than with anti-PD-L1/PD-1 agents.	Heme	24-28	programmed cell death 1	Homo sapiens	122-126
34598945-0	2022	First-in-Class Anti-Immunoglobulin-Like Transcript 4 Myeloid-Specific Antibody MK-4830 Abrogates a PD-1-Resistance Mechanism in Patients With Advanced Solid Tumors.	mk-4830	79-86	programmed cell death 1	Homo sapiens	99-103
34727389-0	2022	CPI-203 improves the efficacy of anti-PD-1 therapy by inhibiting the induced PD-L1 overexpression in liver cancer.	CPI203	0-7	programmed cell death 1	Homo sapiens	38-42
34918599-9	2021	PD-1 and CTL antigen 4 expressions were significantly reduced in peripheral blood CTLs after MLN removal by VAMLA (p = 0.01 and p = 0.01, respectively).	vamla	108-113	programmed cell death 1	Homo sapiens	0-4
34952044-5	2022	In this study, we prepared a lipid nanoparticle encapsulating docetaxel (DTX-VNS), and associated it with the immune checkpoint inhibitor anti-PD-1 antibody (alphaPD-1) for the treatment of malignant tumors.	Docetaxel	62-71	programmed cell death 1	Homo sapiens	143-147
34952044-5	2022	In this study, we prepared a lipid nanoparticle encapsulating docetaxel (DTX-VNS), and associated it with the immune checkpoint inhibitor anti-PD-1 antibody (alphaPD-1) for the treatment of malignant tumors.	dtx-vns	73-80	programmed cell death 1	Homo sapiens	143-147
34953979-5	2022	The innovative liposomal nanosystem was rationally designed by a remote loading of BMS-202 (a small molecule PD-1/PD-L1 inhibitor) and PSN into the liposomes for a ROS-sensitive paclitaxel release and sustained BMS-202 release.	Reactive Oxygen Species	164-167	programmed cell death 1	Homo sapiens	109-113
34953979-5	2022	The innovative liposomal nanosystem was rationally designed by a remote loading of BMS-202 (a small molecule PD-1/PD-L1 inhibitor) and PSN into the liposomes for a ROS-sensitive paclitaxel release and sustained BMS-202 release.	Paclitaxel	178-188	programmed cell death 1	Homo sapiens	109-113
34965944-1	2022	PURPOSE: To determine whether SD-101, a Toll-like receptor 9 agonist, potentiates the anti-tumor activity of anti-PD-1 antibodies in patients with anti-PD-1/PD-L1 naive, recurrent/metastatic head and neck squamous cell carcinoma (HNSCC).	sd-101	30-36	programmed cell death 1	Homo sapiens	114-118
34965944-1	2022	PURPOSE: To determine whether SD-101, a Toll-like receptor 9 agonist, potentiates the anti-tumor activity of anti-PD-1 antibodies in patients with anti-PD-1/PD-L1 naive, recurrent/metastatic head and neck squamous cell carcinoma (HNSCC).	sd-101	30-36	programmed cell death 1	Homo sapiens	152-156
34958422-2	2022	METHODS: 18F-FDG PET/CT images of 58 MM patients treated with anti-PD-1 or anti-CTLA-4 ICI were retrospectively analyzed for indication of irAE.	Fluorodeoxyglucose F18	9-16	programmed cell death 1	Homo sapiens	67-71
34933913-0	2022	Remodeling chondroitin-6-sulfate-mediated immune exclusion enhances anti-PD-1 response in colorectal cancer with microsatellite stability.	Chondroitin Sulfates	11-32	programmed cell death 1	Homo sapiens	73-77
34933913-5	2022	In vivo experiments with C-6-S-targeted strategies decreased M2 macrophages and reprogrammed the immunosuppressive TME, leading to enhanced response to anti-PD-1 in MSS CRC.	Chondroitin Sulfates	25-30	programmed cell death 1	Homo sapiens	157-161
34927389-4	2022	Consequently, sulfisoxazole effectively reinvigorates exhausted T cells, thereby eliciting robust antitumor effects in combination with anti-PD-1 antibody.	Sulfisoxazole	14-27	programmed cell death 1	Homo sapiens	141-145
34927389-5	2022	Overall, sulfisoxazole regulates immunosuppression through the inhibition of exosomal PD-L1, implying its potential to improve the response rate of anti-PD-1 antibodies.	Sulfisoxazole	9-22	programmed cell death 1	Homo sapiens	153-157
34942439-0	2022	Assessment of the albumin-bilirubin grade as a prognostic factor in patients with non-small-cell lung cancer receiving anti-PD-1-based therapy.	Bilirubin	26-35	programmed cell death 1	Homo sapiens	124-128
34944985-12	2021	A focus is made on the capacity of lactose and Gal-9 to modulate both the TIM-3/Gal-9 and PD-1/PD-L1 immune checkpoints in oncology.	Lactose	35-42	programmed cell death 1	Homo sapiens	90-94
34950838-2	2021	In skin cancers, as high TMB is mostly because of ultraviolet (UV) exposure, we hypothesized a correlation between the primary melanoma cutaneous location according to sun exposure and response to anti-PD-1 monotherapy.	1,2,4,5-tetramethoxybenzene	25-28	programmed cell death 1	Homo sapiens	202-206
34950838-3	2021	METHODS: The aim of this study was to analyze, in advanced melanoma, the relationship between TMB, locations according to sun exposure, and response to PD-1 inhibitors.	1,2,4,5-tetramethoxybenzene	94-97	programmed cell death 1	Homo sapiens	152-156
34950838-8	2021	Melanomas bearing a high TMB had a higher probability of response to PD-1 inhibitors compared with melanomas with a low TMB, with a dose-dependent effect following an exponential curve and a negative odds ratio of 0.40 (95% CI, 0.20 to 0.72, P = .004) between log-TMB and 6-month progression.	1,2,4,5-tetramethoxybenzene	25-28	programmed cell death 1	Homo sapiens	69-73
34950838-8	2021	Melanomas bearing a high TMB had a higher probability of response to PD-1 inhibitors compared with melanomas with a low TMB, with a dose-dependent effect following an exponential curve and a negative odds ratio of 0.40 (95% CI, 0.20 to 0.72, P = .004) between log-TMB and 6-month progression.	1,2,4,5-tetramethoxybenzene	264-267	programmed cell death 1	Homo sapiens	69-73
34914185-7	2022	Notably, a tumor microenvironment activatable prodrug nanoparticle is presented for triple-modality cancer therapy that functions by simultaneously activating ICD and altering the phenotype of TAMs when combined with PD-1 blockade therapy, which efficiently elicits a strong systemic antitumor immune response.	tams	193-197	programmed cell death 1	Homo sapiens	217-221
34855343-4	2021	The released alphaPD-L1 sequentially synergizes with PTX released in the cytoplasm for boosted chemoimmunotherapy due to direct killing of PTX and intensified immune responses through immunogenic cell death (ICD) as well as suppression of immune escape by blocking the PD-1/PD-L1 axis.	Paclitaxel	53-56	programmed cell death 1	Homo sapiens	269-273
34948129-3	2021	Oligosaccharides on PD-1/PD-L1 proteins are specifically fucosylated, leading to functional modifications.	Oligosaccharides	0-16	programmed cell death 1	Homo sapiens	20-24
34889232-6	2021	Herein, we designed clinical trial of co-administrating imatinib mesylate and pembrolizumab (anti-PD-1 antibody) to evaluate its safety and efficacy.	Imatinib Mesylate	56-73	programmed cell death 1	Homo sapiens	98-102
34889243-14	2021	LESSONS: Our case suggests that TACE combined with TKIs, PD-1 inhibitor, and RT may be a suitable treatment option for advanced HCC patients with IVC tumor thrombus and/or RA tumor thrombus, and/or adrenal gland metastasis.	Chlorotrianisene	32-36	programmed cell death 1	Homo sapiens	57-61
34866423-2	2022	We report the outcomes of using combination of programmed cell death protein-1 (PD-1) inhibitor and RT in the treatment of inoperable LA-cSCC.	la-cscc	134-141	programmed cell death 1	Homo sapiens	47-78
34866423-2	2022	We report the outcomes of using combination of programmed cell death protein-1 (PD-1) inhibitor and RT in the treatment of inoperable LA-cSCC.	la-cscc	134-141	programmed cell death 1	Homo sapiens	80-84
34520820-2	2021	This article reviews recent studies in a range of tumor types indicating novel functions for flubendazole in its control of processes associated with tumor growth, spread and renewal including ferroptosis, autophagy, cancer stem-like cell killing and suppression of intratumoral myeloid-derived suppressor cell accumulation and programmed cell death protein 1.	flubendazole	93-105	programmed cell death 1	Homo sapiens	328-359
34620772-5	2021	RECENT FINDINGS: PD-1/PD-L1 immune checkpoint inhibitors (ICIs) have demonstrated activity in the postplatinum and platinum-ineligible settings.	postplatinum	98-110	programmed cell death 1	Homo sapiens	17-21
34620772-5	2021	RECENT FINDINGS: PD-1/PD-L1 immune checkpoint inhibitors (ICIs) have demonstrated activity in the postplatinum and platinum-ineligible settings.	Platinum	115-123	programmed cell death 1	Homo sapiens	17-21
33975498-0	2021	Synergistic effect of the anti-PD-1 antibody with blood stable and reduction sensitive curcumin micelles on colon cancer.	Curcumin	87-95	programmed cell death 1	Homo sapiens	31-35
33975498-8	2021	Furthermore, Cur/DCMs exhibit synergistic anticancer efficacy when combined with the anti-PD-1 antibody in an MC-38 colon cancer xenograft model.	mc-38	110-115	programmed cell death 1	Homo sapiens	90-94
34887262-7	2021	We determined the efficacy of low-dose SN-38 or metformin in sensitizing unresponsive tumors to respond to anti-PD-1 therapy in a syngeneic tumor system.	Irinotecan	39-44	programmed cell death 1	Homo sapiens	112-116
34887262-7	2021	We determined the efficacy of low-dose SN-38 or metformin in sensitizing unresponsive tumors to respond to anti-PD-1 therapy in a syngeneic tumor system.	Metformin	48-57	programmed cell death 1	Homo sapiens	112-116
34767024-2	2021	Objective: To compare the effectiveness of the immune checkpoint inhibitors atezolizumab (programmed cell death ligand 1 inhibitor) and nivolumab (programmed cell death 1 inhibitor) and the chemotherapy drug docetaxel in patients with advanced NSCLC resistant to platinum-based chemotherapy.	Platinum	263-271	programmed cell death 1	Homo sapiens	147-170
34841741-4	2022	The photothermal MPNs were assembled via coordination between tannic acid (TA) and metal ion complex of Fe3+ /Mn2+ , through which a PD-L1 inhibiting DNAzyme (DZ) was loaded to regulate the immunosuppressive PD-1/PD-L1 pathway.	Tannins	62-73	programmed cell death 1	Homo sapiens	208-212
34841741-4	2022	The photothermal MPNs were assembled via coordination between tannic acid (TA) and metal ion complex of Fe3+ /Mn2+ , through which a PD-L1 inhibiting DNAzyme (DZ) was loaded to regulate the immunosuppressive PD-1/PD-L1 pathway.	Tannins	75-77	programmed cell death 1	Homo sapiens	208-212
34841741-4	2022	The photothermal MPNs were assembled via coordination between tannic acid (TA) and metal ion complex of Fe3+ /Mn2+ , through which a PD-L1 inhibiting DNAzyme (DZ) was loaded to regulate the immunosuppressive PD-1/PD-L1 pathway.	Metals	83-88	programmed cell death 1	Homo sapiens	208-212
34841741-4	2022	The photothermal MPNs were assembled via coordination between tannic acid (TA) and metal ion complex of Fe3+ /Mn2+ , through which a PD-L1 inhibiting DNAzyme (DZ) was loaded to regulate the immunosuppressive PD-1/PD-L1 pathway.	ferric sulfate	104-108	programmed cell death 1	Homo sapiens	208-212
34841741-4	2022	The photothermal MPNs were assembled via coordination between tannic acid (TA) and metal ion complex of Fe3+ /Mn2+ , through which a PD-L1 inhibiting DNAzyme (DZ) was loaded to regulate the immunosuppressive PD-1/PD-L1 pathway.	Manganese(2+)	110-114	programmed cell death 1	Homo sapiens	208-212
34838121-0	2021	Amplification of spatially isolated adenosine pathway by tumor-macrophage interaction induces anti-PD1 resistance in hepatocellular carcinoma.	Adenosine	36-45	programmed cell death 1	Homo sapiens	99-102
34792359-1	2021	In this work, we study the water-gas shift (WGS) reaction catalyzed by alpha-MoC(100) supported typical platinum group metal (PGM) single atoms (Rh1, Pd1, and Pt1) and Au1 via density functional theory calculations.	Water	27-32	programmed cell death 1	Homo sapiens	150-153
34792359-1	2021	In this work, we study the water-gas shift (WGS) reaction catalyzed by alpha-MoC(100) supported typical platinum group metal (PGM) single atoms (Rh1, Pd1, and Pt1) and Au1 via density functional theory calculations.	Platinum	104-112	programmed cell death 1	Homo sapiens	150-153
34792359-1	2021	In this work, we study the water-gas shift (WGS) reaction catalyzed by alpha-MoC(100) supported typical platinum group metal (PGM) single atoms (Rh1, Pd1, and Pt1) and Au1 via density functional theory calculations.	Metals	119-124	programmed cell death 1	Homo sapiens	150-153
34849012-16	2021	The PD-1 expression in the high TMB group showed higher.	1,2,4,5-tetramethoxybenzene	32-35	programmed cell death 1	Homo sapiens	4-8
34881181-9	2021	Animal experiments confirmed that metformin downregulated PD-L1 expression and that combination treatment with metformin and PD-1 inhibitors synergistically enhanced the antitumor response.	Metformin	34-43	programmed cell death 1	Homo sapiens	125-129
34803090-5	2021	Two RET-rearranged NSCLC patients experienced severe skin toxicity with alectinib after first undergoing anti-PD-1 antibody treatment with an ICI.	alectinib	72-81	programmed cell death 1	Homo sapiens	110-114
34797860-9	2021	Furthermore, TAMs positively and significantly correlated with PD-1 expression (p = 0.011), PD-L1 expression (p = 0.024), and tended to correlate with IDO expression (p = 0.078).	tams	13-17	programmed cell death 1	Homo sapiens	63-67
34830888-3	2021	In this retrospective study, TMB and PD-L1 were measured by commercially available methodologies and were correlated to demographics, outcome, and response to PD-1 inhibitors.	1,2,4,5-tetramethoxybenzene	29-32	programmed cell death 1	Homo sapiens	159-163
34610423-0	2021	Design, synthesis, and structure-activity relationship of PD-1/PD-L1 inhibitors with a benzo(d)isoxazole scaffold.	benzo(d)isoxazole	87-104	programmed cell death 1	Homo sapiens	58-62
34610423-2	2021	A novel series of compounds bearing a benzo(d)isoxazole scaffold was developed as PD-1/PD-L1 inhibitors, among them, compound P20 exhibited the most potent inhibitory activity, with an IC50 value of 26.8 nM.	benzo(d)isoxazole	38-55	programmed cell death 1	Homo sapiens	82-86
34767045-6	2021	Moreover, ex vivo PD-1 blockade could restore the cytolytic capacity of tumor-infiltrating CD8+CD103+ TRMs, and such anti-PD-1-mediated reinvigoration of CD8+CD103+ TRMs could be further enhanced by 4-1BB co-stimulation.	4-1bb	199-204	programmed cell death 1	Homo sapiens	18-22
34767045-6	2021	Moreover, ex vivo PD-1 blockade could restore the cytolytic capacity of tumor-infiltrating CD8+CD103+ TRMs, and such anti-PD-1-mediated reinvigoration of CD8+CD103+ TRMs could be further enhanced by 4-1BB co-stimulation.	4-1bb	199-204	programmed cell death 1	Homo sapiens	122-126
34844980-0	2022	Anlotinib induces a T cell-inflamed tumor microenvironment by facilitating vessel normalization and enhances the efficacy of PD1 checkpoint blockade in neuroblastoma.	anlotinib	0-9	programmed cell death 1	Homo sapiens	125-128
34858816-0	2021	Disulfiram Improves the Anti-PD-1 Therapy Efficacy by Regulating PD-L1 Expression via Epigenetically Reactivation of IRF7 in Triple Negative Breast Cancer.	Disulfiram	0-10	programmed cell death 1	Homo sapiens	29-33
34737267-3	2021	Here we show that a CD137/PD-1 bispecific antibody, IBI319, is able to overcome these limitations by coupling CD137 activation to PD-1-crosslinking.	ibi319	52-58	programmed cell death 1	Homo sapiens	26-30
34737267-3	2021	Here we show that a CD137/PD-1 bispecific antibody, IBI319, is able to overcome these limitations by coupling CD137 activation to PD-1-crosslinking.	ibi319	52-58	programmed cell death 1	Homo sapiens	130-134
34727963-11	2021	Grade >= 3 toxicities occurred in 23 patients (54.8%) in the anti-PD-1/TA + SBRT group, and in 21 patients (65.6%) in the anti-PD-1/TA alone group.	Tantalum	132-134	programmed cell death 1	Homo sapiens	127-131
34370219-0	2021	18F-FDG PET/CT for monitoring anti-PD-1 therapy in patients with non-small cell lung cancer using SUV harmonization of results obtained with various types of PET/CT scanners used at different centers.	Fluorodeoxyglucose F18	0-7	programmed cell death 1	Homo sapiens	35-39
34520751-0	2021	Thalidomide suppresses angiogenesis and immune evasion via lncRNA FGD5-AS1/miR-454-3p/ZEB1 axis-mediated VEGFA expression and PD-1/PD-L1 checkpoint in NSCLC.	Thalidomide	0-11	programmed cell death 1	Homo sapiens	126-130
34520751-17	2021	CONCLUSION: Thalidomide inhibits NSCLC angiogenesis and immune evasion via FGD5-AS1/miR-454-3p/ZEB1 axis-mediated regulation of VEGFA expression and PD-1/PD-L1 checkpoint.	Thalidomide	12-23	programmed cell death 1	Homo sapiens	149-153
34631053-14	2021	Overall, these cases may indicate that the immune adjuvant actions of immunomodulatory arabinomannan extracted from Mycobacterium tuberculosis improves the effect of PD-1 antibody treatments.	arabinomannan	87-100	programmed cell death 1	Homo sapiens	166-170
34899684-8	2021	Moreover, TMCs 4-8 were correlated with tumor mutation burden and expression of PD-1/PD-L1/CTLA4 in 33 cancers.	trimethylsilyl chloride	10-14	programmed cell death 1	Homo sapiens	80-84
34778042-4	2021	Interestingly, distinct clinical and pathological characteristics were observed that differed from those of the reported cases of severe cutaneous reactions induced by anti-PD-1 antibodies alone; thus, we speculate that it was induced by the combination of camrelizumab and apatinib.	apatinib	274-282	programmed cell death 1	Homo sapiens	173-177
34853812-10	2021	The immunosuppression markers including PDCD1, TIGIT, LAG3, and HAVCR2 were significantly upregulated in the T cells bearing a high glucose uptake signature score.	Glucose	132-139	programmed cell death 1	Homo sapiens	40-45
34702832-2	2021	In this work, two types of atomically dispersed Pd species stabilized on the defect-rich nanodiamond-graphene (ND@G) hybrid support: single Pd atoms (Pd1/ND@G) and fully exposed Pd clusters with average three Pd atoms (Pdn/ND@G), were fabricated.	Palladium	48-50	programmed cell death 1	Homo sapiens	150-153
34702832-4	2021	The Pd1/ND@G catalyst preferentially generates secondary amines (Turnover frequency (TOF@333 K 709 h-1, selectivity >98%), while the Pdn/ND@G catalyst exhibits high selectivity towards primary amines (TOF@313 K 543 h-1, selectivity >98%) under mild reaction conditions.	Amines	57-63	programmed cell death 1	Homo sapiens	4-7
34702832-4	2021	The Pd1/ND@G catalyst preferentially generates secondary amines (Turnover frequency (TOF@333 K 709 h-1, selectivity >98%), while the Pdn/ND@G catalyst exhibits high selectivity towards primary amines (TOF@313 K 543 h-1, selectivity >98%) under mild reaction conditions.	Amines	193-199	programmed cell death 1	Homo sapiens	4-7
34702832-5	2021	Detailed characterizations and density functional theory (DFT) calculations show that the structure of atomically dispersed Pd catalysts governs the dissociative adsorption pattern of H2 and also the hydrogenation pathway of the benzylideneimine (BI) intermediate, resulting in different product selectivity over Pd1/ND@G and Pdn/ND@G, respectively.	Deuterium	184-186	programmed cell death 1	Homo sapiens	313-316
34702832-5	2021	Detailed characterizations and density functional theory (DFT) calculations show that the structure of atomically dispersed Pd catalysts governs the dissociative adsorption pattern of H2 and also the hydrogenation pathway of the benzylideneimine (BI) intermediate, resulting in different product selectivity over Pd1/ND@G and Pdn/ND@G, respectively.	benzylideneimine	229-245	programmed cell death 1	Homo sapiens	313-316
34832863-0	2021	EGCG Inhibits Tumor Growth in Melanoma by Targeting JAK-STAT Signaling and Its Downstream PD-L1/PD-L2-PD1 Axis in Tumors and Enhancing Cytotoxic T-Cell Responses.	epigallocatechin gallate	0-4	programmed cell death 1	Homo sapiens	102-105
34832863-8	2021	Dissimilar to anti-PD-1 treatment that blocks PD-1/PD-L1 interaction, EGCG inhibited JAK/STAT signaling and PD-L1 expression in tumor cells, leading to the re-activation of T cells.	epigallocatechin gallate	70-74	programmed cell death 1	Homo sapiens	19-23
34702832-5	2021	Detailed characterizations and density functional theory (DFT) calculations show that the structure of atomically dispersed Pd catalysts governs the dissociative adsorption pattern of H2 and also the hydrogenation pathway of the benzylideneimine (BI) intermediate, resulting in different product selectivity over Pd1/ND@G and Pdn/ND@G, respectively.	Bismuth	247-249	programmed cell death 1	Homo sapiens	313-316
34832863-8	2021	Dissimilar to anti-PD-1 treatment that blocks PD-1/PD-L1 interaction, EGCG inhibited JAK/STAT signaling and PD-L1 expression in tumor cells, leading to the re-activation of T cells.	epigallocatechin gallate	70-74	programmed cell death 1	Homo sapiens	46-50
34760687-10	2021	Moreover, we found that PD-1 and PD-L1 were dramatically upregulated in a subset of high-risk patients with abundant M2 and Treg infiltration, implying these patients may benefit from anti-PD-1 and PD-L1 immunotherapy.	treg	124-128	programmed cell death 1	Homo sapiens	24-28
34650975-10	2021	Calcium-related risk scores were significantly associated with characteristic clinical features, immune infiltrating signatures of tumor microenvironment, and exhausted T cell markers including programmed cell death 1 (PD-1), lymphocyte activating 3 (LAG3), and T cell membrane protein 3 (TIM-3), which contribute to an adverse therapeutic effect of immunotherapy.	Calcium	0-7	programmed cell death 1	Homo sapiens	194-217
34649778-2	2022	In this study, we aimed to investigate whether pre-treatment magnetic resonance imaging (MRI) features and MRI-based nomogram could predict the risk of disease progression of unresectable HCC after first-line lenvatinib/anti-PD-1 antibody therapy.	lenvatinib	209-219	programmed cell death 1	Homo sapiens	225-229
34692478-3	2021	Our research investigated the relationship between pretreatment LIPI and the prognosis of patients receiving first-line PD-1/PD-L1 inhibitors plus chemotherapy.	lipi	64-68	programmed cell death 1	Homo sapiens	120-124
34692478-11	2021	Subgroup analysis showed that pretreatment LIPI good was associated with better PFS and OS in males, extensive disease (ED), PD-1 inhibitor treatment, smokers, and liver metastasis (p < 0.05).	lipi	43-47	programmed cell death 1	Homo sapiens	125-129
34692478-12	2021	Conclusions: Pretreatment LIPI could serve as a prognostic biomarker for advanced SCLC patients receiving first-line PD-1/PD-L1 inhibitors plus chemotherapy.	lipi	26-30	programmed cell death 1	Homo sapiens	117-121
34692475-17	2021	Conclusions: The preliminary data showed that the combination of anlotinib and anti-PD-1 antibodies demonstrated promising durable antitumor efficacy with acceptable toxicity in patients with various advance tumors, and promoted favorable changes in serum IL-2, IL-4, IL-10, TNF-alpha, IFN-gamma levels and circulating immune cell subsets in clinical responders.	anlotinib	65-74	programmed cell death 1	Homo sapiens	84-88
34545738-1	2021	In this study, we loaded Pd catalysts onto a reduced graphene oxide (rGO) support in an atomically dispersed fashion (i.e., Pd single-atom catalysts (SACs) on rGO or Pd1/rGO) via a facile and scalable synthesis based on anchor-site and photoreduction techniques.	graphene oxide	53-67	programmed cell death 1	Homo sapiens	166-169
34545738-2	2021	The as-synthesized Pd1/rGO significantly outperformed the Pd nanoparticle (Pdnano) counterparts in the electrocatalytic hydrodechlorination of chlorinated phenols.	chlorinated phenols	143-162	programmed cell death 1	Homo sapiens	19-22
34545738-5	2021	Characterization and experimental results demonstrate that the superior performance of Pd1/rGO originates from (1) enhanced interfacial electron transfer through Pd-O bonds due to the electronic metal-support interaction and (2) increased atomic H (H*) utilization efficiency by inhibiting H2 evolution on Pd1.	Metals	195-200	programmed cell death 1	Homo sapiens	87-90
34545738-5	2021	Characterization and experimental results demonstrate that the superior performance of Pd1/rGO originates from (1) enhanced interfacial electron transfer through Pd-O bonds due to the electronic metal-support interaction and (2) increased atomic H (H*) utilization efficiency by inhibiting H2 evolution on Pd1.	Deuterium	290-292	programmed cell death 1	Homo sapiens	87-90
34545738-5	2021	Characterization and experimental results demonstrate that the superior performance of Pd1/rGO originates from (1) enhanced interfacial electron transfer through Pd-O bonds due to the electronic metal-support interaction and (2) increased atomic H (H*) utilization efficiency by inhibiting H2 evolution on Pd1.	Deuterium	290-292	programmed cell death 1	Homo sapiens	306-309
34676181-1	2021	Background: Lenvatinib (LEN) combined with anti-PD-1 antibodies (PD-1) exerted promising effects on unresectable hepatocellular carcinoma (uHCC).	lenvatinib	12-22	programmed cell death 1	Homo sapiens	48-52
34676181-1	2021	Background: Lenvatinib (LEN) combined with anti-PD-1 antibodies (PD-1) exerted promising effects on unresectable hepatocellular carcinoma (uHCC).	lenvatinib	12-22	programmed cell death 1	Homo sapiens	65-69
34339918-10	2021	PD-1 antibody and BMS-1 were each successfully conjugated to decellularized rat thoracic artery patches, respectively, by hyaluronic acid.	Hyaluronic Acid	122-137	programmed cell death 1	Homo sapiens	0-4
34547581-1	2021	BACKGROUND: In preclinical studies trifluridine/tipiracil (FTD/TPI) plus oxaliplatin (Industriestrasse, Holzkirchen, Germany) sensitised microsatellite stable (MSS) metastatic colorectal cancer (mCRC) to anti-programmed cell death protein-1; the addition of oxaliplatin or bevacizumab (F Hoffmann- la ROCHE AG, Kaiseraugst, Switzerland) enhanced the antitumour effects of FTD/TPI.	Trifluridine	35-47	programmed cell death 1	Homo sapiens	209-240
34547581-1	2021	BACKGROUND: In preclinical studies trifluridine/tipiracil (FTD/TPI) plus oxaliplatin (Industriestrasse, Holzkirchen, Germany) sensitised microsatellite stable (MSS) metastatic colorectal cancer (mCRC) to anti-programmed cell death protein-1; the addition of oxaliplatin or bevacizumab (F Hoffmann- la ROCHE AG, Kaiseraugst, Switzerland) enhanced the antitumour effects of FTD/TPI.	tipiracil	48-57	programmed cell death 1	Homo sapiens	209-240
34547581-1	2021	BACKGROUND: In preclinical studies trifluridine/tipiracil (FTD/TPI) plus oxaliplatin (Industriestrasse, Holzkirchen, Germany) sensitised microsatellite stable (MSS) metastatic colorectal cancer (mCRC) to anti-programmed cell death protein-1; the addition of oxaliplatin or bevacizumab (F Hoffmann- la ROCHE AG, Kaiseraugst, Switzerland) enhanced the antitumour effects of FTD/TPI.	Oxaliplatin	73-84	programmed cell death 1	Homo sapiens	209-240
34414762-9	2021	Our research demonstrated that simultaneous inhibition of ER stress and oxidative stress could effectively repolarize M2-TAMs under hypoxia, which not only filled the current gap in regulating the biological repolarization of macrophages under hypoxia but provided a meaningful reference for the clinical immunotherapy of sensitized anti-PD-1.	m2-tams	118-125	programmed cell death 1	Homo sapiens	338-342
34581869-9	2022	Mechanistically, CpG-2722 shaped a tumor microenvironment that is favorable for the action of anti-PD-1, which included promoting the expression of different cytokines such as IL-12, IFN-beta, and IFN-gamma, and increasing the presence of plasmacytoid dendritic cells, M1 macrophages, and CD8 positive T cells.	cpg-2722	17-25	programmed cell death 1	Homo sapiens	99-103
34662227-4	2021	After this interaction, the immunoreceptor tyrosine-based inhibition motif/switch motif (ITIM/ITSM) containing PD-1 domain present in the CRASH-IT switch induces robust inhibition of T cell signaling, and CRASH-IT-mediated suppression of T cell activity can be reversed by small molecule-induced switch proteolysis.	Tyrosine	43-51	programmed cell death 1	Homo sapiens	111-115
34133404-7	2021	Taken together, these data suggest that DFMO might represent a potential immunomodulatory agent that can enhance current PD-1-based checkpoint therapies.	Eflornithine	40-44	programmed cell death 1	Homo sapiens	121-125
34385682-4	2021	We demonstrate that sphingomyelin-derived camptothecin nanovesicles (camptothesomes) elicit potent granzyme-B- and perforin-mediated cytotoxic T lymphocyte (CTL) responses, potentiating PD-L1/PD-1 co-blockade to eradicate subcutaneous MC38 adenocarcinoma with developed memory immunity.	Sphingomyelins	20-33	programmed cell death 1	Homo sapiens	192-196
34385682-4	2021	We demonstrate that sphingomyelin-derived camptothecin nanovesicles (camptothesomes) elicit potent granzyme-B- and perforin-mediated cytotoxic T lymphocyte (CTL) responses, potentiating PD-L1/PD-1 co-blockade to eradicate subcutaneous MC38 adenocarcinoma with developed memory immunity.	Camptothecin	42-54	programmed cell death 1	Homo sapiens	192-196
34650975-10	2021	Calcium-related risk scores were significantly associated with characteristic clinical features, immune infiltrating signatures of tumor microenvironment, and exhausted T cell markers including programmed cell death 1 (PD-1), lymphocyte activating 3 (LAG3), and T cell membrane protein 3 (TIM-3), which contribute to an adverse therapeutic effect of immunotherapy.	Calcium	0-7	programmed cell death 1	Homo sapiens	219-223
34506118-8	2021	An excellent therapeutic effect is achieved when the immune checkpoint PD-1 antibody (aPD-1) is utilized to cooperate with the PEG/PEI/CAD NPs for blocking tumor immune escape and maintaining antitumor activity of the ICD-instigated T cells.	Polyethylene Glycols	127-130	programmed cell death 1	Homo sapiens	71-75
34506118-8	2021	An excellent therapeutic effect is achieved when the immune checkpoint PD-1 antibody (aPD-1) is utilized to cooperate with the PEG/PEI/CAD NPs for blocking tumor immune escape and maintaining antitumor activity of the ICD-instigated T cells.	Polyethyleneimine	131-134	programmed cell death 1	Homo sapiens	71-75
34506118-8	2021	An excellent therapeutic effect is achieved when the immune checkpoint PD-1 antibody (aPD-1) is utilized to cooperate with the PEG/PEI/CAD NPs for blocking tumor immune escape and maintaining antitumor activity of the ICD-instigated T cells.	CyADIC regimen	135-138	programmed cell death 1	Homo sapiens	71-75
34552135-1	2021	Our aim was to analyse whether biomarkers extracted from baseline 18F-FDG PET before anti-PD1 treatment contribute to prognostic survival information for early risk stratification in metastatic melanoma.	Fluorodeoxyglucose F18	66-73	programmed cell death 1	Homo sapiens	90-93
34403371-7	2021	In contrast, the more immunogenic and highly mutated GL261 model responded best to anti-PD-1 and anti-CTLA-4 therapy and more modestly to BAL101553 and anti-CD40 combination.	gl261	53-58	programmed cell death 1	Homo sapiens	88-92
34117723-0	2021	Identification of the FDA-approved drug Pyrvinium as a small-molecule inhibitor of PD-1/PD-L1 interaction.	pyrvinium	40-49	programmed cell death 1	Homo sapiens	83-87
34544358-5	2021	RESULTS: In the GSE51032 dataset, cg06291111 (PDCD-1) and cg10191002 (LAG-3) were screened as the candidate CpG sites for the following study.	cg06291111	34-44	programmed cell death 1	Homo sapiens	46-52
34572586-0	2021	Dual Blockade of Lactate/GPR81 and PD-1/PD-L1 Pathways Enhances the Anti-Tumor Effects of Metformin.	Metformin	90-99	programmed cell death 1	Homo sapiens	35-39
34572586-6	2021	In addition, considering that 3-OBA could recover the inhibitory effects of metformin on PD-1 expression, we further determined the dual blockade effects of PD-1/PD-L1 and lactate/GPR81 on the antitumor activity of metformin.	3-oba	30-35	programmed cell death 1	Homo sapiens	89-93
34572586-6	2021	In addition, considering that 3-OBA could recover the inhibitory effects of metformin on PD-1 expression, we further determined the dual blockade effects of PD-1/PD-L1 and lactate/GPR81 on the antitumor activity of metformin.	3-oba	30-35	programmed cell death 1	Homo sapiens	157-161
34572586-6	2021	In addition, considering that 3-OBA could recover the inhibitory effects of metformin on PD-1 expression, we further determined the dual blockade effects of PD-1/PD-L1 and lactate/GPR81 on the antitumor activity of metformin.	Metformin	76-85	programmed cell death 1	Homo sapiens	89-93
34572586-6	2021	In addition, considering that 3-OBA could recover the inhibitory effects of metformin on PD-1 expression, we further determined the dual blockade effects of PD-1/PD-L1 and lactate/GPR81 on the antitumor activity of metformin.	Metformin	76-85	programmed cell death 1	Homo sapiens	157-161
34572586-6	2021	In addition, considering that 3-OBA could recover the inhibitory effects of metformin on PD-1 expression, we further determined the dual blockade effects of PD-1/PD-L1 and lactate/GPR81 on the antitumor activity of metformin.	Metformin	215-224	programmed cell death 1	Homo sapiens	89-93
34572586-6	2021	In addition, considering that 3-OBA could recover the inhibitory effects of metformin on PD-1 expression, we further determined the dual blockade effects of PD-1/PD-L1 and lactate/GPR81 on the antitumor activity of metformin.	Metformin	215-224	programmed cell death 1	Homo sapiens	157-161
34117723-7	2021	It is noteworthy that Pyrvinium, being an approved drug, may prove especially suitable as a good starting point for further medicinal chemistry efforts, leading to design and development of even more potent structural analogs as selective PD-1/PD-L1 inhibitors.	pyrvinium	22-31	programmed cell death 1	Homo sapiens	239-243
34296473-3	2021	Here, it is demonstrated that 2D black phosphorus (BP) acts as giant phosphorus (P) ligand to confine a high density of single atoms (e.g., Pd1 , Pt1 ) via atomic layer deposition.	Phosphorus	51-53	programmed cell death 1	Homo sapiens	140-143
34572736-8	2021	Beyond its well-known pleiotropic effects, RSV affects PD-L1 and PD-1 expression as well as PD-L1 subcellular localization and post-translational modifications, which we review here.	Resveratrol	43-46	programmed cell death 1	Homo sapiens	65-69
34572736-10	2021	Finally, we discuss their potential use in combination with chemotherapies, and, using RSV as a model, we propose polyphenols as adjuvants to enhance the efficacy of anti-PD-1/anti-PD-L1 immunotherapies.	Polyphenols	114-125	programmed cell death 1	Homo sapiens	171-175
34488792-5	2021	RESULTS: Nano-DOX were first shown to stimulate the tumor cells and the TAMs to release the cytokine HMGB1 which, regardless of its source, acted through the RAGE/NF-kappaB pathway to induce PD-L1 in the tumor cells and PD-L1/PD-1 in the TAMs.	Doxorubicin	14-17	programmed cell death 1	Homo sapiens	226-230
34488792-7	2021	Then, BMS-1 was shown to enhance Nano-DOX-stimulated M1-type activation of TAMs both by blocking Nano-DOX-induced PD-L1 in the TAMs and by blocking tumor cell PD-L1 ligation with TAM PD-1.	Doxorubicin	38-41	programmed cell death 1	Homo sapiens	183-187
34488792-7	2021	Then, BMS-1 was shown to enhance Nano-DOX-stimulated M1-type activation of TAMs both by blocking Nano-DOX-induced PD-L1 in the TAMs and by blocking tumor cell PD-L1 ligation with TAM PD-1.	tams	75-79	programmed cell death 1	Homo sapiens	183-187
34488792-11	2021	CONCLUSIONS: PD-L1/PD-1 upregulation mediated by autocrine and paracrine activation of the HMGB1/RAGE/NF-kappaB signaling is a key response of lung cancer cells and their TAMs to stress, which can be induced by Nano-DOX.	Doxorubicin	216-219	programmed cell death 1	Homo sapiens	19-23
34477160-8	2021	LESSON: Our case report suggests that the use of anti-PD-1 therapy does show efficacy in the treatment of PPA and may provide a viable treatment option for patients.	ppa	106-109	programmed cell death 1	Homo sapiens	54-58
34296473-3	2021	Here, it is demonstrated that 2D black phosphorus (BP) acts as giant phosphorus (P) ligand to confine a high density of single atoms (e.g., Pd1 , Pt1 ) via atomic layer deposition.	Phosphorus	69-79	programmed cell death 1	Homo sapiens	140-143
34296473-5	2021	Metallic Pd1 /BP SAC shows a highly selective semi-hydrogenation of phenylacetylene toward styrene, distinct from metallic Pd nanoparticles that facilitate the formation of fully hydrogenated products.	phenylacetylene	68-83	programmed cell death 1	Homo sapiens	9-12
34296473-5	2021	Metallic Pd1 /BP SAC shows a highly selective semi-hydrogenation of phenylacetylene toward styrene, distinct from metallic Pd nanoparticles that facilitate the formation of fully hydrogenated products.	Styrene	91-98	programmed cell death 1	Homo sapiens	9-12
34628927-6	2021	CONCLUSIONS: Anti PD-1/L1 blockade combined with therapeutic approaches is safe and effective in BC, in particular for PD-L1 antibody atezolizumab plus nab-paclitaxel by inducing PD-1/L1 expression and the number of cytotoxic T cells.	Paclitaxel	156-166	programmed cell death 1	Homo sapiens	18-22
34628927-6	2021	CONCLUSIONS: Anti PD-1/L1 blockade combined with therapeutic approaches is safe and effective in BC, in particular for PD-L1 antibody atezolizumab plus nab-paclitaxel by inducing PD-1/L1 expression and the number of cytotoxic T cells.	Paclitaxel	156-166	programmed cell death 1	Homo sapiens	179-183
34413168-5	2021	Cytotoxic drugs, crude tobacco products, benzo(a)pyrene, nicotine, and multiple other toxic compounds were shown to exhibit rapid PD-L1/PD-1 upregulation.	Benzo(a)pyrene	41-55	programmed cell death 1	Homo sapiens	136-140
34153830-10	2021	In network meta-analyses, pembrolizumab plus lenvatinib seemed the worst tolerated anti-PD-1 combination therapy.	lenvatinib	45-55	programmed cell death 1	Homo sapiens	88-92
34371308-0	2021	Corrigendum to "RECIST 1.1, Choi and mChoi criteria in the evaluation of tumor response in patients with metastatic colorectal cancer treated with Regorafenib and anti-PD-1 antibody" (Eur.	regorafenib	147-158	programmed cell death 1	Homo sapiens	168-172
34224361-3	2021	Nonetheless, intratumoral injection of NDVmuGM-CSF conferred antitumor effects in three syngeneic models in vivo; with efficacy further augmented by concomitant treatment with anti-PD-1/L-1 or T cell agonists.	ndvmugm-csf	39-50	programmed cell death 1	Homo sapiens	181-185
34512366-6	2021	Anti-PD-1 and anti-PD-L1 antibodies increase KCa3.1 and Kv1.3 function in CD8+ PBTs of HNSCC patients.	pbts	79-83	programmed cell death 1	Homo sapiens	5-9
34433253-0	2021	Combination of Chidamide-Mediated Epigenetic Modulation with Immunotherapy: Boosting Tumor Immunogenicity and Response to PD-1/PD-L1 Blockade.	N-(2-amino-5-fluorobenzyl)-4-(N-(pyridine-3-acrylyl)aminomethyl)benzamide	15-24	programmed cell death 1	Homo sapiens	122-126
34502071-0	2021	Allicin May Promote Reversal of T-Cell Dysfunction in Periodontitis via the PD-1 Pathway.	allicin	0-7	programmed cell death 1	Homo sapiens	76-80
34442054-10	2021	CONCLUSIONS: Patients administered systemic steroids for irAEs due to PD-1 blockade treatment exhibited shorter PFS than those who were not.	Steroids	44-52	programmed cell death 1	Homo sapiens	70-74
34442054-11	2021	Systemic steroids might affect survival after PD-1 blockade even for patients who once acquired its clinical benefit.	Steroids	9-17	programmed cell death 1	Homo sapiens	46-50
34456725-6	2021	Conclusion: Compared with the docetaxel chemotherapy regimen, the anti-PD-1/PD-L1 Inhibitors has certain advantages in terms of efficacy and safety.	Docetaxel	30-39	programmed cell death 1	Homo sapiens	71-75
34434936-5	2021	Here we discover that fucoidan-supplemented diet significantly improves the antitumor activities of PD-1 antibodies in vivo.	fucoidan	22-30	programmed cell death 1	Homo sapiens	100-104
34434936-6	2021	Specifically, fucoidan as a dietary ingredient strongly inhibits tumor growth when co-administrated with PD-1 antibodies, which effects can be further strengthened when fucoidan is applied before PD-1 treatments.	fucoidan	14-22	programmed cell death 1	Homo sapiens	105-109
34434936-6	2021	Specifically, fucoidan as a dietary ingredient strongly inhibits tumor growth when co-administrated with PD-1 antibodies, which effects can be further strengthened when fucoidan is applied before PD-1 treatments.	fucoidan	14-22	programmed cell death 1	Homo sapiens	196-200
34434936-6	2021	Specifically, fucoidan as a dietary ingredient strongly inhibits tumor growth when co-administrated with PD-1 antibodies, which effects can be further strengthened when fucoidan is applied before PD-1 treatments.	fucoidan	169-177	programmed cell death 1	Homo sapiens	105-109
34362362-1	2021	BACKGROUND: This study aimed to investigate, if different physiological concentrations of vitamin D (25(OH)D3) and single nucleotide polymorphisms in vitamin D receptor (VDR) gene have an impact on gene expression in human periodontal ligament (hPDL) fibroblasts induced by simulated orthodontic compressive strain.	Vitamin D	90-99	programmed cell death 1	Homo sapiens	245-249
34581869-10	2022	Overall, CpG-2722 provided a priming effect for CD8 positive T cells by sharpening the tumor microenvironment, whereas anti-PD-1 released the brake for their tumor-killing effect, resulting in an enhanced efficacy of the combined CpG-2722 and anti-PD-1.	cpg-2722	9-17	programmed cell death 1	Homo sapiens	248-252
34581869-10	2022	Overall, CpG-2722 provided a priming effect for CD8 positive T cells by sharpening the tumor microenvironment, whereas anti-PD-1 released the brake for their tumor-killing effect, resulting in an enhanced efficacy of the combined CpG-2722 and anti-PD-1.	cpg-2722	230-238	programmed cell death 1	Homo sapiens	124-128
34512388-15	2021	Osteoblasts showed significantly reduced opg expression in the presence of supernatant derived of hPDL fibroblasts treated with autophagy inhibitor and sIL-6R.	sil-6r	152-158	programmed cell death 1	Homo sapiens	98-102
34950184-0	2021	Higher Enhancement Intrahepatic Nodules on the Hepatobiliary Phase of Gd-EOB-DTPA-Enhanced MRI as a Poor Responsive Marker of Anti-PD-1/PD-L1 Monotherapy for Unresectable Hepatocellular Carcinoma.	gadolinium ethoxybenzyl DTPA	70-81	programmed cell death 1	Homo sapiens	131-135
34950184-11	2021	Conclusion: The TTnP on HCC nodules with higher enhancement and the median PFS in patients who carried higher enhancement intrahepatic HCC nodules were significantly shorter than those in hypointense HCC nodules with anti-PD-1/PD-L1 monotherapy.	ttnp	16-20	programmed cell death 1	Homo sapiens	222-226
34950184-12	2021	The intensity of the nodule on the hepatobiliary phase of Gd-EOB-DTPA-enhanced MRI is a promising imaging biomarker for predicting unfavorable response with anti-PD-1/PD-L1 monotherapy in patients with HCC.	gadolinium ethoxybenzyl DTPA	58-69	programmed cell death 1	Homo sapiens	162-166
34289694-13	2021	Finally, liposome-formulated resiquimod significantly enhanced the efficacy of PD1 blockade against syngeneic ovarian tumors.	resiquimod	29-39	programmed cell death 1	Homo sapiens	79-82
34434611-5	2021	Individual responses to PD-1 inhibition were found ex vivo and combination with chemotherapy or t-lymphocyte activation led to enhanced antitumoral effects in PDTCs.	prolinedithiocarbamate	159-164	programmed cell death 1	Homo sapiens	24-28
34396984-5	2021	Entinostat promoted a T cell-inflamed phenotype and had substantial antitumor efficacy when used in combination with anti-PD-1 therapy.	entinostat	0-10	programmed cell death 1	Homo sapiens	122-126
34413168-5	2021	Cytotoxic drugs, crude tobacco products, benzo(a)pyrene, nicotine, and multiple other toxic compounds were shown to exhibit rapid PD-L1/PD-1 upregulation.	Nicotine	57-65	programmed cell death 1	Homo sapiens	136-140
34584855-2	2021	We performed a prospective study to investigate the effect of CCS on treatment outcomes in patients with non-oncogene driven metastatic non-small cell lung cancer (NSCLC) undergoing therapy with programmed cell death protein 1 (PD-1)/programmed death ligand 1 (PD-L1) inhibitors.	ovex	62-65	programmed cell death 1	Homo sapiens	228-232
34326162-3	2021	In the dose-escalation part of this phase 1b study, vidutolimod was administered intratumorally at escalating doses with intravenous pembrolizumab to 44 patients with advanced melanoma who had progressive disease or stable disease on prior anti-PD-1 therapy.	vidutolimod	52-63	programmed cell death 1	Homo sapiens	245-249
34368325-4	2021	The aim of this case report is to evaluate the combination approach of low-dose decitabine plus a PD-1 inhibitor in relapsed/ refractory cHL patients with prior PD-1 inhibitor exposure.	Decitabine	80-90	programmed cell death 1	Homo sapiens	161-165
34458266-7	2021	In addition, we identified 31 DMEGs that were able to distinguish PD-1-negative samples from normal samples.	dmegs	30-35	programmed cell death 1	Homo sapiens	66-70
34307420-0	2021	Case Report: PD-1 Blockade Combined Autologous Hematopoietic Stem Cell Transplantation With Modified BEAM Regimen Containing High-Dose Cytarabine to Treat R/R Hodgkin"s Lymphoma.	Cytarabine	135-145	programmed cell death 1	Homo sapiens	13-17
34295326-9	2021	We reviewed responses for patients with chemotherapy, decitabine or everolimus combination therapies with PD-1 antibodies, and found that PD-1 antibody combined with decitabine showed potential efficacy in pediatric patients with advanced embryonal rhabdomyosarcoma and lymphoepitheliomatoid-like carcinoma.	Decitabine	54-64	programmed cell death 1	Homo sapiens	106-110
34295326-9	2021	We reviewed responses for patients with chemotherapy, decitabine or everolimus combination therapies with PD-1 antibodies, and found that PD-1 antibody combined with decitabine showed potential efficacy in pediatric patients with advanced embryonal rhabdomyosarcoma and lymphoepitheliomatoid-like carcinoma.	Everolimus	68-78	programmed cell death 1	Homo sapiens	138-142
34295341-6	2021	The results of in vivo experiments show that chloroquine can increase the expression of PD-1 in tumor tissues.	Chloroquine	45-56	programmed cell death 1	Homo sapiens	88-92
34295341-8	2021	The mechanism underlying this phenomenon is the occurrence of chloroquine-induced apoptosis and the effective immune response caused by the attenuated Salmonella carrying PD-1 siRNA.	Chloroquine	62-73	programmed cell death 1	Homo sapiens	171-175
34230109-4	2021	RESULTS: Functional evaluation using effector cells expressing both 4-1BB and PD-1 revealed superior biological activity of ABL503 compared with the combination of each monoclonal antibody.	abl503	124-130	programmed cell death 1	Homo sapiens	78-82
34301816-3	2021	We determined whether changes in 3"-deoxy-3"-(18F)-fluorothymidine (18F-FLT) PET parameters before and soon after treatment initiation predicted the therapeutic effect of anti-PD-1 antibody.	alovudine	33-66	programmed cell death 1	Homo sapiens	176-180
34084221-5	2021	The programmed cell death ligand 1 (PD-L1) and programmed cell death protein 1 (PD1) expression before TACE treatment were significantly higher in patients with poor TACE response compared with those patients with well response.	Chlorotrianisene	103-107	programmed cell death 1	Homo sapiens	47-78
34084221-5	2021	The programmed cell death ligand 1 (PD-L1) and programmed cell death protein 1 (PD1) expression before TACE treatment were significantly higher in patients with poor TACE response compared with those patients with well response.	Chlorotrianisene	103-107	programmed cell death 1	Homo sapiens	80-83
34084221-5	2021	The programmed cell death ligand 1 (PD-L1) and programmed cell death protein 1 (PD1) expression before TACE treatment were significantly higher in patients with poor TACE response compared with those patients with well response.	Chlorotrianisene	166-170	programmed cell death 1	Homo sapiens	47-78
34084221-5	2021	The programmed cell death ligand 1 (PD-L1) and programmed cell death protein 1 (PD1) expression before TACE treatment were significantly higher in patients with poor TACE response compared with those patients with well response.	Chlorotrianisene	166-170	programmed cell death 1	Homo sapiens	80-83
34084221-7	2021	After TACE treatment, the proportion of CD4+/CD8+ cells were decreased while the expression levels of programmed cell death protein 1 (PD1) were significantly increased.	Chlorotrianisene	6-10	programmed cell death 1	Homo sapiens	102-133
34084221-7	2021	After TACE treatment, the proportion of CD4+/CD8+ cells were decreased while the expression levels of programmed cell death protein 1 (PD1) were significantly increased.	Chlorotrianisene	6-10	programmed cell death 1	Homo sapiens	135-138
34084221-9	2021	The expression levels of PD1 and PD-L1 were closely related to the therapeutic effect of TACE and the prognosis of patients with HCC.	Chlorotrianisene	89-93	programmed cell death 1	Homo sapiens	25-28
34188068-0	2021	YIV-906 potentiated anti-PD1 action against hepatocellular carcinoma by enhancing adaptive and innate immunity in the tumor microenvironment.	yiv-906	0-7	programmed cell death 1	Homo sapiens	25-28
34146911-3	2021	METHOD: We retrospectively recruited patients treated with Regorafenib and anti-PD-1 antibody in a single institution.	regorafenib	59-70	programmed cell death 1	Homo sapiens	80-84
34221914-11	2021	When PD-1/PD-L1 was activated, the glycogen uptake rate and expression levels of Glut1, HK2, and PKM2 showed a decreasing trend (ACLF+PD-1 group compared to ACLF group , all p<0.05).	Glycogen	35-43	programmed cell death 1	Homo sapiens	5-9
34221914-11	2021	When PD-1/PD-L1 was activated, the glycogen uptake rate and expression levels of Glut1, HK2, and PKM2 showed a decreasing trend (ACLF+PD-1 group compared to ACLF group , all p<0.05).	Glycogen	35-43	programmed cell death 1	Homo sapiens	129-138
34170847-8	2021	PD-1 antibody or BMS-1 was successfully conjugated to the decellularized rat thoracic artery patch by hyaluronic acid with altered morphology and reduced the water contact angle (WCA).	Hyaluronic Acid	102-117	programmed cell death 1	Homo sapiens	0-4
34170847-8	2021	PD-1 antibody or BMS-1 was successfully conjugated to the decellularized rat thoracic artery patch by hyaluronic acid with altered morphology and reduced the water contact angle (WCA).	Water	158-163	programmed cell death 1	Homo sapiens	0-4
34239776-8	2021	IBI323 bound to PD-L1 and LAG-3 with similar potency as its parental antibodies and blocked the interaction of PD-1/PD-L1, CD80/PD-L1, and LAG-3/MHC-II.	ibi323	0-6	programmed cell death 1	Homo sapiens	111-115
34207286-7	2021	In fact, clinical evidence has verified that TAMs, representing up to 50% of the tumor mass, exert both protumor and immunosuppressive effects in promoting tumor metastasis through secretion of interleukin 10 (IL10), transforming growth factor beta (TGFbeta), and VEGF, expression of PD-1 and consumption of arginine to inhibit T cell anti-tumor function.	tams	45-49	programmed cell death 1	Homo sapiens	284-288
34224377-0	2021	Correction: Cyclophosphamide and Vinorelbine Activate Stem-Like CD8+ T Cells and Improve Anti-PD-1 Efficacy in Triple-Negative Breast Cancer.	Cyclophosphamide	12-28	programmed cell death 1	Homo sapiens	94-98
34224377-0	2021	Correction: Cyclophosphamide and Vinorelbine Activate Stem-Like CD8+ T Cells and Improve Anti-PD-1 Efficacy in Triple-Negative Breast Cancer.	Vinorelbine	33-44	programmed cell death 1	Homo sapiens	94-98
34203761-2	2021	MSI and TMB are closely related to DNA mismatch repair (MMR) pathway functionality, while the PD-L1 checkpoint mediates cancer cell evasion from immune surveillance via the PD-L1/PD-1 axis.	1,2,4,5-tetramethoxybenzene	8-11	programmed cell death 1	Homo sapiens	179-183
34423116-4	2021	Such an in-silico experimentation and predictive model, based on the in vitro microfluidic chip-measured end-point data and patient-specific immunological characteristics, allowed for a comprehensive and dynamic analysis of multiple TAM-associated immunosuppression mechanisms against the anti-PD-1 immunotherapy.	tam	233-236	programmed cell death 1	Homo sapiens	294-298
34423116-6	2021	Our prediction results indicated that a combination therapy co-targeting of PD-1 checkpoint and TAM-associated CSF-1R signaling could enhance the immune responses of GBM patients, especially those patients with mesenchymal GBM who are irresponsive to the single anti-PD-1 therapy.	tam	96-99	programmed cell death 1	Homo sapiens	267-271
34103659-0	2021	PD-1 derived CA-170 is an oral immune checkpoint inhibitor that exhibits preclinical anti-tumor efficacy.	PD-1-IN-1	13-19	programmed cell death 1	Homo sapiens	0-4
34099731-5	2021	When combined, lorlatinib also improves the response to anti-PD-1 blockade resulting in more activated CD8 + T cells in PDAC tumors.	lorlatinib	15-25	programmed cell death 1	Homo sapiens	61-65
34368325-10	2021	CONCLUSION: The strategy of combining low-dose decitabine with tislelizumab could reverse the resistance to PD-1 inhibitors in patients with heavily pretreated relapsed/ refractory cHL.	Decitabine	47-57	programmed cell death 1	Homo sapiens	108-112
34061898-3	2021	Since TGF-beta activates Tregs, TGF-beta inhibitor may overcome primary resistance to anti-PD-1.	tregs	25-30	programmed cell death 1	Homo sapiens	91-95
34073458-3	2021	We show that, while CD4 CTL are resistant to suppression by Tregs in vitro, the conditioned medium of CD4 CTL accentuates the suppressive phenotype of Tregs by upregulating IL-10, Granzyme B, CTLA-4, and PD-1.	tregs	60-65	programmed cell death 1	Homo sapiens	204-208
34073458-3	2021	We show that, while CD4 CTL are resistant to suppression by Tregs in vitro, the conditioned medium of CD4 CTL accentuates the suppressive phenotype of Tregs by upregulating IL-10, Granzyme B, CTLA-4, and PD-1.	tregs	151-156	programmed cell death 1	Homo sapiens	204-208
34079767-6	2021	Further, we analyzed resected samples from 120 patients with MIBC and found that individuals with PD-1-positive TAMs showed a reduction in 5-year overall survival and disease-free survival.	4-METHYL-2-PENTANOL	61-65	programmed cell death 1	Homo sapiens	98-102
34113555-8	2021	Moreover, the PD-L1 expression and TMB might be the potential predictors of PD-1 blockade response for colorectal SCC patients.	1,2,4,5-tetramethoxybenzene	35-38	programmed cell death 1	Homo sapiens	76-80
34113560-10	2021	Moreover, the use of PD-1/PD-L1 blockade prior to or concurrent with osimertinib has been reported to increase the risk of pulmonary toxicity.	osimertinib	69-80	programmed cell death 1	Homo sapiens	21-25
34069461-0	2021	Polyphenols Modulating Effects of PD-L1/PD-1 Checkpoint and EMT-Mediated PD-L1 Overexpression in Breast Cancer.	Polyphenols	0-11	programmed cell death 1	Homo sapiens	40-44
34079767-2	2021	Previous studies have shown that the programmed cell death protein 1 (PD-1)-positive TAMs have an M2 macrophage phenotype.	tams	85-89	programmed cell death 1	Homo sapiens	37-68
34079767-2	2021	Previous studies have shown that the programmed cell death protein 1 (PD-1)-positive TAMs have an M2 macrophage phenotype.	tams	85-89	programmed cell death 1	Homo sapiens	70-74
35220552-8	2022	In addition, the low-WM score group was expected to be more sensitive to programmed cell death protein 1 (PD-1) therapy and showed lower predicted IC50 of chemotherapy drugs paclitaxel and cisplatin treatment.	Paclitaxel	174-184	programmed cell death 1	Homo sapiens	73-104
35220552-8	2022	In addition, the low-WM score group was expected to be more sensitive to programmed cell death protein 1 (PD-1) therapy and showed lower predicted IC50 of chemotherapy drugs paclitaxel and cisplatin treatment.	Paclitaxel	174-184	programmed cell death 1	Homo sapiens	106-110
35537335-0	2022	Corrigendum to "Combining anti-PD-1 antibodies with Mn2+-drug coordinated multifunctional nanoparticles for enhanced cancer therapy" (Biomaterials 275 (2021) 120897).	Manganese(2+)	52-56	programmed cell death 1	Homo sapiens	31-35
35613652-6	2022	The SB415286 nanoformulation efficiently inhibited PD-1 expression in chimeric antigen receptor (CAR)-T cells co-cultured with tumour cells expressing the CAR target, and improved their survival and proliferation.	3-(3-chloro-4-hydroxyphenylamino)-4-(4-nitrophenyl)-1H-pyrrole-2,5-dione	4-12	programmed cell death 1	Homo sapiens	51-55
34163753-4	2021	To showcase the applicability of our approach, we developed two new inhibitors (PD-i3 and PD-i6) of programmed cell death 1 (PD-1), a key immune checkpoint in oncology.	pd-i3	80-85	programmed cell death 1	Homo sapiens	100-123
34163753-4	2021	To showcase the applicability of our approach, we developed two new inhibitors (PD-i3 and PD-i6) of programmed cell death 1 (PD-1), a key immune checkpoint in oncology.	pd-i6	90-95	programmed cell death 1	Homo sapiens	100-123
34163753-4	2021	To showcase the applicability of our approach, we developed two new inhibitors (PD-i3 and PD-i6) of programmed cell death 1 (PD-1), a key immune checkpoint in oncology.	pd-i6	90-95	programmed cell death 1	Homo sapiens	125-129
35526308-2	2022	Recent preclinical data suggest that regorafenib may enhance the antitumor activity of anti-PD-1 immunotherapy.	regorafenib	37-48	programmed cell death 1	Homo sapiens	92-96
35575994-10	2022	Patients with immune-related myasthenia gravis experience increased mortality and morbidity but if steroid-responsive, may benefit from the reintroduction of anti-programmed cell death protein 1 therapy for end-stage malignancy with close monitoring.	Steroids	99-106	programmed cell death 1	Homo sapiens	163-194
35429911-0	2022	Pyrazolones as inhibitors of immune checkpoint blocking the PD-1/PD-L1 interaction.	Pyrazolones	0-11	programmed cell death 1	Homo sapiens	60-64
35417536-1	2022	Preliminary data from a phase I trial of MEDI5752, a bispecific antibody targeting both PD-1 and CTLA4, indicate the drug is well tolerated and active, with durable responses seen across diverse tumor types.	medi5752	41-49	programmed cell death 1	Homo sapiens	88-92
35276694-6	2022	RESULTS: Prolonged exposure of colorectal tumors to GZ17-6.02 enhanced the efficacy of 5-fluorouracil and of an anti-PD1 antibody, significantly prolonging animal survival.	gz17-6.02	52-61	programmed cell death 1	Homo sapiens	117-120
35405572-0	2022	Discovery of benzo(d)isothiazole derivatives as novel scaffold inhibitors targeting the programmed cell death-1/programmed cell death-ligand 1 (PD-1/PD-L1) interaction through "ring fusion" strategy.	benzo(d)isothiazole	13-32	programmed cell death 1	Homo sapiens	88-142
35437196-0	2022	Corrigendum to "Docetaxel downregulates PD-1 expression via STAT3 in Tlymphocytes" (Clinical Lung Cancer 19 (2018) e675-e683).	Docetaxel	16-25	programmed cell death 1	Homo sapiens	40-44
35366156-12	2022	Therefore, immune checkpoint inhibitors that target the PD-1/PD-L1 pathway may be a treatment option for TCs.	Technetium	105-108	programmed cell death 1	Homo sapiens	56-60
35630791-2	2022	Different molecular scaffolds have been reported, including phenyl-pyrazolone derivatives which potently inhibit binding of PD-L1 to PD-1.	phenyl-pyrazolone	60-77	programmed cell death 1	Homo sapiens	133-137
34079767-6	2021	Further, we analyzed resected samples from 120 patients with MIBC and found that individuals with PD-1-positive TAMs showed a reduction in 5-year overall survival and disease-free survival.	tams	112-116	programmed cell death 1	Homo sapiens	98-102
34079767-7	2021	Additionally, PD-1-positive TAMs showed a significant association with higher programmed death-ligand 1 (PD-L1) expression, the Ki67 index, the pT stage and fewer CD8-positive T cells.	tams	28-32	programmed cell death 1	Homo sapiens	14-18
34079767-11	2021	Together, these results indicate for the first time that CD68/PD-1 may be a novel target for the prognosis of patients with MIBC.	4-METHYL-2-PENTANOL	124-128	programmed cell death 1	Homo sapiens	62-66
35536197-12	2022	CONCLUSIONS: The combination of TACE with a PD-1 inhibitor and lenvatinib in patients with BCLC stage B HCC might result in significantly improved clinical outcomes with a manageable safety profile compared with TACE with a PD-1 inhibitor.	Chlorotrianisene	32-36	programmed cell death 1	Homo sapiens	44-48
35547095-2	2022	Immune checkpoint inhibitors (ICIs) based on programmed death-1/programmed death ligand-1 (PD-1/PD-L1) blockade have made a breakthrough with the approval of PD-1 inhibitor for refractory recurrence and/or metastatic (R/M NPC) and the approval of PD-1 inhibitor in combination with gemcitabine and cisplatin as first line for R/M NPC in 2021 in China.	gemcitabine	282-293	programmed cell death 1	Homo sapiens	91-95
35626016-7	2022	We conclude that GNP-LLO91-99 nanovaccines can work as monotherapies or combinatory immunotherapies with anti-CTLA-4 or anti-PD-1 antibodies for solid tumors with high T cell infiltration, such as bladder cancer or melanoma.	gnp-llo91-99	17-29	programmed cell death 1	Homo sapiens	125-129
35626016-7	2022	We conclude that GNP-LLO91-99 nanovaccines can work as monotherapies or combinatory immunotherapies with anti-CTLA-4 or anti-PD-1 antibodies for solid tumors with high T cell infiltration, such as bladder cancer or melanoma.	nanovaccines	30-42	programmed cell death 1	Homo sapiens	125-129
35547095-2	2022	Immune checkpoint inhibitors (ICIs) based on programmed death-1/programmed death ligand-1 (PD-1/PD-L1) blockade have made a breakthrough with the approval of PD-1 inhibitor for refractory recurrence and/or metastatic (R/M NPC) and the approval of PD-1 inhibitor in combination with gemcitabine and cisplatin as first line for R/M NPC in 2021 in China.	gemcitabine	282-293	programmed cell death 1	Homo sapiens	158-162
35547095-2	2022	Immune checkpoint inhibitors (ICIs) based on programmed death-1/programmed death ligand-1 (PD-1/PD-L1) blockade have made a breakthrough with the approval of PD-1 inhibitor for refractory recurrence and/or metastatic (R/M NPC) and the approval of PD-1 inhibitor in combination with gemcitabine and cisplatin as first line for R/M NPC in 2021 in China.	Cisplatin	298-307	programmed cell death 1	Homo sapiens	91-95
35547095-2	2022	Immune checkpoint inhibitors (ICIs) based on programmed death-1/programmed death ligand-1 (PD-1/PD-L1) blockade have made a breakthrough with the approval of PD-1 inhibitor for refractory recurrence and/or metastatic (R/M NPC) and the approval of PD-1 inhibitor in combination with gemcitabine and cisplatin as first line for R/M NPC in 2021 in China.	Cisplatin	298-307	programmed cell death 1	Homo sapiens	158-162
35199927-2	2022	In this study, we show that SiC monolayers are promising substrates for the development of highly stable single-atom catalysts (Pd1 /SiC) within the density functional theory.	sic	28-31	programmed cell death 1	Homo sapiens	128-131
35199927-3	2022	In presence of a Si-vacancy, the diffusion barrier energy of a Pd1 atom embedded in the SiC monolayer is substantially enhanced from 2.3 to 7.8 eV, which is much higher than the reported diffusion barrier energies of graphene, boron nitride and defective MgO of the same catalytic system.	Silicon	17-19	programmed cell death 1	Homo sapiens	63-66
35199927-3	2022	In presence of a Si-vacancy, the diffusion barrier energy of a Pd1 atom embedded in the SiC monolayer is substantially enhanced from 2.3 to 7.8 eV, which is much higher than the reported diffusion barrier energies of graphene, boron nitride and defective MgO of the same catalytic system.	Graphite	217-225	programmed cell death 1	Homo sapiens	63-66
35199927-3	2022	In presence of a Si-vacancy, the diffusion barrier energy of a Pd1 atom embedded in the SiC monolayer is substantially enhanced from 2.3 to 7.8 eV, which is much higher than the reported diffusion barrier energies of graphene, boron nitride and defective MgO of the same catalytic system.	boron nitride	227-240	programmed cell death 1	Homo sapiens	63-66
35199927-3	2022	In presence of a Si-vacancy, the diffusion barrier energy of a Pd1 atom embedded in the SiC monolayer is substantially enhanced from 2.3 to 7.8 eV, which is much higher than the reported diffusion barrier energies of graphene, boron nitride and defective MgO of the same catalytic system.	mgo	255-258	programmed cell death 1	Homo sapiens	63-66
35199927-4	2022	Ab initio molecular dynamic calculations at 500 K also confirm the enhanced stability of Pd1 /SiC monolayer (Si-vacancy) such that the Pd1 atom remains embedded in the vacancy.	Silicon	109-111	programmed cell death 1	Homo sapiens	89-92
35199927-4	2022	Ab initio molecular dynamic calculations at 500 K also confirm the enhanced stability of Pd1 /SiC monolayer (Si-vacancy) such that the Pd1 atom remains embedded in the vacancy.	Silicon	109-111	programmed cell death 1	Homo sapiens	135-138
35199927-5	2022	Additionally, the Pd1 /SiC monolayer (Si-vacancy) catalysts show a ~34 % reduction of activation barrier energy for CO oxidation as compared to pristine catalysts.	Silicon	38-40	programmed cell death 1	Homo sapiens	18-21
35592338-4	2022	There are several therapies available to recover the anticancer efficacy of PD-1/PD-L1 inhibitors by targeting TAMs, including the inhibition of TAM differentiation and re-education of TAM activation.	tams	111-115	programmed cell death 1	Homo sapiens	76-80
35135862-4	2022	By attaching a Toll-like receptor 7 agonist (TLR7-1A) to fluorescein, we enable the anti-fluorescein CAR to bind and internalize TLR7-1A, leading to both downregulation of exhaustion markers (i.e. PD-1, TIM3, LAG3) and reactivation of exhausted CAR T-cells without causing the toxicities commonly associated with systemic administration of TLR7 agonists.	Fluorescein	57-68	programmed cell death 1	Homo sapiens	197-201
35135862-4	2022	By attaching a Toll-like receptor 7 agonist (TLR7-1A) to fluorescein, we enable the anti-fluorescein CAR to bind and internalize TLR7-1A, leading to both downregulation of exhaustion markers (i.e. PD-1, TIM3, LAG3) and reactivation of exhausted CAR T-cells without causing the toxicities commonly associated with systemic administration of TLR7 agonists.	Fluorescein	89-100	programmed cell death 1	Homo sapiens	197-201
35592338-4	2022	There are several therapies available to recover the anticancer efficacy of PD-1/PD-L1 inhibitors by targeting TAMs, including the inhibition of TAM differentiation and re-education of TAM activation.	tam	145-148	programmed cell death 1	Homo sapiens	76-80
35592338-4	2022	There are several therapies available to recover the anticancer efficacy of PD-1/PD-L1 inhibitors by targeting TAMs, including the inhibition of TAM differentiation and re-education of TAM activation.	tam	185-188	programmed cell death 1	Homo sapiens	76-80
35592338-5	2022	In this review, we will summarize the roles and mechanisms of TAMs in PD-1/PD-L1 blocker resistance.	tams	62-66	programmed cell death 1	Homo sapiens	70-74
35190965-3	2022	We previously found that programmed cell death 1 (Pdcd1), an immune checkpoint receptor, inhibits DOX-induced cardiomyocyte apoptosis.	Doxorubicin	98-101	programmed cell death 1	Homo sapiens	50-55
35176764-2	2022	In preclinical models, 4-1BB costimulation synergizes with CPIs targeting the PD-1/PD-L1 axis by activating cytotoxic T-cell-mediated antitumor immunity.	cpis	59-63	programmed cell death 1	Homo sapiens	78-82
35120032-4	2022	Herein, we present the clinical, histopathologic, and immunofluorescence findings of 3 patients diagnosed with lichen planus pemphigoides (LPP) after treatment with anti-PD-1 inhibitors.	lichen planus pemphigoides	111-137	programmed cell death 1	Homo sapiens	170-174
35120032-4	2022	Herein, we present the clinical, histopathologic, and immunofluorescence findings of 3 patients diagnosed with lichen planus pemphigoides (LPP) after treatment with anti-PD-1 inhibitors.	Linalyl diphosphate	139-142	programmed cell death 1	Homo sapiens	170-174
35039625-9	2022	CONCLUSIONS: TIGIT/PD-1-based risk stratification with distinct immune and molecular features could be served as a predictor for systematic therapeutic response including adjuvant chemotherapy and immunotherapy in MIBC patients.	4-METHYL-2-PENTANOL	214-218	programmed cell death 1	Homo sapiens	19-23
35622442-0	2022	Steroid treatment in the management of destructive thyrotoxicosis induced by PD1 blockade.	Steroids	0-7	programmed cell death 1	Homo sapiens	77-80
35524455-5	2022	The absence of sEVsCD73 enhanced the sensitivity of anti-PD-1 therapy through reversed immunosuppression.	sevscd73	15-23	programmed cell death 1	Homo sapiens	57-61
35548349-7	2022	These findings suggest that beta-glucan could be used as an immune adjuvant to reverse anti-PD-1/PD-L1 resistance by regulating the immune system.	beta-Glucans	28-39	programmed cell death 1	Homo sapiens	92-96
35537782-2	2022	Camrelizumab is a monoclonal antibody against PD-1, and famitinib is a multitargeted receptor tyrosine kinase inhibitor with antiangiogenesis and antiproliferation activities against tumor cells.	famitinib	56-65	programmed cell death 1	Homo sapiens	46-50
35577504-11	2022	CONCLUSIONS: Our findings revealed a previously unappreciated role of ABZ in antitumor immunity by inducing ubiquitin-mediated PD-L1 protein degradation, identified predictors for assessing the therapeutic efficacy of anti-PD-1 therapy, and provided novel therapeutic possibility by combination treatment of ABZ and CD73 blockade in cancers.	Albendazole	70-73	programmed cell death 1	Homo sapiens	223-227
35516457-9	2022	Furthermore, the high-risk group with higher TMB levels and expression of immune checkpoints was more likely to benefit from immune checkpoint therapy such as PD-1 and CTLA-4 inhibitors.	1,2,4,5-tetramethoxybenzene	45-48	programmed cell death 1	Homo sapiens	159-163
35473608-4	2022	It also evaluates the association between removal of oral albuterol from the PDL and dispensing levels.	Albuterol	58-67	programmed cell death 1	Homo sapiens	77-80
35473608-6	2022	Using a difference-in-differences model, we examine the association between removal of oral albuterol from Arkansas" Medicaid PDL in 2014 and dispensing of this drug through Medicaid, with Iowa as a control state.	Albuterol	92-101	programmed cell death 1	Homo sapiens	126-129
35473608-11	2022	Removal of oral albuterol syrup from the Arkansas PDL in March 2014 was associated with a more rapid decline in dispensing compared with Iowa which maintained this medication on their PDL.	Albuterol	16-25	programmed cell death 1	Homo sapiens	50-53
35451929-9	2022	Besides, PD-L1 expression in tumor cells was significantly higher in the 2-ME-treated group than in the control group, indicating that 2-ME could exhibit stronger anti-tumor effects against melanoma if combined with PD-1 blockade therapy.Conclusion: 2-ME suppresses melanoma in vivo and in vitro and is a promising synergistic enhancer of PD-1 blockade immunotherapy.	2-Methoxyestradiol	73-77	programmed cell death 1	Homo sapiens	216-220
35451929-9	2022	Besides, PD-L1 expression in tumor cells was significantly higher in the 2-ME-treated group than in the control group, indicating that 2-ME could exhibit stronger anti-tumor effects against melanoma if combined with PD-1 blockade therapy.Conclusion: 2-ME suppresses melanoma in vivo and in vitro and is a promising synergistic enhancer of PD-1 blockade immunotherapy.	2-Methoxyestradiol	73-77	programmed cell death 1	Homo sapiens	339-343
35451929-9	2022	Besides, PD-L1 expression in tumor cells was significantly higher in the 2-ME-treated group than in the control group, indicating that 2-ME could exhibit stronger anti-tumor effects against melanoma if combined with PD-1 blockade therapy.Conclusion: 2-ME suppresses melanoma in vivo and in vitro and is a promising synergistic enhancer of PD-1 blockade immunotherapy.	2-Methoxyestradiol	135-139	programmed cell death 1	Homo sapiens	339-343
35451929-9	2022	Besides, PD-L1 expression in tumor cells was significantly higher in the 2-ME-treated group than in the control group, indicating that 2-ME could exhibit stronger anti-tumor effects against melanoma if combined with PD-1 blockade therapy.Conclusion: 2-ME suppresses melanoma in vivo and in vitro and is a promising synergistic enhancer of PD-1 blockade immunotherapy.	2-Methoxyestradiol	250-254	programmed cell death 1	Homo sapiens	216-220
35530353-1	2022	Purpose: To compare the efficacy and safety of the combination of transcatheter arterial chemoembolization (TACE), Lenvatinib, and programmed cell death protein-1 (PD-1) inhibitors (combination group) with TACE (TACE group) in the treatment of patients with unresectable hepatocellular carcinoma (uHCC).	Chlorotrianisene	212-216	programmed cell death 1	Homo sapiens	131-162
35530353-1	2022	Purpose: To compare the efficacy and safety of the combination of transcatheter arterial chemoembolization (TACE), Lenvatinib, and programmed cell death protein-1 (PD-1) inhibitors (combination group) with TACE (TACE group) in the treatment of patients with unresectable hepatocellular carcinoma (uHCC).	Chlorotrianisene	212-216	programmed cell death 1	Homo sapiens	164-168
35449134-4	2022	Antibody blockade of Treg PD-1, Teff CD80 (the alternative ligand for PD-L1), or LEC PD-L1 impairs Treg or Teff migration in vitro and in vivo.	treg	99-103	programmed cell death 1	Homo sapiens	26-30
35611193-4	2022	CASE SUMMARY: A 39-year-old male presented with erythema, blisters and erosions on the face, neck, trunk and limbs 1 wk after receiving combination therapy with lenvatinib and toripalimab, a PD-1 inhibitor.	lenvatinib	161-171	programmed cell death 1	Homo sapiens	191-195
35418130-5	2022	To overcome this challenge and take advantage of PD-L1 upregulation upon gemcitabine treatment, we generated recombinant PD-L1xCD3 bispecific T cell engagers (BiTEs) to simultaneously block PD-1/PD-L1 signaling and recruit T lymphocytes to eliminate CCA cells.	gemcitabine	73-84	programmed cell death 1	Homo sapiens	190-194
35419588-0	2022	Correction: First-in-Class Anti-Immunoglobulin-like Transcript 4 Myeloid-Specific Antibody MK-4830 Abrogates a PD-1 Resistance Mechanism in Patients with Advanced Solid Tumors.	mk-4830	91-98	programmed cell death 1	Homo sapiens	111-115
35454162-1	2022	Dual Blockade of Lactate/GPR81 and PD-1/PD-L1 Pathways Enhances the Anti-Tumor Effects of Metformin.	Metformin	90-99	programmed cell death 1	Homo sapiens	35-39
35444660-8	2022	The CLV3 dAb also exhibits the highest blocking efficacy of the PD-1/PD-L1 interaction.	3,3'-Diaminobenzidine	9-12	programmed cell death 1	Homo sapiens	64-68
35495754-11	2022	Anlotinib can inhibit the expression of PD-L1, and achieve better therapeutic effects after combined with PD-1 antibody.	anlotinib	0-9	programmed cell death 1	Homo sapiens	106-110
35142017-7	2022	The identity of the donor chlorophyll (ChlD1 or PD1) is wavelength-dependent and conformational dynamics broaden the sampling of far-red by the two charge-transfer states.	Chlorophyll	26-37	programmed cell death 1	Homo sapiens	48-51
35088497-3	2022	We demonstrate here that anti-fluorescein CAR-mediated uptake of a fluorescein-TLR7-3 conjugate can reactivate exhausted CAR T cells, leading to dramatic reduction in T cell exhaustion markers (PD-1 + Tim-3 + ) and shrinkage of otherwise resistant tumors without inducing systemic activation of the immune system.	Fluorescein	30-41	programmed cell death 1	Homo sapiens	194-198
35088497-3	2022	We demonstrate here that anti-fluorescein CAR-mediated uptake of a fluorescein-TLR7-3 conjugate can reactivate exhausted CAR T cells, leading to dramatic reduction in T cell exhaustion markers (PD-1 + Tim-3 + ) and shrinkage of otherwise resistant tumors without inducing systemic activation of the immune system.	Fluorescein	67-78	programmed cell death 1	Homo sapiens	194-198
35243806-8	2022	Mitochondria-targeted atovaquone also improves the anti-tumor activity of PD-1 blockade immunotherapy.	Atovaquone	22-32	programmed cell death 1	Homo sapiens	74-78
35212057-2	2022	Herein, a synergistic function between single Pd atoms (Pd1 ) and Pd nanoparticles (PdNPs ) on graphitic carbon nitride (C3 N4 ) for photocatalytic CO2 methanation is presented.	Palladium	46-48	programmed cell death 1	Homo sapiens	56-59
35212057-2	2022	Herein, a synergistic function between single Pd atoms (Pd1 ) and Pd nanoparticles (PdNPs ) on graphitic carbon nitride (C3 N4 ) for photocatalytic CO2 methanation is presented.	graphitic	95-104	programmed cell death 1	Homo sapiens	56-59
35212057-2	2022	Herein, a synergistic function between single Pd atoms (Pd1 ) and Pd nanoparticles (PdNPs ) on graphitic carbon nitride (C3 N4 ) for photocatalytic CO2 methanation is presented.	cyanogen	105-119	programmed cell death 1	Homo sapiens	56-59
35212057-2	2022	Herein, a synergistic function between single Pd atoms (Pd1 ) and Pd nanoparticles (PdNPs ) on graphitic carbon nitride (C3 N4 ) for photocatalytic CO2 methanation is presented.	c3 n4	121-126	programmed cell death 1	Homo sapiens	56-59
35212057-2	2022	Herein, a synergistic function between single Pd atoms (Pd1 ) and Pd nanoparticles (PdNPs ) on graphitic carbon nitride (C3 N4 ) for photocatalytic CO2 methanation is presented.	Carbon Dioxide	148-151	programmed cell death 1	Homo sapiens	56-59
35212057-5	2022	Mechanistic studies revealed that Pd1 sites activated CO2 , while PdNPs sites boosted water (H2 O) dissociation for increased H* coverage.	Carbon Dioxide	54-57	programmed cell death 1	Homo sapiens	34-37
35212057-6	2022	The H* produced by PdNPs migrate to the Pd1 sites to promote multiple proton-electron coupling transfer via hydrogen spillover.	Hydrogen	108-116	programmed cell death 1	Homo sapiens	40-43
35212057-7	2022	Moreover, the adjacent Pd1 and PdNPs effectively stabilized intermediates such as *CHO, thereby favoring the pathway for CH4 production.	Methane	121-124	programmed cell death 1	Homo sapiens	23-26
35362647-2	2022	A low-affinity PD-1 binder was incubated with a library of >100 D-peptides under thiol-exchange favoring conditions, in the presence of the target protein PD-1, and we determined the S-linked dimeric species that resulted amplified in the protein samples versus the controls.	Sulfhydryl Compounds	81-86	programmed cell death 1	Homo sapiens	15-19
35189139-9	2022	Collectively, our findings unveil the beneficial effect of V9302 in boosting antitumor immune response in breast cancer and illustrate that anti-PD-1 together with V9302 treatment may provide synergistic effects in the treatment of patients insensitive to anti-PD-1 therapy.	v9302	59-64	programmed cell death 1	Homo sapiens	145-149
35091445-13	2022	High expression of co-inhibitory receptors PD1/LAG3/CD39 on tumor-infiltrating Treg associated with worse DFS (HR=5.6, 95% CI: 0.83-37.8, p=0.08).	treg	79-83	programmed cell death 1	Homo sapiens	43-46
35294071-3	2022	We generated orthotopic HCC-bearing mice, which have typical features in common with human patients, and then treated them with LipC6 in combination with the antibodies (Abs) for programmed cell death protein 1 (PD-1) or cytotoxic T-lymphocyte antigen 4 (CTLA4).	lipc6	128-133	programmed cell death 1	Homo sapiens	179-210
35294071-3	2022	We generated orthotopic HCC-bearing mice, which have typical features in common with human patients, and then treated them with LipC6 in combination with the antibodies (Abs) for programmed cell death protein 1 (PD-1) or cytotoxic T-lymphocyte antigen 4 (CTLA4).	lipc6	128-133	programmed cell death 1	Homo sapiens	212-216
35378172-12	2022	LAY SUMMARY: Non-alcoholic fatty liver disease impairs motility, metabolic function and response to anti-PD-1 treatment of hepatic CD8+ T cells, which can be rescued by metformin treatment.	Metformin	169-178	programmed cell death 1	Homo sapiens	105-109
35444059-11	2022	Response to BEMPEG+NKTR-262 was characterized by a significant expansion of activated CD8+ T cells (GzmA+; Ki-67+; ICOS+; PD-1+) in the blood, which correlated with reduced tumor size (p<0.05).	bempeg	12-18	programmed cell death 1	Homo sapiens	122-126
35444059-12	2022	In the tumor, BEMPEG+NKTR-262 induced higher frequencies of GzmA+ CD8+ T cells exhibiting reduced expression of suppressive molecules (PD-1+), compared with BEMPEG+RT (p<0.05).	bempeg	14-20	programmed cell death 1	Homo sapiens	135-139
35194944-8	2022	In a syngeneic CRC model, DCZ0415 treatment induced an immune response by decreasing PD1 and CTLA4 levels and increasing granzyme B, perforin and interferon gamma.	DCZ0415	26-33	programmed cell death 1	Homo sapiens	85-88
35386213-3	2022	Methods: In this systematic review and network meta-analysis, we searched PubMed, Embase, and Cochrane Library databases for randomized controlled trials (RCTs) with the time set from database establishment to December 10, 2021, using programmed death factor 1 (PD-1) inhibitors, nivolumab, and sunitinib in the treatment of mRCC.	Sunitinib	295-304	programmed cell death 1	Homo sapiens	235-260
35386213-3	2022	Methods: In this systematic review and network meta-analysis, we searched PubMed, Embase, and Cochrane Library databases for randomized controlled trials (RCTs) with the time set from database establishment to December 10, 2021, using programmed death factor 1 (PD-1) inhibitors, nivolumab, and sunitinib in the treatment of mRCC.	Sunitinib	295-304	programmed cell death 1	Homo sapiens	262-266
35346313-14	2022	CONCLUSIONS: DDR mutations may contribute to DDR-induced STING pathway with sustained innate immunity activation following cetuximab plus avelumab combination in previously treated, PD-1 inhibitor responsive NSCLC patients.	ddr	45-48	programmed cell death 1	Homo sapiens	182-186
35454072-9	2022	Basic cell studies revealed that the utilization of MTAM-HFA in PD-1/PD-L1+ combination therapy revealed enhanced T-cell activity upon the administration of the PD-1/PD-L1 drug; thereby resulting in the reduction of tumor cell viability by up to 70%, and the cytotoxic effects by 82%.	methyl 4-thio-alpha-maltoside	52-56	programmed cell death 1	Homo sapiens	64-68
35454072-11	2022	This suggested that the MTAM-HFA system is suitable for use in PD-1/PD-L1+ screening and the accuracy, rapidity and cost effectiveness made it extremely suitable for application as a companion diagnostic system in both personalized medicine for cancer treatment and could potentially be applied to screen for candidate compounds in the development of next generation PD-1/PD-L1+ combination therapies.	methyl 4-thio-alpha-maltoside	24-28	programmed cell death 1	Homo sapiens	63-67
35454072-11	2022	This suggested that the MTAM-HFA system is suitable for use in PD-1/PD-L1+ screening and the accuracy, rapidity and cost effectiveness made it extremely suitable for application as a companion diagnostic system in both personalized medicine for cancer treatment and could potentially be applied to screen for candidate compounds in the development of next generation PD-1/PD-L1+ combination therapies.	methyl 4-thio-alpha-maltoside	24-28	programmed cell death 1	Homo sapiens	367-371
35278107-10	2022	Response rates to PD-1-based ICB were higher in patients with low TREM2+ TAMs (31.58%) compared to high TREM2+ TAMs (14.29%).	tams	73-77	programmed cell death 1	Homo sapiens	18-22
35583064-0	2022	(Artesunate upregulates the expression of CD39, CD279 and granzyme B in CD4+ and CD8+ T lymphocytes of patients with lung cancer).	Artesunate	1-11	programmed cell death 1	Homo sapiens	48-53
35462489-0	2022	(Observation of PD-1+CXCR5+CD4+T lymphocyte and sPD-1 levels in HBeAg positive chronic hepatitis B virus carriers treated with entecavir).	entecavir	127-136	programmed cell death 1	Homo sapiens	16-20
35462489-1	2022	Objective: To dynamically observe the clinical efficacy of entecavir and the changes of PD-1+CXCR5+CD4+T lymphocytes and sPD-1 levels in peripheral blood of HBeAg-positive chronic hepatitis B virus carriers treated with entecavir, and further explore its clinical significance.	entecavir	220-229	programmed cell death 1	Homo sapiens	88-92
35371031-11	2022	In patients who were treated with an EGFR antibody instead of a PD-1 inhibitor, a significant difference in PFS and clinical benefits was only observed between patients with CPS >= 1 and CPS < 1.	cps	174-177	programmed cell death 1	Homo sapiens	64-68
35236323-10	2022	The correlation analysis between this signature and immunosuppressive molecules, Immunophenoscore (IPS) and chemotherapeutic efficacy demonstrated that low-risk group had a higher  IC50 of cisplatin, mitomycin and doxorubicin and negatively related with CTLA4, HAVCR2, LAG3, PDCD1, TIGIT and ICIs treatment represented by CTLA4-/PD-1-, CTLA4 + /PD-1-, CTLA4-/PD-1 + .	Cisplatin	189-198	programmed cell death 1	Homo sapiens	275-280
35236323-10	2022	The correlation analysis between this signature and immunosuppressive molecules, Immunophenoscore (IPS) and chemotherapeutic efficacy demonstrated that low-risk group had a higher  IC50 of cisplatin, mitomycin and doxorubicin and negatively related with CTLA4, HAVCR2, LAG3, PDCD1, TIGIT and ICIs treatment represented by CTLA4-/PD-1-, CTLA4 + /PD-1-, CTLA4-/PD-1 + .	Cisplatin	189-198	programmed cell death 1	Homo sapiens	329-333
35236323-10	2022	The correlation analysis between this signature and immunosuppressive molecules, Immunophenoscore (IPS) and chemotherapeutic efficacy demonstrated that low-risk group had a higher  IC50 of cisplatin, mitomycin and doxorubicin and negatively related with CTLA4, HAVCR2, LAG3, PDCD1, TIGIT and ICIs treatment represented by CTLA4-/PD-1-, CTLA4 + /PD-1-, CTLA4-/PD-1 + .	Cisplatin	189-198	programmed cell death 1	Homo sapiens	345-349
35236323-10	2022	The correlation analysis between this signature and immunosuppressive molecules, Immunophenoscore (IPS) and chemotherapeutic efficacy demonstrated that low-risk group had a higher  IC50 of cisplatin, mitomycin and doxorubicin and negatively related with CTLA4, HAVCR2, LAG3, PDCD1, TIGIT and ICIs treatment represented by CTLA4-/PD-1-, CTLA4 + /PD-1-, CTLA4-/PD-1 + .	Cisplatin	189-198	programmed cell death 1	Homo sapiens	359-363
35236323-10	2022	The correlation analysis between this signature and immunosuppressive molecules, Immunophenoscore (IPS) and chemotherapeutic efficacy demonstrated that low-risk group had a higher  IC50 of cisplatin, mitomycin and doxorubicin and negatively related with CTLA4, HAVCR2, LAG3, PDCD1, TIGIT and ICIs treatment represented by CTLA4-/PD-1-, CTLA4 + /PD-1-, CTLA4-/PD-1 + .	Doxorubicin	214-225	programmed cell death 1	Homo sapiens	275-280
35236323-10	2022	The correlation analysis between this signature and immunosuppressive molecules, Immunophenoscore (IPS) and chemotherapeutic efficacy demonstrated that low-risk group had a higher  IC50 of cisplatin, mitomycin and doxorubicin and negatively related with CTLA4, HAVCR2, LAG3, PDCD1, TIGIT and ICIs treatment represented by CTLA4-/PD-1-, CTLA4 + /PD-1-, CTLA4-/PD-1 + .	Doxorubicin	214-225	programmed cell death 1	Homo sapiens	329-333
35236323-10	2022	The correlation analysis between this signature and immunosuppressive molecules, Immunophenoscore (IPS) and chemotherapeutic efficacy demonstrated that low-risk group had a higher  IC50 of cisplatin, mitomycin and doxorubicin and negatively related with CTLA4, HAVCR2, LAG3, PDCD1, TIGIT and ICIs treatment represented by CTLA4-/PD-1-, CTLA4 + /PD-1-, CTLA4-/PD-1 + .	Doxorubicin	214-225	programmed cell death 1	Homo sapiens	345-349
35236323-10	2022	The correlation analysis between this signature and immunosuppressive molecules, Immunophenoscore (IPS) and chemotherapeutic efficacy demonstrated that low-risk group had a higher  IC50 of cisplatin, mitomycin and doxorubicin and negatively related with CTLA4, HAVCR2, LAG3, PDCD1, TIGIT and ICIs treatment represented by CTLA4-/PD-1-, CTLA4 + /PD-1-, CTLA4-/PD-1 + .	Doxorubicin	214-225	programmed cell death 1	Homo sapiens	359-363
35371873-3	2022	Aspirin may have a synergistic effect with PD-1 inhibitors via inhibition of prostaglandin E2 (PGE2) production, which can reverse the ability of tumor cells to evade the immune system.	Aspirin	0-7	programmed cell death 1	Homo sapiens	43-47
35220243-1	2022	BACKGROUND/AIM: Recent evidence suggests potential synergistic antitumor effects of the combination of programmed death-1 (PD-1)/programmed death-ligand 1 (PD-L1) immune checkpoint inhibitors with the oral hypoglycemic agent metformin.	Metformin	225-234	programmed cell death 1	Homo sapiens	103-121
35220243-1	2022	BACKGROUND/AIM: Recent evidence suggests potential synergistic antitumor effects of the combination of programmed death-1 (PD-1)/programmed death-ligand 1 (PD-L1) immune checkpoint inhibitors with the oral hypoglycemic agent metformin.	Metformin	225-234	programmed cell death 1	Homo sapiens	123-127
35133489-0	2022	Pharmacokinetics and pharmacodynamics of MEDI0680, a fully human anti-PD-1 monoclonal antibody, in patients with advanced malignancies.	medi0680	41-49	programmed cell death 1	Homo sapiens	70-74
35133489-6	2022	The estimated half-maximal effective concentration for MEDI0680 binding to the PD-1 antigen was approximately 1.88 microg/mL.	medi0680	55-63	programmed cell death 1	Homo sapiens	79-83
35233733-10	2022	The GSVA revealed that high PD-1 expression was associated with various immune-associated pathways, such as T cell/B cell receptor signaling pathway or natural killer cell-mediated cytotoxicity.	gsva	4-8	programmed cell death 1	Homo sapiens	28-32
35371873-3	2022	Aspirin may have a synergistic effect with PD-1 inhibitors via inhibition of prostaglandin E2 (PGE2) production, which can reverse the ability of tumor cells to evade the immune system.	Dinoprostone	77-93	programmed cell death 1	Homo sapiens	43-47
35371873-3	2022	Aspirin may have a synergistic effect with PD-1 inhibitors via inhibition of prostaglandin E2 (PGE2) production, which can reverse the ability of tumor cells to evade the immune system.	Dinoprostone	95-99	programmed cell death 1	Homo sapiens	43-47
35318258-9	2022	1alpha,25(OH)2D3, the active form of vitamin D, promotes the nuclear translocation of VDR, which binds to the promoter region of Pdcd1, Tim3, and Tigit genes and inhibits their expression.	Calcitriol	0-16	programmed cell death 1	Homo sapiens	129-134
35241494-12	2022	Patients with EBVaGC with a high cytotoxic T lymphocyte-associated antigen-4 (CTLA-4) level were less responsive to anti-programmed death-1/ligand 1 (PD-1/L1) monotherapy, and the combination of anti-CTLA-4 plus anti-PD-1/L1 checkpoint blockade benefited patients with EBVaGC more than anti-PD-1/L1 monotherapy with a trend close to significance (p=0.074).	ebvagc	14-20	programmed cell death 1	Homo sapiens	150-157
35241494-12	2022	Patients with EBVaGC with a high cytotoxic T lymphocyte-associated antigen-4 (CTLA-4) level were less responsive to anti-programmed death-1/ligand 1 (PD-1/L1) monotherapy, and the combination of anti-CTLA-4 plus anti-PD-1/L1 checkpoint blockade benefited patients with EBVaGC more than anti-PD-1/L1 monotherapy with a trend close to significance (p=0.074).	ebvagc	14-20	programmed cell death 1	Homo sapiens	217-221
35241494-12	2022	Patients with EBVaGC with a high cytotoxic T lymphocyte-associated antigen-4 (CTLA-4) level were less responsive to anti-programmed death-1/ligand 1 (PD-1/L1) monotherapy, and the combination of anti-CTLA-4 plus anti-PD-1/L1 checkpoint blockade benefited patients with EBVaGC more than anti-PD-1/L1 monotherapy with a trend close to significance (p=0.074).	ebvagc	14-20	programmed cell death 1	Homo sapiens	291-295
35241494-12	2022	Patients with EBVaGC with a high cytotoxic T lymphocyte-associated antigen-4 (CTLA-4) level were less responsive to anti-programmed death-1/ligand 1 (PD-1/L1) monotherapy, and the combination of anti-CTLA-4 plus anti-PD-1/L1 checkpoint blockade benefited patients with EBVaGC more than anti-PD-1/L1 monotherapy with a trend close to significance (p=0.074).	ebvagc	269-275	programmed cell death 1	Homo sapiens	150-157
35281267-13	2022	Conclusion: Metformin combining PD-1 inhibitor enhanced anti-tumor efficacy in STK11 mutant lung cancer through inhibition of RNF5-mediated K48-linked ubiquitination of STING, which was dependent on AXIN-1.	Metformin	12-21	programmed cell death 1	Homo sapiens	32-36
35273594-2	2022	We recently conducted a clinical study that combined neoantigen nanovaccine with anti-PD-1 antibody.	neoantigen	53-63	programmed cell death 1	Homo sapiens	86-90
34985925-2	2022	After more than two decades without clinical progress, the addition of programmed cell death protein 1 axis blockade to platinum-based chemotherapy has demonstrated sustained overall survival benefit and represents the current standard of care in the first-line setting.	Platinum	120-128	programmed cell death 1	Homo sapiens	71-102
35170879-11	2022	Platinum-based regimens combined with targeted therapies (Bev, PARPi, and PD-1/PD-L1 inhibitor) also improve the pCR rate beyond that with AT alone, but this benefit is accompanied by greater toxicity.	Platinum	0-8	programmed cell death 1	Homo sapiens	74-78
35170879-11	2022	Platinum-based regimens combined with targeted therapies (Bev, PARPi, and PD-1/PD-L1 inhibitor) also improve the pCR rate beyond that with AT alone, but this benefit is accompanied by greater toxicity.	Astatine	139-141	programmed cell death 1	Homo sapiens	74-78
35241815-2	2022	Here we report the design and performance of systemically administered protease activity sensors conjugated to anti-programmed cell death protein 1 (alphaPD1) antibodies for the monitoring of antitumour responses to ICB therapy.	indole-2-carboxylic acid	216-219	programmed cell death 1	Homo sapiens	116-147
35267557-8	2022	In conclusion, the patients who developed clinically significant hypothyroidism requiring replacement therapy with L-thyroxin were the group who benefitted most from anti-PD-1 treatment.	Thyroxine	115-125	programmed cell death 1	Homo sapiens	171-175
35192052-0	2022	TMB and BRAF mutation status are independent predictive factors in high-risk melanoma patients with adjuvant anti-PD-1 therapy.	1,2,4,5-tetramethoxybenzene	0-3	programmed cell death 1	Homo sapiens	114-118
35192052-13	2022	A classification based on BRAF mutation status and TMB is proposed to predict RFS in melanoma patients with adjuvant anti-PD-1 therapy.	1,2,4,5-tetramethoxybenzene	51-54	programmed cell death 1	Homo sapiens	122-126
35265212-5	2022	Moreover, oral DPAICP@ME augmented the action of immunotherapy by Anti-PD1 through the further T-cell activation.	dpaicp@me	15-24	programmed cell death 1	Homo sapiens	71-74
35261780-6	2022	With the response rate of 81.8%, duration of response of 15.2 months, median progression-free survival of 15.5 months, median overall survival of 21.5 months and manageable toxicity in patients with advanced ESCC, we demonstrated that cisplatin-based chemotherapy plus anti-PD-1 antibody is an effective and safe option.	Cisplatin	235-244	programmed cell death 1	Homo sapiens	274-278
35261780-8	2022	These results highlight the effectiveness of cisplatin combining with anti-PD-1 antibody in patients with advanced ESCC, revealed its capability to promote the PD-L1 expression in ESCC cells and act synergistically with anti-PD-1 antibody to restore exhausted immune cells activities, thus providing a theoretical basis for further explorations in the mechanism of the combination treatment of cisplatin-based chemotherapy with immune checkpoint inhibitors in ESCC.	Cisplatin	45-54	programmed cell death 1	Homo sapiens	75-79
35261780-8	2022	These results highlight the effectiveness of cisplatin combining with anti-PD-1 antibody in patients with advanced ESCC, revealed its capability to promote the PD-L1 expression in ESCC cells and act synergistically with anti-PD-1 antibody to restore exhausted immune cells activities, thus providing a theoretical basis for further explorations in the mechanism of the combination treatment of cisplatin-based chemotherapy with immune checkpoint inhibitors in ESCC.	Cisplatin	45-54	programmed cell death 1	Homo sapiens	225-229
35261780-8	2022	These results highlight the effectiveness of cisplatin combining with anti-PD-1 antibody in patients with advanced ESCC, revealed its capability to promote the PD-L1 expression in ESCC cells and act synergistically with anti-PD-1 antibody to restore exhausted immune cells activities, thus providing a theoretical basis for further explorations in the mechanism of the combination treatment of cisplatin-based chemotherapy with immune checkpoint inhibitors in ESCC.	Cisplatin	394-403	programmed cell death 1	Homo sapiens	75-79
35261780-8	2022	These results highlight the effectiveness of cisplatin combining with anti-PD-1 antibody in patients with advanced ESCC, revealed its capability to promote the PD-L1 expression in ESCC cells and act synergistically with anti-PD-1 antibody to restore exhausted immune cells activities, thus providing a theoretical basis for further explorations in the mechanism of the combination treatment of cisplatin-based chemotherapy with immune checkpoint inhibitors in ESCC.	Cisplatin	394-403	programmed cell death 1	Homo sapiens	225-229
35318258-9	2022	1alpha,25(OH)2D3, the active form of vitamin D, promotes the nuclear translocation of VDR, which binds to the promoter region of Pdcd1, Tim3, and Tigit genes and inhibits their expression.	Vitamin D	37-46	programmed cell death 1	Homo sapiens	129-134
34981715-10	2022	Low-expressing singlenucleotide polymorphisms of interferon regulatory factor 4 could enhance the downstream gene expression of programmed cell death 1 and Helios immunoregulatory molecules.	singlenucleotide	15-31	programmed cell death 1	Homo sapiens	128-151
35178344-10	2022	Conclusions: NLR, PLR, MLR, dNLR, and SII can reflect the short-term efficacy of immunotherapy in patients who underwent anti-PD-1 therapy with AGC.	agc	144-147	programmed cell death 1	Homo sapiens	126-130
35135866-6	2022	Given the broad activity but known limitations of anti-programmed cell death protein (PD1) therapy and other checkpoint inhibitors, ongoing studies have sought to augment the successful outcomes of anti-PD1 therapy with combinatorial approaches, particularly adenosine signaling blockade.	Adenosine	259-268	programmed cell death 1	Homo sapiens	86-89
35135866-6	2022	Given the broad activity but known limitations of anti-programmed cell death protein (PD1) therapy and other checkpoint inhibitors, ongoing studies have sought to augment the successful outcomes of anti-PD1 therapy with combinatorial approaches, particularly adenosine signaling blockade.	Adenosine	259-268	programmed cell death 1	Homo sapiens	203-206
35153753-0	2021	Case Report: Successful Avatrombopag Treatment for Two Cases of Anti-PD-1 Antibody-Induced Acquired Amegakaryocytic Thrombocytopenia.	avatrombopag	24-36	programmed cell death 1	Homo sapiens	69-73
35153753-4	2021	Case summary: We reported for the first time the successful treatment of avatrombopag in two cases of anti-PD1 antibody-induced AAT (in particular, one case had progressed to aplastic anemia), which was refractory or intolerant to glucocorticoids, ciclosporin, intravenous immunoglobulin (IVIG), recombinant human thrombopoietin (rh-TPO) and even TPO receptor agonist (TPO-RA) eltrombopag.	avatrombopag	73-85	programmed cell death 1	Homo sapiens	107-110
35153753-6	2021	Conclusion: Anti-PD1 antibody-induced AAT occurs with low frequency but is often serious and difficult to manage, for which this study proposed vatrombopag as a potential curative and safe approach.	vatrombopag	144-155	programmed cell death 1	Homo sapiens	17-20
35079117-6	2022	Multianalyte biomarkers based on TCS estimates predicted response to anti-PD-1 therapy in three different cancers and outperformed the indicated PD-L1 test, as well as Tumor Mutational Burden.	9-ethyl-N-(3,4,5-trimethoxyphenyl)carbazole-3-sulfonamide	33-36	programmed cell death 1	Homo sapiens	74-78
35096488-3	2022	Importantly, in a small cohort of melanoma patients, the plasma levels of vitamin B5 positively correlate with responses to PD-1-targeted immunotherapy.	Pantothenic Acid	74-84	programmed cell death 1	Homo sapiens	124-128
35042864-0	2022	PDCD1 (PD-1) is a direct target of miR-15a-5p and miR-16-5p.	-15a-	38-43	programmed cell death 1	Homo sapiens	0-5
35093211-4	2022	PD-1 blockade synergizes with lactic acid to enhance Treg suppression and impede antitumor immunity.	Lactic Acid	30-41	programmed cell death 1	Homo sapiens	0-4
35042864-0	2022	PDCD1 (PD-1) is a direct target of miR-15a-5p and miR-16-5p.	-15a-	38-43	programmed cell death 1	Homo sapiens	7-11
35022908-1	2022	BACKGROUND: Anti-PD-1 antibodies plus lenvatinib therapeutic regimens have demonstrated a relatively high antitumor response in many solid cancers; however, the efficacy and safety of anti-PD-1 antibodies plus lenvatinib in patients with advanced gallbladder cancer (GBC) has not been reported.	lenvatinib	210-220	programmed cell death 1	Homo sapiens	17-21
35015785-4	2022	In the present paper we develop a mathematical model to assess the efficacy of any combination of ADT with cancer vaccine, PD-1 inhibitor, and CTLA-4 inhibitor.	adt	98-101	programmed cell death 1	Homo sapiens	123-127
35121988-5	2022	Following small-molecule compound C26-A6 treatment to disrupt the MTDH-SND1 complex, we showed enhanced immune surveillance and sensitivity to anti-programmed cell death protein 1 therapy in preclinical models of metastatic breast cancer, in support of this combination therapy as a viable approach to increase immune-checkpoint blockade therapy responses in metastatic breast cancer.	c26-a6	34-40	programmed cell death 1	Homo sapiens	148-179
34996924-5	2022	Of all 6, CH-4 displayed the lowest cytotoxicity and strongest inhibitory activity towards the PD-1/PD-L1 interaction.	CH-4	10-14	programmed cell death 1	Homo sapiens	95-99
34996924-6	2022	The experiments revealed that CH-4 inhibited the interaction of soluble form PD-L1 (sPD-L1) with PD-1 surface protein expressed by KG-1 cells.	CH-4	30-34	programmed cell death 1	Homo sapiens	97-101
35058326-14	2022	CONCLUSIONS: The present study suggests that CD38 and PD-1 modulation by Isa+Cemi has a manageable safety profile, reduces CD38+ immune cells in the TME, and activates peripheral T cells; however, such CD38 inhibition was not associated with significant antitumor activity.	isa+cemi	73-81	programmed cell death 1	Homo sapiens	54-58
35141051-5	2022	A humanized CEACAM6-blocking antibody, BAY 1834942, was developed and characterized for its immunomodulating effects in co-culture experiments with T cells and solid cancer cells and in comparison to antibodies targeting the immune checkpoints programmed cell death protein 1 (PD-1), programmed death-ligand 1 (PD-L1), and T cell immunoglobulin mucin-3 (TIM-3).	bay 1834942	39-50	programmed cell death 1	Homo sapiens	277-281
35003748-13	2022	Our results suggest that SKI-G-801 has the potential to overcome anti-PD-1 therapy resistance and allow more patients to benefit from anti-PD-1 therapy.	ski-g-801	25-34	programmed cell death 1	Homo sapiens	70-74
35003748-13	2022	Our results suggest that SKI-G-801 has the potential to overcome anti-PD-1 therapy resistance and allow more patients to benefit from anti-PD-1 therapy.	ski-g-801	25-34	programmed cell death 1	Homo sapiens	139-143
33687756-6	2021	Surprisingly, we observed that C-REV treatment increased the abundance of activated CD8+ PD-1- tumor-infiltrating lymphocytes (TILs) in the tumor on both the injected and contralateral sides, although infiltration of CD8+ PD-1high TILs into the tumor was observed in the control group.	c-rev	31-36	programmed cell death 1	Homo sapiens	89-93
35003793-0	2022	Cooperating minimalist nanovaccine with PD-1 blockade for effective and feasible cancer immunotherapy.	nanovaccine	23-34	programmed cell death 1	Homo sapiens	40-44
35003793-3	2022	Objectives: Our study aims to solve the above dilemmas by cooperating minimalist nanovaccine with PD-1 blockade for effective and feasible cancer immunotherapy.	nanovaccine	81-92	programmed cell death 1	Homo sapiens	98-102
35003793-5	2022	On that basis, PD-1 antibody (aPD-1) was utilized to block the tumor immune escape and cooperate with the nanovaccine by maintaining the tumoricidal-activity of the vaccine-induced T cells.	nanovaccine	106-117	programmed cell death 1	Homo sapiens	15-19
35356198-0	2022	Incorporation of SKI-G-801, a Novel AXL Inhibitor, With Anti-PD-1 Plus Chemotherapy Improves Anti-Tumor Activity and Survival by Enhancing T Cell Immunity.	ski-g-801	17-26	programmed cell death 1	Homo sapiens	61-65
35356229-4	2022	This patient achieved clinical remission after platinum-based effective chemotherapy and programmed death 1 (PD-1) immunotherapy.	Platinum	47-55	programmed cell death 1	Homo sapiens	109-113
7106165-8	1982	The pharmacodynamic half-life (Pd 1/2) of TC approximated a mean first fast Pd 1/2 of 1.3 d and a slower phase of 14.2 d. During treatment with the highest TC dose, resting blood pressure was significantly elevated from 120 to 128 mm Hg, and the pressor sensitivity to NE (S NE) in 4 of the 6 subjects rose, the mean was 1.7 (n = 6).	Technetium	42-44	programmed cell death 1	Homo sapiens	31-37
7106165-8	1982	The pharmacodynamic half-life (Pd 1/2) of TC approximated a mean first fast Pd 1/2 of 1.3 d and a slower phase of 14.2 d. During treatment with the highest TC dose, resting blood pressure was significantly elevated from 120 to 128 mm Hg, and the pressor sensitivity to NE (S NE) in 4 of the 6 subjects rose, the mean was 1.7 (n = 6).	Technetium	42-44	programmed cell death 1	Homo sapiens	76-82
7428796-2	1980	A combined pharmacodynamic and pharmacokinetic approach was made to study the pharmacodynamic half-life (Pd1/2) of amitriptyline (AT).	Amitriptyline	115-128	programmed cell death 1	Homo sapiens	105-110
7428796-6	1980	It was possible to detect DTS for 228-300 h after the last oral dose and the mean Pd1/2 of this decline of pharmacodynamic effect was observed to be 135 h. However, no measurable amount of AT or NT was present after 84 h and the mean elimination plasma half-life (t1/2) of AT and NT were 37.7 and 38.9 h, respectively.	Nortriptyline	280-282	programmed cell death 1	Homo sapiens	82-87
7428796-9	1980	Pd1/2, as assessed by DTS, correlated directly with the t1/2 (r = 0.91) and inversely with the plasma clearance rate (r = 0.60) of NT.	dibenzyl trisulfide	22-25	programmed cell death 1	Homo sapiens	0-5
33957086-10	2021	These results indicate that oleic acid and OEA inhibit PD-1 expression, and induce apoptosis via STAT phosphorylation.	Oleic Acid	28-38	programmed cell death 1	Homo sapiens	55-59
33957086-10	2021	These results indicate that oleic acid and OEA inhibit PD-1 expression, and induce apoptosis via STAT phosphorylation.	oleoylethanolamide	43-46	programmed cell death 1	Homo sapiens	55-59
33687756-7	2021	Moreover, the difference in PD-1 expression was observed only in tumors after treatment with C-REV, whereas most CD8+ T cells in the spleen, tumor-draining lymph nodes, and blood were PD-1-negative, and this did not change after C-REV treatment.	c-rev	93-98	programmed cell death 1	Homo sapiens	28-32
34059019-9	2021	The TMB and the effectiveness of anti-PD-1 treatment were significantly increased in the PD-L1-high expression groups compared with the PD-L1-low expression groups.	1,2,4,5-tetramethoxybenzene	4-7	programmed cell death 1	Homo sapiens	38-42
33997867-6	2021	The release of D-PPA could not only lead to instability and aggregation of NPs for enhanced tumor retention but also block PD-1/PD-L1 to avoid immune escape and elicit enhanced immune response.	diphenylphosphorazidate	15-20	programmed cell death 1	Homo sapiens	123-127
33997867-7	2021	In addition, DOX could induce immunogenic cell death (ICD) of cancer cells and promote anti-tumor immune response with the combination of PD-1/PD-L1 blocking.	Doxorubicin	13-16	programmed cell death 1	Homo sapiens	138-142
34036623-0	2021	Lenvatinib Targets FGFR4 to Enhance Antitumor Immune Response of Anti-PD-1 in Hepatocellular Carcinoma.	lenvatinib	0-10	programmed cell death 1	Homo sapiens	70-74
34036623-10	2021	CONCLUSIONS: Lenvatinib reduced tumor PD-L1 level and Treg differentiation to improve anti-PD-1 efficacy by blocking FGFR4.	lenvatinib	13-23	programmed cell death 1	Homo sapiens	91-95
34021735-6	2021	D PPA is an inhibitory peptide of the PD-1/PD-L1 immune checkpoint pathway.	ppa	2-5	programmed cell death 1	Homo sapiens	38-42
34016641-9	2021	Finally, in line with our results, we showed significant sex-based differences in the association between TMB and outcome of patients with advanced NSCLC treated with anti-PD1/PDL1 drugs.	1,2,4,5-tetramethoxybenzene	106-109	programmed cell death 1	Homo sapiens	172-175
34016716-6	2021	Soluble programmed cell death protein 1 and sTIM-3 both positively correlated with hepatitis B virus (HBV) DNA level and increased in entecavir or tenofovir used group.	entecavir	134-143	programmed cell death 1	Homo sapiens	8-39
34016716-6	2021	Soluble programmed cell death protein 1 and sTIM-3 both positively correlated with hepatitis B virus (HBV) DNA level and increased in entecavir or tenofovir used group.	Tenofovir	147-156	programmed cell death 1	Homo sapiens	8-39
34055609-8	2021	These findings suggest that bTMB is a validated predictive biomarker for determining the clinical outcome of advanced NSCLC patients and may serve as a feasible predictor of the clinical benefit of immunotherapies (anti-PD-1 antibody) in the advanced NSCLC population in Yunnan Province.	3,5-Bis(trimethylsilyl)benzoic acid	28-32	programmed cell death 1	Homo sapiens	220-224
34055595-5	2021	An independent cohort of 23 patients with solid tumors was used to evaluate the value of selected radiomic features in predicting the expression of the programmed cell death 1 (PD1), using 18F-FDG PET/CT images and RNA-seq genomic data.	Fluorodeoxyglucose F18	189-196	programmed cell death 1	Homo sapiens	152-175
33986285-7	2021	Ex vivo expansion of Tregs from patients with PD restored and enhanced their suppressive functions while expanded Tregs displayed increased expression of foxp3, il2ra (CD25), nt5e (CD73), il10, il13, ctla4, pdcd1 (PD1), and gzmb.	tregs	114-119	programmed cell death 1	Homo sapiens	207-212
33986285-7	2021	Ex vivo expansion of Tregs from patients with PD restored and enhanced their suppressive functions while expanded Tregs displayed increased expression of foxp3, il2ra (CD25), nt5e (CD73), il10, il13, ctla4, pdcd1 (PD1), and gzmb.	tregs	114-119	programmed cell death 1	Homo sapiens	214-217
34055595-5	2021	An independent cohort of 23 patients with solid tumors was used to evaluate the value of selected radiomic features in predicting the expression of the programmed cell death 1 (PD1), using 18F-FDG PET/CT images and RNA-seq genomic data.	Fluorodeoxyglucose F18	189-196	programmed cell death 1	Homo sapiens	177-180
33979178-14	2021	CONCLUSION: Lifileucel demonstrated durable responses and addresses a major unmet need in patients with metastatic melanoma with limited treatment options after approved therapy, including the primary refractory to anti-PD-1 or PD-L1 therapy subset.	lifileucel	12-22	programmed cell death 1	Homo sapiens	220-224
33991512-18	2021	INTERPRETATION: Treatment with enfortumab vedotin was tolerable and confirmed responses were seen in 52% of cisplatin-ineligible patients with locally advanced or metastatic urothelial carcinoma who were previously treated with PD-1 or PD-L1 inhibitors.	vedotin	42-49	programmed cell death 1	Homo sapiens	228-232
33930312-0	2021	Evaluation of TMB as a predictive biomarker in patients with solid cancers treated with anti-PD-1/CTLA-4 combination immunotherapy.	1,2,4,5-tetramethoxybenzene	14-17	programmed cell death 1	Homo sapiens	93-97
34026621-0	2021	IL-21 Is an Accomplice of PD-L1 in the Induction of PD-1-Dependent Treg Generation in Head and Neck Cancer.	treg	67-71	programmed cell death 1	Homo sapiens	52-56
34026621-3	2021	Here, we demonstrated that IL-21-polarized inflammation was enriched in the tumor microenvironment in head and neck squamous cell carcinoma (HNSCC) and that IL-21 could promote PD-L1-induced Treg generation in a PD-1-dependent manner.	treg	191-195	programmed cell death 1	Homo sapiens	212-216
34026621-5	2021	Importantly, an anti-PD-1 antibody could inhibit only Treg expansion induced by clinical tumor explants with high expression of IL-21/PD-L1.	treg	54-58	programmed cell death 1	Homo sapiens	21-25
34026621-6	2021	In addition, neutralizing IL-21 could enhance the anti-PD-1 antibody-mediated inhibitory effect on Treg expansion.	treg	99-103	programmed cell death 1	Homo sapiens	55-59
34026621-8	2021	These findings indicate that IL-21 in the tumor microenvironment may promote PD-L1-induced, Treg-mediated immune escape in a PD-1-dependent manner and that an IL-21 neutralization strategy may enhance PD-1 blockade-based antitumor immunotherapy by targeting Treg-mediated immune evasion in patients with high expression of IL-21 and PD-L1.	treg	92-96	programmed cell death 1	Homo sapiens	125-129
33382454-0	2021	Efficacy and safety of PD1/PDL1 blockade with platinum-based chemotherapy for extensive small cell lung cancer: a pooled analysis of randomized trials.	Platinum	46-54	programmed cell death 1	Homo sapiens	23-26
33980416-0	2021	Anti-PD-1 checkpoint blockade improves the efficacy of a melphalan-based therapy in experimental melanoma.	Melphalan	57-66	programmed cell death 1	Homo sapiens	5-9
33855690-1	2021	INTRODUCTION: The phase III KEYNOTE-048 trial showed that the programmed death receptor 1 (PD-1) inhibitor pembrolizumab, in the combined positive score (CPS) >= 1 population and combined with platinum + 5-fluorouracil in the total population, improves survival over cetuximab + platinum + 5-fluorouracil in recurrent or metastatic (R/M) head and neck squamous cell carcinoma (HNSCC).	Fluorouracil	204-218	programmed cell death 1	Homo sapiens	91-95
33855690-1	2021	INTRODUCTION: The phase III KEYNOTE-048 trial showed that the programmed death receptor 1 (PD-1) inhibitor pembrolizumab, in the combined positive score (CPS) >= 1 population and combined with platinum + 5-fluorouracil in the total population, improves survival over cetuximab + platinum + 5-fluorouracil in recurrent or metastatic (R/M) head and neck squamous cell carcinoma (HNSCC).	Platinum	279-287	programmed cell death 1	Homo sapiens	62-89
33855690-1	2021	INTRODUCTION: The phase III KEYNOTE-048 trial showed that the programmed death receptor 1 (PD-1) inhibitor pembrolizumab, in the combined positive score (CPS) >= 1 population and combined with platinum + 5-fluorouracil in the total population, improves survival over cetuximab + platinum + 5-fluorouracil in recurrent or metastatic (R/M) head and neck squamous cell carcinoma (HNSCC).	Platinum	279-287	programmed cell death 1	Homo sapiens	91-95
33855690-1	2021	INTRODUCTION: The phase III KEYNOTE-048 trial showed that the programmed death receptor 1 (PD-1) inhibitor pembrolizumab, in the combined positive score (CPS) >= 1 population and combined with platinum + 5-fluorouracil in the total population, improves survival over cetuximab + platinum + 5-fluorouracil in recurrent or metastatic (R/M) head and neck squamous cell carcinoma (HNSCC).	Fluorouracil	290-304	programmed cell death 1	Homo sapiens	62-89
33855690-1	2021	INTRODUCTION: The phase III KEYNOTE-048 trial showed that the programmed death receptor 1 (PD-1) inhibitor pembrolizumab, in the combined positive score (CPS) >= 1 population and combined with platinum + 5-fluorouracil in the total population, improves survival over cetuximab + platinum + 5-fluorouracil in recurrent or metastatic (R/M) head and neck squamous cell carcinoma (HNSCC).	Fluorouracil	290-304	programmed cell death 1	Homo sapiens	91-95
33581579-0	2021	PD-1/PD-L1 enhanced cisplatin resistance in gastric cancer through PI3K/AKT mediated P-gp expression.	Cisplatin	20-29	programmed cell death 1	Homo sapiens	0-4
33581579-12	2021	CONCLUSION: PD-1/PD-L1 enhanced cisplatin resistance in gastric cancer through PI3K/AKT mediated P-gp expression.	Cisplatin	32-41	programmed cell death 1	Homo sapiens	12-16
34011535-1	2021	BACKGROUND: The Camrelizumab Plus Apatinib in Patients with Advanced Cervical Cancer trial was a single-arm, phase II study that showed promising activity of the programmed death-1 (PD-1) inhibitor camrelizumab plus the vascular endothelial growth factor receptor-2 inhibitor apatinib in patients with advanced cervical cancer.	apatinib	34-42	programmed cell death 1	Homo sapiens	182-186
34055224-0	2021	Design, Synthesis, and Biological Evaluation of Imidazopyridines as PD-1/PD-L1 Antagonists.	imidazopyridine	48-64	programmed cell death 1	Homo sapiens	68-72
33877296-4	2021	Lenalidomide rapidly and transiently induced an activated T-cell phenotype, including HLA-DR, Tim-3, CD137, and programmed cell death protein 1 (PD-1) upregulation.	Lenalidomide	0-12	programmed cell death 1	Homo sapiens	112-143
33903974-8	2021	COM902, either alone or in combination with a PVRIG (COM701) or PD-1 inhibitor, enhances antigen-specific human T cell responses in-vitro.	com902	0-6	programmed cell death 1	Homo sapiens	64-68
33852965-13	2021	CD31 expression on memory CD8 + T cells of HIV-infected individuals was associated higher levels of PD-1 (p = 0.0019) and CD38/HLADR (p = 0.0345), and higher PD-1 expression on CD8 + TEMRA (p = 0.0024), an effect not observed in non-HIV-infected individuals.	temra	183-188	programmed cell death 1	Homo sapiens	158-162
33859108-9	2021	P2 demonstrated a striking increase in the frequency of gag-specific central and effector memory CD8+ T cells producing IFN-gamma, TNF-alpha, and CD107a following anti-PD1 and anti-CTLA-4.	P-2	0-2	programmed cell death 1	Homo sapiens	168-171
33859108-9	2021	P2 demonstrated a striking increase in the frequency of gag-specific central and effector memory CD8+ T cells producing IFN-gamma, TNF-alpha, and CD107a following anti-PD1 and anti-CTLA-4.	Glycosaminoglycans	56-59	programmed cell death 1	Homo sapiens	168-171
33656040-4	2021	Here, cisplatin (CDDP) loaded poly(l-glutamic acid)-graft-methoxy poly(ethylene glycol) complex nanoparticles (CDDP-NPs) are confirmed to increase CD8+ T cells within non-irradiated tumors and boost the abscopal effect of RT plus anti-PD1, and more strongly than CDDP.	Cisplatin	6-15	programmed cell death 1	Homo sapiens	235-238
33656040-4	2021	Here, cisplatin (CDDP) loaded poly(l-glutamic acid)-graft-methoxy poly(ethylene glycol) complex nanoparticles (CDDP-NPs) are confirmed to increase CD8+ T cells within non-irradiated tumors and boost the abscopal effect of RT plus anti-PD1, and more strongly than CDDP.	Cisplatin	17-21	programmed cell death 1	Homo sapiens	235-238
33656040-4	2021	Here, cisplatin (CDDP) loaded poly(l-glutamic acid)-graft-methoxy poly(ethylene glycol) complex nanoparticles (CDDP-NPs) are confirmed to increase CD8+ T cells within non-irradiated tumors and boost the abscopal effect of RT plus anti-PD1, and more strongly than CDDP.	Glutamic Acid	30-51	programmed cell death 1	Homo sapiens	235-238
33656040-4	2021	Here, cisplatin (CDDP) loaded poly(l-glutamic acid)-graft-methoxy poly(ethylene glycol) complex nanoparticles (CDDP-NPs) are confirmed to increase CD8+ T cells within non-irradiated tumors and boost the abscopal effect of RT plus anti-PD1, and more strongly than CDDP.	graft-methoxy poly(ethylene glycol)	52-87	programmed cell death 1	Homo sapiens	235-238
33656040-4	2021	Here, cisplatin (CDDP) loaded poly(l-glutamic acid)-graft-methoxy poly(ethylene glycol) complex nanoparticles (CDDP-NPs) are confirmed to increase CD8+ T cells within non-irradiated tumors and boost the abscopal effect of RT plus anti-PD1, and more strongly than CDDP.	Cisplatin	111-115	programmed cell death 1	Homo sapiens	235-238
33656040-4	2021	Here, cisplatin (CDDP) loaded poly(l-glutamic acid)-graft-methoxy poly(ethylene glycol) complex nanoparticles (CDDP-NPs) are confirmed to increase CD8+ T cells within non-irradiated tumors and boost the abscopal effect of RT plus anti-PD1, and more strongly than CDDP.	Cisplatin	111-115	programmed cell death 1	Homo sapiens	235-238
33897892-0	2021	Enhanced anti-PD-1 therapy in hepatocellular carcinoma by tumor vascular disruption and normalization dependent on combretastatin A4 nanoparticles and DC101.	fosbretabulin	115-132	programmed cell death 1	Homo sapiens	14-18
33554680-8	2021	Cemiplimab is a recombinant IgG4 human monoclonal antibody against the PD-1 protein for the intravenous treatment of lacSCC.	lacscc	117-123	programmed cell death 1	Homo sapiens	71-75
33868266-4	2021	Case Presentation: We reported a case of treated secondary (ts)-AML in a patient who received tislelizumab (an anti-PD-1 antibody) in combination with azacitidine.	Azacitidine	151-162	programmed cell death 1	Homo sapiens	116-120
33869015-3	2021	Our objective was to compare the clinical efficacy and safety of anti-PD-1/PD-L1 therapies in platinum-resistant UC patients.	Platinum	94-102	programmed cell death 1	Homo sapiens	70-74
33496513-14	2021	CONCLUSION: Our study provided up-to-date evidence that pembrolizumab/lenvatinib combination therapy achieved objective responses in both heavily pretreated and anti-PD-1 refractory R/M HNSCC patients.	lenvatinib	70-80	programmed cell death 1	Homo sapiens	166-170
33597150-8	2021	PD1 upregulation is accentuated in the presence of rapamycin but prevented by tacrolimus.	Sirolimus	51-60	programmed cell death 1	Homo sapiens	0-3
33597150-8	2021	PD1 upregulation is accentuated in the presence of rapamycin but prevented by tacrolimus.	Tacrolimus	78-88	programmed cell death 1	Homo sapiens	0-3
33597150-9	2021	These data support a general theory of CoB-resistant cells as Ag-experienced, costimulation-independent cells and suggest a mechanism for the synergy of belatacept and rapamycin, with increased expression of the activation marker PD1 potentiating exhaustion of CoB-resistant cells.	cob	39-42	programmed cell death 1	Homo sapiens	230-233
33597150-9	2021	These data support a general theory of CoB-resistant cells as Ag-experienced, costimulation-independent cells and suggest a mechanism for the synergy of belatacept and rapamycin, with increased expression of the activation marker PD1 potentiating exhaustion of CoB-resistant cells.	Sirolimus	168-177	programmed cell death 1	Homo sapiens	230-233
33597150-9	2021	These data support a general theory of CoB-resistant cells as Ag-experienced, costimulation-independent cells and suggest a mechanism for the synergy of belatacept and rapamycin, with increased expression of the activation marker PD1 potentiating exhaustion of CoB-resistant cells.	cob	261-264	programmed cell death 1	Homo sapiens	230-233
33104972-6	2021	This study aims to evaluate the biodistribution of Zirconium-89 (89Zr)-labeled pembrolizumab, a humanized IgG4 kappa monoclonal antibody targeting PD-1, in healthy cynomolgus monkeys as a translational model of tracking PD-1-positive immune cells.	Zirconium-89	51-63	programmed cell death 1	Homo sapiens	147-151
33877099-3	2021	Treated with first-line encorafenib + binimetinib, the patient reported a complete response lasting 37 months and followed by a partial response, still ongoing after 19 months, to anti-PD-1 antibody second line therapy.	encorafenib	24-35	programmed cell death 1	Homo sapiens	185-189
33877099-3	2021	Treated with first-line encorafenib + binimetinib, the patient reported a complete response lasting 37 months and followed by a partial response, still ongoing after 19 months, to anti-PD-1 antibody second line therapy.	binimetinib	38-49	programmed cell death 1	Homo sapiens	185-189
32737851-4	2021	C8 showed high binding affinity with hPD-1 and could effectively interfere the interaction of PD-1/PD-L1.	1-octene	0-2	programmed cell death 1	Homo sapiens	37-42
32737851-9	2021	The interaction model of C8 with hPD-1 was simulated and confirmed by alanine scanning.	Alanine	70-77	programmed cell death 1	Homo sapiens	33-38
34026438-3	2021	In this study, alcohol induces ligand programmed cell death receptor 1 (PD-L1) expression of CRC cells in vitro and in vivo.	Alcohols	15-22	programmed cell death 1	Homo sapiens	38-70
33094431-0	2021	Detection of pseudoprogression with [18F]-FDG-PET in a patient with pulmonary large cell neuroendocrine carcinoma who received anti-PD-1 treatment.	Fluorodeoxyglucose F18	42-45	programmed cell death 1	Homo sapiens	132-136
33788151-10	2021	Besides, various immune checkpoint proteins expressed on the surface of TAMs, such as PD-1 and CD47, provide the possibility of the application of immune checkpoint inhibitors.	tams	72-76	programmed cell death 1	Homo sapiens	86-90
33786726-0	2022	Design, synthesis and biological evaluation of isoxazole-containing biphenyl derivatives as small-molecule inhibitors targeting the programmed cell death-1/ programmed cell death-ligand 1 immune checkpoint.	Isoxazoles	47-56	programmed cell death 1	Homo sapiens	132-187
33786726-4	2022	A novel series of isoxazole-containing biphenyl compounds were designed, synthesized and evaluated as PD-1/PD-L1 inhibitors in this paper.	Isoxazoles	18-27	programmed cell death 1	Homo sapiens	102-106
33786726-5	2022	The structure-activity relationship of the novel synthesized compounds indicated that the ring-closure strategy of introducing isoxazole could be employed and the 3-cyanobenzyl group was significant for the inhibitory activity against the PD-1/PD-L1 protein-protein interactions.	Isoxazoles	127-136	programmed cell death 1	Homo sapiens	239-243
33786726-5	2022	The structure-activity relationship of the novel synthesized compounds indicated that the ring-closure strategy of introducing isoxazole could be employed and the 3-cyanobenzyl group was significant for the inhibitory activity against the PD-1/PD-L1 protein-protein interactions.	3-cyanobenzyl	163-176	programmed cell death 1	Homo sapiens	239-243
33786726-7	2022	In particular, compound II-12 was a promising anti-PD-1/PD-L1 inhibitor with the IC50 value of 23.0 nM, providing valuable information for future drug development.	ii-12	24-29	programmed cell death 1	Homo sapiens	51-55
33577729-11	2021	CONCLUSIONS: Enfortumab vedotin significantly prolonged survival as compared with standard chemotherapy in patients with locally advanced or metastatic urothelial carcinoma who had previously received platinum-based treatment and a PD-1 or PD-L1 inhibitor.	vedotin	24-31	programmed cell death 1	Homo sapiens	232-236
33879398-0	2021	The Value of 18F-FDG PET/CT in Predicting the Response to PD-1 Blocking Immunotherapy in Advanced NSCLC Patients with High-Level PD-L1 Expression.	Fluorodeoxyglucose F18	13-20	programmed cell death 1	Homo sapiens	58-62
33758937-2	2021	Programmed cell death 1 (PD-1) prompts FoxP3 in Tregs expression and enhances the suppressive activity of Tregs.	tregs	48-53	programmed cell death 1	Homo sapiens	25-29
33758937-2	2021	Programmed cell death 1 (PD-1) prompts FoxP3 in Tregs expression and enhances the suppressive activity of Tregs.	tregs	106-111	programmed cell death 1	Homo sapiens	25-29
33758937-4	2021	OBJECTIVE: To evaluate the role of PD-1 in Tregs function and triiodothyronine (T3) in PD-1 expression in patients with GD and mice treated with T3.	tregs	43-48	programmed cell death 1	Homo sapiens	35-39
33758937-9	2021	RESULTS: PD-1 expression in Tregs and the suppressive function of Tregs significantly decreased in patients with GD.	tregs	28-33	programmed cell death 1	Homo sapiens	9-13
33758937-10	2021	T3 reduced PD-1 expression in human Tregs in a concentration- and time-dependent manner in vitro.	Triiodothyronine	0-2	programmed cell death 1	Homo sapiens	11-15
33758937-10	2021	T3 reduced PD-1 expression in human Tregs in a concentration- and time-dependent manner in vitro.	tregs	36-41	programmed cell death 1	Homo sapiens	11-15
33758937-12	2021	CONCLUSIONS: Tregs dysfunction in GD patients might be due to down-regulation of PD-1 expression in Tregs induced by high levels of serum T3.	tregs	13-18	programmed cell death 1	Homo sapiens	81-85
33758937-12	2021	CONCLUSIONS: Tregs dysfunction in GD patients might be due to down-regulation of PD-1 expression in Tregs induced by high levels of serum T3.	tregs	100-105	programmed cell death 1	Homo sapiens	81-85
33758937-12	2021	CONCLUSIONS: Tregs dysfunction in GD patients might be due to down-regulation of PD-1 expression in Tregs induced by high levels of serum T3.	Triiodothyronine	138-140	programmed cell death 1	Homo sapiens	81-85
33879398-1	2021	BACKGROUND: The objective of this study was to evaluate if 18F-fluorodeoxyglucose positron emission tomography/computed tomography (18F-FDG PET/CT)-derived parameters are useful in predicting response and survival after programmed cell death protein 1 (PD-1) blocking immunotherapy in patients with advanced NSCLC characterized by a high programmed death-ligand 1 (PD-L1) expression (>=50%) on immunohistochemistry.	Fluorodeoxyglucose F18	59-81	programmed cell death 1	Homo sapiens	220-251
33879398-1	2021	BACKGROUND: The objective of this study was to evaluate if 18F-fluorodeoxyglucose positron emission tomography/computed tomography (18F-FDG PET/CT)-derived parameters are useful in predicting response and survival after programmed cell death protein 1 (PD-1) blocking immunotherapy in patients with advanced NSCLC characterized by a high programmed death-ligand 1 (PD-L1) expression (>=50%) on immunohistochemistry.	Fluorodeoxyglucose F18	59-81	programmed cell death 1	Homo sapiens	253-257
33879398-1	2021	BACKGROUND: The objective of this study was to evaluate if 18F-fluorodeoxyglucose positron emission tomography/computed tomography (18F-FDG PET/CT)-derived parameters are useful in predicting response and survival after programmed cell death protein 1 (PD-1) blocking immunotherapy in patients with advanced NSCLC characterized by a high programmed death-ligand 1 (PD-L1) expression (>=50%) on immunohistochemistry.	Fluorodeoxyglucose F18	132-139	programmed cell death 1	Homo sapiens	220-251
33879398-1	2021	BACKGROUND: The objective of this study was to evaluate if 18F-fluorodeoxyglucose positron emission tomography/computed tomography (18F-FDG PET/CT)-derived parameters are useful in predicting response and survival after programmed cell death protein 1 (PD-1) blocking immunotherapy in patients with advanced NSCLC characterized by a high programmed death-ligand 1 (PD-L1) expression (>=50%) on immunohistochemistry.	Fluorodeoxyglucose F18	132-139	programmed cell death 1	Homo sapiens	253-257
32871584-6	2021	Finally, we observed clinical responses to PD-1 blockade in three of five patients with relapsed/refractory TCRLBCL who were enrolled in clinical trials for refractory hematologic malignancies, including two complete responses and one partial response.	tcrlbcl	108-115	programmed cell death 1	Homo sapiens	43-47
33742076-1	2021	With the recent FDA approval of tumor mutational burden-high (TMB-H) status as a biomarker for treatment with a PD-1 inhibitor regardless of tumor type, accurate assessment of patient-specific TMB is more critical now more than ever.	1,2,4,5-tetramethoxybenzene	62-65	programmed cell death 1	Homo sapiens	112-116
33682607-5	2021	Additionally, SNHG14/miR-152-3p inhibits apoptosis and promotes cell proliferation on cytotoxic T lymphocytes (CTLs) in DLBCL via the PD-1/PD-L1 checkpoint.	mir-152-3p	21-31	programmed cell death 1	Homo sapiens	134-138
33616147-2	2021	Herein, we report a nano-educator (NE) that when loaded with all trans retinoic acid (ATRA) and anti-PD-1 antibodies (aPD-1) instructs myeloid cells to assist T cells towards revitalizing anti-PD-1 therapy.	Tretinoin	65-84	programmed cell death 1	Homo sapiens	119-123
33616147-3	2021	In vivo, ATRA converts myeloid-derived suppressor cells (MDSCs) into dendritic cells (DCs), which are essential for anti-PD-1 therapy, while intervening in the polarization of macrophages.	Tretinoin	9-13	programmed cell death 1	Homo sapiens	121-125
32880684-0	2021	Increased thyroid uptake on 18F-FDG PET/CT is associated with the development of permanent hypothyroidism in stage IV melanoma patients treated with anti-PD-1 antibodies.	Fluorodeoxyglucose F18	28-35	programmed cell death 1	Homo sapiens	154-158
33278498-0	2021	Low-dose carboplatin reprograms tumor immune microenvironment through STING signaling pathway and synergizes with PD-1 inhibitors in lung cancer.	Carboplatin	9-20	programmed cell death 1	Homo sapiens	114-118
33278498-5	2021	Further, low-dose carboplatin changed the "cold" tumor into a "hot" tumor via the signaling hub STING, augmenting CD8+ T-cell infiltration, increasing PD-L1 expression, and hence potentiating the anti-tumor effect of PD-1 inhibitors; importantly, there were no adverse effects.	Carboplatin	18-29	programmed cell death 1	Homo sapiens	217-221
33278498-7	2021	Our findings collectively reported a previously unexplored role of low-dose carboplatin targeting in the STING pathway and provided an economical, useful and safe option for improving the efficacy of PD-1 inhibitors in lung cancer.	Carboplatin	76-87	programmed cell death 1	Homo sapiens	200-204
33658304-0	2021	SRC family kinase (SFK) inhibitor dasatinib improves the antitumor activity of anti-PD-1 in NSCLC models by inhibiting Treg cell conversion and proliferation.	Dasatinib	34-43	programmed cell death 1	Homo sapiens	84-88
33658304-16	2021	Dasatinib synergizes with anti-PD-1 to impair tumor growth in NSCLC experimental models.	Dasatinib	0-9	programmed cell death 1	Homo sapiens	31-35
33497367-3	2021	UMCD6 augmented killing of breast, lung or prostate cancer cells through direct effects on both CD8+ T cells and natural killer (NK) cells, increasing cancer cell death and lowering cancer cell survival in vitro more robustly than monoclonal antibody checkpoint inhibitors that interrupt the PD-1/PD-L1 axis.	umcd6	0-5	programmed cell death 1	Homo sapiens	292-296
33199494-5	2021	The U.S. Food and Drug Administration (FDA) has approved the PD-1 inhibitor pembrolizumab as a therapy for all solid tumors with TMB equal to or greater than 10 mutations/megabase as measured by the FoundationOne CDx assay.	1,2,4,5-tetramethoxybenzene	129-132	programmed cell death 1	Homo sapiens	61-65
33199494-5	2021	The U.S. Food and Drug Administration (FDA) has approved the PD-1 inhibitor pembrolizumab as a therapy for all solid tumors with TMB equal to or greater than 10 mutations/megabase as measured by the FoundationOne CDx assay.	Cefadroxil	213-216	programmed cell death 1	Homo sapiens	61-65
33753566-1	2021	BACKGROUND: Regorafenib and other multikinase inhibitors may enhance antitumor efficacy of anti-program cell death-1 (anti-PD1) therapy in hepatocellular carcinoma (HCC).	regorafenib	12-23	programmed cell death 1	Homo sapiens	123-126
33627871-9	2021	Second, Treg cells in tumours show enhanced expression of the PD-1 gene, through a process that depends on SREBP activity and signals via mevalonate metabolism to protein geranylgeranylation.	Mevalonic Acid	138-148	programmed cell death 1	Homo sapiens	62-66
33458968-8	2021	CONCLUSIONS: Patients with NSCLC who co-express NY-ESO-1 or LAG-3 with PD-L1 exhibit greater DCBs and improved long-term survival following anti-PD-1 therapy.	S-(Benzo[d]thiazol-2-yl)-N,N-dicyclohexylthiohydroxylamine	93-97	programmed cell death 1	Homo sapiens	145-149
32361873-5	2021	More recently, several anti-PD-L1 and anti-PD-1 antibodies have shown promising activity in the first-line and post-platinum setting; however, immunotherapy remains ineffective in most patients.	Platinum	116-124	programmed cell death 1	Homo sapiens	43-47
33639962-12	2021	Increased PD-1 lymphocytes were associated with the long-term PEM response group, as PD-L1 expression in tumors was associated with a high incidence of immune-related adverse effects following ICI administration.	Pemetrexed	62-65	programmed cell death 1	Homo sapiens	10-14
33754054-21	2021	Conclusion: Pectin facilitated the anti-PD-1 mAb efficacy in CRC via regulating the T cell infiltration in the tumor microenvironment, which was potentially mediated by the metabolite butyrate.	Butyrates	184-192	programmed cell death 1	Homo sapiens	40-44
33593403-11	2021	In vitro experiments showed that YM101 effectively counteracted the biological effects of TGF-beta and PD-1/PD-L1 pathway, including activating Smad signaling, inducing epithelial-mesenchymal transition, and immunosuppression.	ym101	33-38	programmed cell death 1	Homo sapiens	103-107
33594323-11	2021	In conclusion, the SimTA-based multi-omics serial deep learning provides a promising methodology for predicting response of advanced NSCLC patients to anti-PD-1/PD-L1 monotherapy.	simta	19-24	programmed cell death 1	Homo sapiens	156-160
33408116-6	2021	Furthermore, E7386 showed synergistic antitumor activity against MMTV-Wnt1 tumor in combination with anti-PD-1 antibody.	E-7386	13-18	programmed cell death 1	Homo sapiens	106-110
33408116-7	2021	In conclusion, E7386 demonstrates clear antitumor activity via modulation of the Wnt/beta-catenin signal pathway and alteration of the tumor and immune microenvironments, and its antitumor activity can be enhanced in combination with anti-PD-1 antibody.	E-7386	15-20	programmed cell death 1	Homo sapiens	239-243
33402116-20	2021	CONCLUSIONS: The current study may offer a novel autophagy-related prognostic signature and may identify a promising miRNA-ARG pathway for predicting the efficacy of anti-PD-1 therapy in PCa.	Arginine	123-126	programmed cell death 1	Homo sapiens	171-175
33080152-12	2021	CONCLUSIONS: In this large real-world cohort, effectiveness in terms of TTTTD and OS with PD-1/L1 inhibitors in patients with platinum-refractory locally advanced/unresectable or metastatic urothelial carcinoma was similar.	Platinum	126-134	programmed cell death 1	Homo sapiens	90-94
33290748-11	2021	CONCLUSION: In a 75-patient cohort with non-small cell lung cancer treated with the PD1 antibody nivolumab and systematically screened for cortisol abnormalities, 10.7% of patients showed asymptomatic corticotropic insufficiency.	Hydrocortisone	139-147	programmed cell death 1	Homo sapiens	84-87
33475525-12	2021	Therefore, targeting the PD-1/PD-L1 axis could be a promising strategy for treating BP-NEN.	bp-nen	84-90	programmed cell death 1	Homo sapiens	25-29
32954856-6	2021	On the one hand, the positive effects of platinum-based chemotherapy on immunomodulation can be harnessed to increase the sensitivity of tumor cells to PD-1/PD-L1 inhibitors.	Platinum	41-49	programmed cell death 1	Homo sapiens	152-156
32954856-7	2021	On the other hand, platinum-based chemotherapy may upregulate PD-L1 expression in tumor tissue and exert a negative immunomodulatory effect, which can be counteracted by PD-1/PD-L1 inhibitors through their action pathway.	Platinum	19-27	programmed cell death 1	Homo sapiens	170-174
33523301-0	2021	Real-world outcomes of anti-PD1 antibodies in platinum-refractory, PD-L1-positive recurrent and/or metastatic non-small cell lung cancer, and its potential practical predictors: first report from Korean Cancer Study Group LU19-05.	Platinum	46-54	programmed cell death 1	Homo sapiens	28-31
33708420-6	2021	PD-1 inhibitor with chemotherapy [albumin paclitaxel 100 mg/m2 on days 1 and 8 + carboplatin with an area under the curve (AUC) of 5 on day 1] were administered every 3 weeks intravenously, and surgery was performed approximately 3-5 weeks after the second dose.	Paclitaxel	42-52	programmed cell death 1	Homo sapiens	0-4
33708420-6	2021	PD-1 inhibitor with chemotherapy [albumin paclitaxel 100 mg/m2 on days 1 and 8 + carboplatin with an area under the curve (AUC) of 5 on day 1] were administered every 3 weeks intravenously, and surgery was performed approximately 3-5 weeks after the second dose.	Carboplatin	81-92	programmed cell death 1	Homo sapiens	0-4
33522942-11	2021	The anti-PD-1 related pneumonitis mixed with bacterial infection was clinically diagnosed based on the laboratory and radiological evidences and good response to the prednisolone and antibiotics.	Prednisolone	166-178	programmed cell death 1	Homo sapiens	9-13
31269868-11	2021	Blood glucose monitoring is recommended for all patients receiving anti-PD-1 therapy.	Blood Glucose	0-13	programmed cell death 1	Homo sapiens	72-76
32935617-0	2021	Sequencing of PD-1/L1 Inhibitors and Carboplatin-Based Chemotherapy for Cisplatin-Ineligible Metastatic Urothelial Carcinoma.	Cisplatin	72-81	programmed cell death 1	Homo sapiens	14-18
32935617-7	2021	RESULTS: In this multicenter retrospective study, we identified 146 cisplatin-ineligible patients with mUC treated with first-line (1L) PD-1/L1 inhibitor therapy followed by second-line (2L) carboplatin-containing chemotherapy (Group 1, n=43) or the reverse sequence (Group 2, n=103).	Cisplatin	68-77	programmed cell death 1	Homo sapiens	136-143
32935617-12	2021	CONCLUSIONS: In this biomarker-unselected cohort of cisplatin-ineligible patients with mUC, PD-1/L1 inhibitor followed by carboplatin-containing chemotherapy and the reverse sequence had comparable OS.	Cisplatin	52-61	programmed cell death 1	Homo sapiens	92-99
33507343-4	2021	Increasing the TMB enhanced host anti-tumor T cell responses and improved anti-PD-1 efficacy in syngeneic models across all genetic backgrounds.	1,2,4,5-tetramethoxybenzene	15-18	programmed cell death 1	Homo sapiens	79-83
33507343-5	2021	However, limited anti-PD-1 efficacy was observed in the KPL cell lines with increased TMB, which possessed a distinct immunosuppressed tumor microenvironment (TME) primarily composed of granulocytic myeloid-derived suppressor cells (G-MDSCs).	1,2,4,5-tetramethoxybenzene	86-89	programmed cell death 1	Homo sapiens	22-26
33469052-0	2021	Boosting anti-PD-1 therapy with metformin-loaded macrophage-derived microparticles.	Metformin	32-41	programmed cell death 1	Homo sapiens	14-18
33024998-0	2021	Triggering interferon signaling in T cells with avadomide sensitizes CLL to anti-PD-L1/PD-1 immunotherapy.	3-(5-amino-2-methyl-4-oxoquinazolin-3(4H)-yl)piperidine-2,6-dione	48-57	programmed cell death 1	Homo sapiens	87-91
33441183-0	2021	Value of 18F-FDG-PET to predict PD-L1 expression and outcomes of PD-1 inhibition therapy in human cancers.	Fluorodeoxyglucose F18	9-16	programmed cell death 1	Homo sapiens	65-69
33441183-7	2021	Therefore, we reviewed the clinical significance of 18F-FDG uptake on PET as a predictor of the efficacy of PD-1 blockade therapy, by correlating with the expression of PD-L1, in patients with several neoplasms.	Fluorodeoxyglucose F18	52-59	programmed cell death 1	Homo sapiens	108-112
33436023-2	2021	We conducted this study to evaluate the efficacy and safety of geptanolimab (GB226), an anti-PD-1 antibody, in r/r PTCL patients.	gb226	77-82	programmed cell death 1	Homo sapiens	93-97
33506034-12	2021	Moreover, GSEA showed that several pathways were enriched in CPEB3, such as PD1 signaling, CTLA4 pathway, CTCF pathway, CHEMOKIN signaling, VEGF signaling, and JAK-STAT pathway.	gsea	10-14	programmed cell death 1	Homo sapiens	76-79
33091531-9	2021	The joining of a durable PD-1 blockage significantly boosted the efficacy of PTX@HSST on multiple tumor models, including lung metastatic tumors and even multidrug-resistant tumors.	Paclitaxel	77-80	programmed cell death 1	Homo sapiens	25-29
33430352-3	2021	Here, we investigated whether chemoradiotherapy (CRT), a combination of cisplatin and irradiation, could improve the efficacy of postirradiation anti-programmed cell death 1 (PD-1) treatment in UC.	Cisplatin	72-81	programmed cell death 1	Homo sapiens	175-179
33430403-1	2021	Structure of model bimetallic PdAu nanoparticles is analyzed aiming to find Pd:Au ratios optimal for existence of Pd1 single-atom surface sites inside outer Au atomic shell.	Palladium	30-32	programmed cell death 1	Homo sapiens	114-117
33430403-1	2021	Structure of model bimetallic PdAu nanoparticles is analyzed aiming to find Pd:Au ratios optimal for existence of Pd1 single-atom surface sites inside outer Au atomic shell.	Gold	32-34	programmed cell death 1	Homo sapiens	114-117
33430403-1	2021	Structure of model bimetallic PdAu nanoparticles is analyzed aiming to find Pd:Au ratios optimal for existence of Pd1 single-atom surface sites inside outer Au atomic shell.	Gold	79-81	programmed cell death 1	Homo sapiens	114-117
33430403-5	2021	However, surface Pd1 sites become stable, when Pd content inside a Pd-Au particle reaches ca.	pd-au	67-72	programmed cell death 1	Homo sapiens	17-20
33430403-7	2021	Further Pd content increase up to almost pure Pd core is accompanied by increased concentration of surface Pd atoms, mostly as Pd1 sites, although larger Pd ensembles as dimers and linear trimers are formed as well.	Palladium	8-10	programmed cell death 1	Homo sapiens	127-130
33430403-7	2021	Further Pd content increase up to almost pure Pd core is accompanied by increased concentration of surface Pd atoms, mostly as Pd1 sites, although larger Pd ensembles as dimers and linear trimers are formed as well.	Palladium	46-48	programmed cell death 1	Homo sapiens	127-130
33430403-7	2021	Further Pd content increase up to almost pure Pd core is accompanied by increased concentration of surface Pd atoms, mostly as Pd1 sites, although larger Pd ensembles as dimers and linear trimers are formed as well.	Palladium	46-48	programmed cell death 1	Homo sapiens	127-130
33430403-7	2021	Further Pd content increase up to almost pure Pd core is accompanied by increased concentration of surface Pd atoms, mostly as Pd1 sites, although larger Pd ensembles as dimers and linear trimers are formed as well.	Palladium	46-48	programmed cell death 1	Homo sapiens	127-130
33080152-1	2021	PURPOSE: Five programmed cell death protein 1 (PD-1) or its ligand (L1) inhibitors are approved for treatment of platinum-refractory locally advanced/unresectable or metastatic urothelial carcinoma.	Platinum	113-121	programmed cell death 1	Homo sapiens	14-45
33080152-1	2021	PURPOSE: Five programmed cell death protein 1 (PD-1) or its ligand (L1) inhibitors are approved for treatment of platinum-refractory locally advanced/unresectable or metastatic urothelial carcinoma.	Platinum	113-121	programmed cell death 1	Homo sapiens	47-51
32542563-14	2021	Peritumoral TILs and PD-1 expressions may predict a better response to DPCP.	diphenylcyclopropenone	71-75	programmed cell death 1	Homo sapiens	21-25
33087895-11	2021	CONCLUSIONS: Patients who relapse after adjuvant TT respond well to subsequent anti-PD-1 based therapy and have outcomes similar to those seen when first line anti-PD-1 therapy is used in stage IV melanoma.	6-thiotheophylline	49-51	programmed cell death 1	Homo sapiens	84-88
33268528-0	2021	Cyclophosphamide and vinorelbine activate stem-like CD8+ T cells and improve anti-PD-1 efficacy in triple-negative breast cancer.	Cyclophosphamide	0-16	programmed cell death 1	Homo sapiens	82-86
33268528-0	2021	Cyclophosphamide and vinorelbine activate stem-like CD8+ T cells and improve anti-PD-1 efficacy in triple-negative breast cancer.	Vinorelbine	21-32	programmed cell death 1	Homo sapiens	82-86
33353450-7	2021	5-Aza-2"-deoxycytidine decreased the activity of DNMTs in all the subjects and may have induced a more pronounced upward trend of PD-1 expression in HBV patients.	Decitabine	0-22	programmed cell death 1	Homo sapiens	130-134
33355035-1	2021	BACKGROUND: Several immuno-oncology (IO) agents targeting programmed death-1 or programmed death-ligand 1 (PD-1/L1) are approved second-line therapy options for patients with locally advanced or metastatic urothelial carcinoma (la/mUC) previously treated with platinum-based chemotherapy or first-line options in patients ineligible for cisplatin whose tumors express PD-L1 or for any platinum-based chemotherapy regardless of PD-L1 expression levels.	Platinum	260-268	programmed cell death 1	Homo sapiens	107-111
33355035-1	2021	BACKGROUND: Several immuno-oncology (IO) agents targeting programmed death-1 or programmed death-ligand 1 (PD-1/L1) are approved second-line therapy options for patients with locally advanced or metastatic urothelial carcinoma (la/mUC) previously treated with platinum-based chemotherapy or first-line options in patients ineligible for cisplatin whose tumors express PD-L1 or for any platinum-based chemotherapy regardless of PD-L1 expression levels.	Cisplatin	337-346	programmed cell death 1	Homo sapiens	107-111
33355035-1	2021	BACKGROUND: Several immuno-oncology (IO) agents targeting programmed death-1 or programmed death-ligand 1 (PD-1/L1) are approved second-line therapy options for patients with locally advanced or metastatic urothelial carcinoma (la/mUC) previously treated with platinum-based chemotherapy or first-line options in patients ineligible for cisplatin whose tumors express PD-L1 or for any platinum-based chemotherapy regardless of PD-L1 expression levels.	Platinum	385-393	programmed cell death 1	Homo sapiens	107-111
33613701-0	2021	Baseline lesion number as an efficacy predictive and independent prognostic factor and its joint utility with TMB for PD-1 inhibitor treatment in advanced gastric cancer.	1,2,4,5-tetramethoxybenzene	110-113	programmed cell death 1	Homo sapiens	118-122
33584591-0	2020	Low-Density Granulocytes Affect T-SPOT.TB Assay by Inhibiting the Production of Interferon-gamma in T Cells via PD-L1/PD-1 Pathway.	Terbium	39-41	programmed cell death 1	Homo sapiens	118-122
33747719-6	2021	The improved delivery of irinotecan by the silicasome is accompanied by robust antitumor immunity, which can be synergistically enhanced by anti-PD-1 in the orthotopic model.	Irinotecan	25-35	programmed cell death 1	Homo sapiens	145-149
33584637-0	2020	Lysophosphatidic Acid Is an Inflammatory Lipid Exploited by Cancers for Immune Evasion via Mechanisms Similar and Distinct From CTLA-4 and PD-1.	lysophosphatidic acid	0-21	programmed cell death 1	Homo sapiens	139-143
33460396-9	2021	GSEA identified that the PD1 signaling pathway was negatively associated with these prognostic factors which may explain the cardiovascular side effect of immune checkpoint therapy in anti-tumor treatment.	gsea	0-4	programmed cell death 1	Homo sapiens	25-28
33148676-7	2021	Combination treatment with anti-IL-1b plus anti-PD-1 or cabozantinib showed increased anti-tumor activity that was associated with decreases in immunosuppressive MDSC and increases in M1-like TAM.	tam	192-195	programmed cell death 1	Homo sapiens	48-52
32683672-12	2021	Furthermore, ibrutinib enriched CART cells with less-differentiated naive-like phenotype and decreased expression of exhaustion markers including PD-1, TIM-3, and LAG-3.	ibrutinib	13-22	programmed cell death 1	Homo sapiens	146-150
33024998-7	2021	Patient-derived xenograft tumors treated with avadomide were converted to CD8+ T cell-inflamed tumor microenvironments (TMEs) that responded to anti-PD-L1/PD-1-based combination therapy.	3-(5-amino-2-methyl-4-oxoquinazolin-3(4H)-yl)piperidine-2,6-dione	46-55	programmed cell death 1	Homo sapiens	155-159
33073996-2	2021	N-glycosylation of PD-L1 affects its interaction with PD-1, but little is known about the distribution of glycoforms at its four NXS/T sequons.	Nitrogen	0-1	programmed cell death 1	Homo sapiens	54-58
32467569-6	2021	Intraperitoneal administration of CS1003 (0.1, 0.5, 2.5 mg/kg, once every 3 days) dose-dependently suppressed the growth of MC38-hPD-L1 colon cancer in hPD-1 knock-in mice.	5-(pyrazin-2-yl)pyridin-2-amine	34-40	programmed cell death 1	Homo sapiens	152-157
33078505-1	2021	Although nivolumab, a programmed cell death 1 (PD-1) inhibitor, is a standard therapy for platinum-refractory recurrent or metastatic head and neck squamous cell carcinoma (R/M HNSCC), no definitive biomarkers have been reported thus far.	Platinum	90-98	programmed cell death 1	Homo sapiens	47-51
33239433-5	2021	Concurrent dexamethasone also abrogated survival following anti-PD-1 therapy with or without radiotherapy in immune-resistant CT-2A models.	Dexamethasone	11-24	programmed cell death 1	Homo sapiens	64-68
33112279-4	2021	Case: We report a patient with ACTH-secreting pituitary carcinoma, progressive after multiple lines of therapy including chemotherapy with TMZ, who demonstrated disease stabilization by a combination of ipilimumab (anti-CTLA-4) and nivolumab (anti-PD-1) ICI therapy.	Temozolomide	139-142	programmed cell death 1	Homo sapiens	248-252
32281670-8	2021	DAA treatment restored ADCC ability and reduced PD1 expression.	daa	0-3	programmed cell death 1	Homo sapiens	48-51
33129113-4	2021	The aim of this study is to demonstrate the potential of deep learning to facilitate the prediction of anti-PD-1 response from H&E images directly.	Helium	127-130	programmed cell death 1	Homo sapiens	108-112
33129113-9	2021	INTERPRETATION: To our knowledge, this is the first study of using deep learning to determine patients" anti-PD-1 response from H&E slides directly.	Helium	128-131	programmed cell death 1	Homo sapiens	109-113
33221685-1	2021	BACKGROUND: This study aimed to evaluate the effect of salvage therapy with nab-paclitaxel (nab-p) or temozolomide (TMZ) combined with antiangiogenic drugs in programmed death 1 (PD-1) inhibitor-resistant patients with unresectable metastatic melanoma.	nab	76-79	programmed cell death 1	Homo sapiens	159-177
33221685-1	2021	BACKGROUND: This study aimed to evaluate the effect of salvage therapy with nab-paclitaxel (nab-p) or temozolomide (TMZ) combined with antiangiogenic drugs in programmed death 1 (PD-1) inhibitor-resistant patients with unresectable metastatic melanoma.	nab	76-79	programmed cell death 1	Homo sapiens	179-183
33221685-1	2021	BACKGROUND: This study aimed to evaluate the effect of salvage therapy with nab-paclitaxel (nab-p) or temozolomide (TMZ) combined with antiangiogenic drugs in programmed death 1 (PD-1) inhibitor-resistant patients with unresectable metastatic melanoma.	Paclitaxel	80-90	programmed cell death 1	Homo sapiens	159-177
33221685-1	2021	BACKGROUND: This study aimed to evaluate the effect of salvage therapy with nab-paclitaxel (nab-p) or temozolomide (TMZ) combined with antiangiogenic drugs in programmed death 1 (PD-1) inhibitor-resistant patients with unresectable metastatic melanoma.	Paclitaxel	80-90	programmed cell death 1	Homo sapiens	179-183
33221685-1	2021	BACKGROUND: This study aimed to evaluate the effect of salvage therapy with nab-paclitaxel (nab-p) or temozolomide (TMZ) combined with antiangiogenic drugs in programmed death 1 (PD-1) inhibitor-resistant patients with unresectable metastatic melanoma.	Temozolomide	102-114	programmed cell death 1	Homo sapiens	159-177
33221685-1	2021	BACKGROUND: This study aimed to evaluate the effect of salvage therapy with nab-paclitaxel (nab-p) or temozolomide (TMZ) combined with antiangiogenic drugs in programmed death 1 (PD-1) inhibitor-resistant patients with unresectable metastatic melanoma.	Temozolomide	102-114	programmed cell death 1	Homo sapiens	179-183
33221685-1	2021	BACKGROUND: This study aimed to evaluate the effect of salvage therapy with nab-paclitaxel (nab-p) or temozolomide (TMZ) combined with antiangiogenic drugs in programmed death 1 (PD-1) inhibitor-resistant patients with unresectable metastatic melanoma.	Temozolomide	116-119	programmed cell death 1	Homo sapiens	159-177
33221685-1	2021	BACKGROUND: This study aimed to evaluate the effect of salvage therapy with nab-paclitaxel (nab-p) or temozolomide (TMZ) combined with antiangiogenic drugs in programmed death 1 (PD-1) inhibitor-resistant patients with unresectable metastatic melanoma.	Temozolomide	116-119	programmed cell death 1	Homo sapiens	179-183
33099251-1	2020	OBJECTIVE: To investigate whether cynaroside protects human periodontal ligament (hPDL) cells from lipopolysaccharide (LPS)-induced damage and inflammation and to analyze the underlying mechanism.	luteolin-7-glucoside	34-44	programmed cell death 1	Homo sapiens	82-86
33073996-6	2021	Molecular modeling of PD-L1/PD-1 interaction with N-glycans suggests that glycans at the N219 site of PD-L1 and N74 and N116 of PD-1 may be involved in glycan-glycan interactions, but the impact of this potential interaction on the protein function remains at this point unknown.	n-glycans	50-59	programmed cell death 1	Homo sapiens	28-32
33073996-6	2021	Molecular modeling of PD-L1/PD-1 interaction with N-glycans suggests that glycans at the N219 site of PD-L1 and N74 and N116 of PD-1 may be involved in glycan-glycan interactions, but the impact of this potential interaction on the protein function remains at this point unknown.	n-glycans	50-59	programmed cell death 1	Homo sapiens	128-132
33073996-6	2021	Molecular modeling of PD-L1/PD-1 interaction with N-glycans suggests that glycans at the N219 site of PD-L1 and N74 and N116 of PD-1 may be involved in glycan-glycan interactions, but the impact of this potential interaction on the protein function remains at this point unknown.	Polysaccharides	52-59	programmed cell death 1	Homo sapiens	28-32
33073996-6	2021	Molecular modeling of PD-L1/PD-1 interaction with N-glycans suggests that glycans at the N219 site of PD-L1 and N74 and N116 of PD-1 may be involved in glycan-glycan interactions, but the impact of this potential interaction on the protein function remains at this point unknown.	Polysaccharides	52-59	programmed cell death 1	Homo sapiens	128-132
33073996-6	2021	Molecular modeling of PD-L1/PD-1 interaction with N-glycans suggests that glycans at the N219 site of PD-L1 and N74 and N116 of PD-1 may be involved in glycan-glycan interactions, but the impact of this potential interaction on the protein function remains at this point unknown.	Polysaccharides	52-58	programmed cell death 1	Homo sapiens	28-32
33073996-6	2021	Molecular modeling of PD-L1/PD-1 interaction with N-glycans suggests that glycans at the N219 site of PD-L1 and N74 and N116 of PD-1 may be involved in glycan-glycan interactions, but the impact of this potential interaction on the protein function remains at this point unknown.	Polysaccharides	52-58	programmed cell death 1	Homo sapiens	128-132
33073996-6	2021	Molecular modeling of PD-L1/PD-1 interaction with N-glycans suggests that glycans at the N219 site of PD-L1 and N74 and N116 of PD-1 may be involved in glycan-glycan interactions, but the impact of this potential interaction on the protein function remains at this point unknown.	Polysaccharides	74-80	programmed cell death 1	Homo sapiens	28-32
33073996-6	2021	Molecular modeling of PD-L1/PD-1 interaction with N-glycans suggests that glycans at the N219 site of PD-L1 and N74 and N116 of PD-1 may be involved in glycan-glycan interactions, but the impact of this potential interaction on the protein function remains at this point unknown.	Polysaccharides	74-80	programmed cell death 1	Homo sapiens	128-132
33099251-6	2020	RESULTS: Cynaroside inhibited the expression of iNOS, COX-2, TNF-alpha, and IL-6 in LPS-stimulated hPDL and RAW264.7 cells without cytotoxicity.	luteolin-7-glucoside	9-19	programmed cell death 1	Homo sapiens	99-103
33099251-9	2020	Moreover, cynaroside could restore the mineralization ability of hPDL cells reduced by LPS.	luteolin-7-glucoside	10-20	programmed cell death 1	Homo sapiens	65-69
33099251-10	2020	CONCLUSION: Cynaroside protected hPDL cells from LPS-induced damage and inflammation via inhibition of NF-kappaB activation.	luteolin-7-glucoside	12-22	programmed cell death 1	Homo sapiens	33-37
33230973-6	2020	Genomic profiling revealed that compared with the patient"s samples collected at baseline, the post-TMZ-treatment samples had markedly higher levels of tumor mutational burden (TMB) associated with characteristic alkylating mutational signature representing a positive correlation with favorable response to anti-PD-1 treatment.	Temozolomide	100-103	programmed cell death 1	Homo sapiens	313-317
33230973-8	2020	This case suggests that anti-PD-1 therapy could be a treatment option for PanNET patients with increased TMB after TMZ-based treatment.	1,2,4,5-tetramethoxybenzene	105-108	programmed cell death 1	Homo sapiens	29-33
33230973-8	2020	This case suggests that anti-PD-1 therapy could be a treatment option for PanNET patients with increased TMB after TMZ-based treatment.	Temozolomide	115-118	programmed cell death 1	Homo sapiens	29-33
33418913-4	2021	Recent data suggest that, among the potential mechanisms behind the lack of responsiveness or resistance to anti-PD-L1/PD-1 antibodies, the CD38 metabolic pathways involving the immune-suppressive factor, adenosine, could play an important role.	Adenosine	205-214	programmed cell death 1	Homo sapiens	119-123
33643804-3	2021	Herein, an oxygen-enriched X-ray nanoprocessor Hb@Hf-Ce6 nanoparticle is developed for improving the therapeutic effect of RT-radiodynamic therapy (RDT), enhancing modulation of hypoxia tumor microenvironment (TME) and promoting antitumor immune response in combination with programmed cell death protein 1 (PD-1) immune checkpoint blockade.	Oxygen	11-17	programmed cell death 1	Homo sapiens	275-306
33643804-3	2021	Herein, an oxygen-enriched X-ray nanoprocessor Hb@Hf-Ce6 nanoparticle is developed for improving the therapeutic effect of RT-radiodynamic therapy (RDT), enhancing modulation of hypoxia tumor microenvironment (TME) and promoting antitumor immune response in combination with programmed cell death protein 1 (PD-1) immune checkpoint blockade.	Oxygen	11-17	programmed cell death 1	Homo sapiens	308-312
33457080-0	2020	M1-like TAMs are required for the efficacy of PD-L1/PD-1 blockades in gastric cancer.	Tamoxifen	8-12	programmed cell death 1	Homo sapiens	52-56
33376237-2	2020	Here, we report the efficacy of anti-programmed death 1 (PD-1) antibody with the P-GEMOX (pegaspargase, gemcitabine, and oxaliplatin) regimen in advanced NKTL.	p-gemox	81-88	programmed cell death 1	Homo sapiens	57-61
33376237-2	2020	Here, we report the efficacy of anti-programmed death 1 (PD-1) antibody with the P-GEMOX (pegaspargase, gemcitabine, and oxaliplatin) regimen in advanced NKTL.	pegaspargase	90-102	programmed cell death 1	Homo sapiens	57-61
33376237-2	2020	Here, we report the efficacy of anti-programmed death 1 (PD-1) antibody with the P-GEMOX (pegaspargase, gemcitabine, and oxaliplatin) regimen in advanced NKTL.	gemcitabine	104-115	programmed cell death 1	Homo sapiens	57-61
33376237-2	2020	Here, we report the efficacy of anti-programmed death 1 (PD-1) antibody with the P-GEMOX (pegaspargase, gemcitabine, and oxaliplatin) regimen in advanced NKTL.	Oxaliplatin	121-132	programmed cell death 1	Homo sapiens	57-61
33375291-9	2020	In mice, the anti-tumor efficacy of anti-PD-1 can be enhanced by depleting Tregs.	tregs	75-80	programmed cell death 1	Homo sapiens	41-45
33375291-10	2020	This suggests Tregs pose resistance to anti-PD-1 therapy.	tregs	14-19	programmed cell death 1	Homo sapiens	44-48
33375291-11	2020	In this article, we review the relevant Treg functions that suppress tumor immunity and the potential effects anti-PD-1 could have on Tregs which are counter-productive to the treatment of cancer, occasionally causing HPD.	tregs	134-139	programmed cell death 1	Homo sapiens	115-119
33377131-6	2020	Susceptible tumors are characterized by a stemness signature, an activated interferon pathway, and suppression of PD-1 ligands in response to 5-FU+irinotecan.	Fluorouracil	142-146	programmed cell death 1	Homo sapiens	114-118
33377131-6	2020	Susceptible tumors are characterized by a stemness signature, an activated interferon pathway, and suppression of PD-1 ligands in response to 5-FU+irinotecan.	Irinotecan	147-157	programmed cell death 1	Homo sapiens	114-118
33377134-3	2020	In vitro, MGD019 mediates the combinatorial blockade of PD-1 and CTLA-4, confirming dual inhibition via a single molecule.	mgd019	10-16	programmed cell death 1	Homo sapiens	56-60
33377134-4	2020	MGD019 is well tolerated in non-human primates, with evidence of both PD-1 and CTLA-4 blockade, including increases in Ki67+CD8 and ICOS+CD4 T cells, respectively.	mgd019	0-6	programmed cell death 1	Homo sapiens	70-74
33390946-0	2020	Choosing PD-1 Inhibitors in Oncology Setting, Left or Right?-Lessons From Value Assessment With ASCO-VF and ESMO-MCBS.	esmo-mcbs	108-117	programmed cell death 1	Homo sapiens	9-13
33326644-11	2021	CONCLUSION: Our results, showing an increase in PD-1 and PD-L1 expression in HCC following TACE, support the use of TACE in combination with immunotherapy in selected cases to optimize tumor response.	Chlorotrianisene	91-95	programmed cell death 1	Homo sapiens	48-52
33326644-11	2021	CONCLUSION: Our results, showing an increase in PD-1 and PD-L1 expression in HCC following TACE, support the use of TACE in combination with immunotherapy in selected cases to optimize tumor response.	Chlorotrianisene	116-120	programmed cell death 1	Homo sapiens	48-52
33311449-0	2020	Anti-PD1 therapy induces lymphocyte-derived exosomal miRNA-4315 release inhibiting Bim-mediated apoptosis of tumor cells.	mirna-4315	53-63	programmed cell death 1	Homo sapiens	5-8
33311449-7	2020	We found that anti-PD1 exposure of T-cell promotes an enrichment of exosomal miRNA-4315.	mirna-4315	77-87	programmed cell death 1	Homo sapiens	19-22
33311449-11	2020	A longitudinal study using patient blood showed that miRNA-4315 and cytochrome c can be used to define the time period during which the addition of ABT263 therapy may effectively increase cancer cell death and bypass anti-PD1 resistance.This work provides a blood biomarker (exosomal miRNA-4315) for patient stratification developing a phenomenon of resistance to anti-PD1 antibody therapy and also identifies a therapeutic alternative (the use of a BH3 mimetic drug) to limit this resistance phenomenon.	navitoclax	148-154	programmed cell death 1	Homo sapiens	222-225
33311449-11	2020	A longitudinal study using patient blood showed that miRNA-4315 and cytochrome c can be used to define the time period during which the addition of ABT263 therapy may effectively increase cancer cell death and bypass anti-PD1 resistance.This work provides a blood biomarker (exosomal miRNA-4315) for patient stratification developing a phenomenon of resistance to anti-PD1 antibody therapy and also identifies a therapeutic alternative (the use of a BH3 mimetic drug) to limit this resistance phenomenon.	navitoclax	148-154	programmed cell death 1	Homo sapiens	369-372
33311449-11	2020	A longitudinal study using patient blood showed that miRNA-4315 and cytochrome c can be used to define the time period during which the addition of ABT263 therapy may effectively increase cancer cell death and bypass anti-PD1 resistance.This work provides a blood biomarker (exosomal miRNA-4315) for patient stratification developing a phenomenon of resistance to anti-PD1 antibody therapy and also identifies a therapeutic alternative (the use of a BH3 mimetic drug) to limit this resistance phenomenon.	mirna-4315	53-63	programmed cell death 1	Homo sapiens	369-372
33311600-6	2021	Here, we develop a PD-L1-targeting immune liposome (P-Lipo) for co-delivering irinotecan (IRI) and JQ1, and this system can successfully elicit antitumor immunity in colorectal cancer through inducing ICD by IRI and interfering in the immunosuppressive PD-1/PD-L1 pathway by JQ1.	Irinotecan	78-88	programmed cell death 1	Homo sapiens	253-257
33363038-6	2020	This case indicates that the combination of PD-1 inhibitor and HDAC inhibitor might be a treatment choice for immunotherapy-resistant NKTCL.	nktcl	134-139	programmed cell death 1	Homo sapiens	44-48
32860704-8	2020	NMR spectroscopy revealed changes in tumor lactate as a potential early biomarker for IL17/PD-1 combination efficacy.	Lactic Acid	43-50	programmed cell death 1	Homo sapiens	91-95
33311988-0	2020	Complete Response to the Sequential Treatment with Regorafenib Followed by PD-1 Inhibitor in a Sorafenib-Refractory Hepatocellular Carcinoma Patient.	Sorafenib	95-104	programmed cell death 1	Homo sapiens	75-79
33311988-13	2020	Data from this clinical case report suggest that sequential treatment with regorafenib followed by PD-1 inhibitor is a promising therapeutic option for sorafenib-refractory cases of HCCs.	Sorafenib	152-161	programmed cell death 1	Homo sapiens	99-103
33289336-3	2020	Herein, a photoswitched CRISPR/Cas9 system for genomic disruption of the PD-L1 gene is developed to achieve permanent blockade of the PD-1/PD-L1 pathway; this system is constructed by using a photoactivated self-degradable polyethyleneimine derivative and the plasmid pX330/sgPD-L1 (expression of the Cas9 protein and single-guide RNA targeting PD-L1).	aziridine	223-240	programmed cell death 1	Homo sapiens	134-138
32393842-5	2020	Among patients receiving tacrolimus/sirolimus, nivolumab-exposed patients had a higher incidence of severe aGVHD and a more effector T-cell profile compared with anti-PD-1-naive patients.	Tacrolimus	25-35	programmed cell death 1	Homo sapiens	167-171
32662522-7	2020	This case indicates that the addition of nintedanib and glucocorticoid might possibly have potentially therapeutic effects of PD-1 induced pulmonary fibrosis and hypercytokinaemia.	nintedanib	41-51	programmed cell death 1	Homo sapiens	126-130
32393842-5	2020	Among patients receiving tacrolimus/sirolimus, nivolumab-exposed patients had a higher incidence of severe aGVHD and a more effector T-cell profile compared with anti-PD-1-naive patients.	Sirolimus	36-45	programmed cell death 1	Homo sapiens	167-171
32851941-7	2020	A month after the onset of the endocrinopathy, the patient also developed steroid-responsive encephalitis, considered as a consequence of anti-PD-1 therapy.	Steroids	74-81	programmed cell death 1	Homo sapiens	143-147
33020660-6	2020	Furthermore, supplementation with nicotinamide riboside enhanced T cell mitochondrial fitness and improved responsiveness to anti-PD-1 treatment.	nicotinamide-beta-riboside	34-55	programmed cell death 1	Homo sapiens	130-134
32920330-5	2020	Here, we found that anti-PD-1 treatment boosted circulating Tregs levels, which presented the most remarkable augment during the first two therapeutic cycles, in NSCLC patients.	tregs	60-65	programmed cell death 1	Homo sapiens	25-29
32920330-9	2020	Consistently, Tregs levels robustly increased in the syngeneic tumor model after anti-mouse PD-1 Ab treatment.	tregs	14-19	programmed cell death 1	Homo sapiens	92-96
32920330-12	2020	In conclusion, anti-PD-1 therapy upregulates Tregs levels in NSCLC patients, and the M-MDSC levels are associated with the anti-tumor efficacy of anti-PD-1 treatment.	tregs	45-50	programmed cell death 1	Homo sapiens	20-24
32920330-12	2020	In conclusion, anti-PD-1 therapy upregulates Tregs levels in NSCLC patients, and the M-MDSC levels are associated with the anti-tumor efficacy of anti-PD-1 treatment.	tregs	45-50	programmed cell death 1	Homo sapiens	151-155
33299657-0	2020	Soluble forms of PD-L1 and PD-1 as prognostic and predictive markers of sunitinib efficacy in patients with metastatic clear cell renal cell carcinoma.	Sunitinib	72-81	programmed cell death 1	Homo sapiens	27-31
33330386-2	2020	Programmed cell death 1 (PD-1) could be phosphorylated at its immunoreceptor tyrosine-based inhibitory motif (ITIM) and immunoreceptor tyrosine-based switch motif (ITSM) and can bind to SHP2 to initiate T cell inactivation.	Tyrosine	77-85	programmed cell death 1	Homo sapiens	0-23
33143424-5	2020	A homogenous cancer cell membrane was coated on the surfaces of these DLMSNs, followed by conjugation with the anti-PD-1 peptide AUNP-12 through a polyethylene glycol linker with an acid-labile benzoic-imine bond.	AUNP-12	129-136	programmed cell death 1	Homo sapiens	116-120
32790005-4	2020	The Pd 1 /alpha-MoC catalyst exhibits high activity and excellent selectivity for both liquid-phase hydrogenation of substituted nitroaromatics (> 99%) and gas-phase hydrogenation of CO 2 to CO (> 98%), which is far superior to their nanoparticles analogues.	nitroaromatics	129-143	programmed cell death 1	Homo sapiens	4-8
32790005-4	2020	The Pd 1 /alpha-MoC catalyst exhibits high activity and excellent selectivity for both liquid-phase hydrogenation of substituted nitroaromatics (> 99%) and gas-phase hydrogenation of CO 2 to CO (> 98%), which is far superior to their nanoparticles analogues.	Carbon Dioxide	183-187	programmed cell death 1	Homo sapiens	4-8
32790005-4	2020	The Pd 1 /alpha-MoC catalyst exhibits high activity and excellent selectivity for both liquid-phase hydrogenation of substituted nitroaromatics (> 99%) and gas-phase hydrogenation of CO 2 to CO (> 98%), which is far superior to their nanoparticles analogues.	Carbon Monoxide	183-185	programmed cell death 1	Homo sapiens	4-8
33330386-2	2020	Programmed cell death 1 (PD-1) could be phosphorylated at its immunoreceptor tyrosine-based inhibitory motif (ITIM) and immunoreceptor tyrosine-based switch motif (ITSM) and can bind to SHP2 to initiate T cell inactivation.	Tyrosine	77-85	programmed cell death 1	Homo sapiens	25-29
33330386-2	2020	Programmed cell death 1 (PD-1) could be phosphorylated at its immunoreceptor tyrosine-based inhibitory motif (ITIM) and immunoreceptor tyrosine-based switch motif (ITSM) and can bind to SHP2 to initiate T cell inactivation.	Tyrosine	135-143	programmed cell death 1	Homo sapiens	0-23
33330386-2	2020	Programmed cell death 1 (PD-1) could be phosphorylated at its immunoreceptor tyrosine-based inhibitory motif (ITIM) and immunoreceptor tyrosine-based switch motif (ITSM) and can bind to SHP2 to initiate T cell inactivation.	Tyrosine	135-143	programmed cell death 1	Homo sapiens	25-29
33095222-0	2020	Conjugation of biphenyl groups with poly(ethylene glycol) to enhance inhibitory effects on the PD-1/PD-L1 immune checkpoint interaction.	Polyethylene Glycols	36-57	programmed cell death 1	Homo sapiens	95-99
33095222-5	2020	However, the inhibitory effect on PD-1/PD-L1 interaction was further enhanced by using branched PEG conjugates.	Polyethylene Glycols	96-99	programmed cell death 1	Homo sapiens	34-38
32602900-4	2020	Compared with NNK-induced lung tumors, NNK+LPS-induced lung tumors exhibited an immunosuppressive microenvironment characterized by higher relative abundances of PD-1+ tumor-associated macrophages, PD-L1+ tumor cells, PD-1+ CD4 and CD8 T lymphocytes and FOXP3+ CD4 and CD8 T lymphocytes.	4-(N-methyl-N-nitrosamino)-1-(3-pyridyl)-1-butanone	39-42	programmed cell death 1	Homo sapiens	162-166
32966436-4	2020	When the proton is at D1-His190, Em(TyrZ) is the lowest and can serve as an electron donor to the oxidized chlorophyll PD1 +.	Chlorophyll	107-118	programmed cell death 1	Homo sapiens	119-122
33192094-6	2020	Anti-PD-1 single/combination therapy may be used as a strategy for treating advanced refractory TC.	Technetium	96-98	programmed cell death 1	Homo sapiens	5-9
33209062-2	2020	Recently, TAMs have become increasingly recognised as an attractive target in combination therapy with PD-1/PD-L1 immuno-checkpoint blockades (ICBs).	tams	10-14	programmed cell death 1	Homo sapiens	103-107
33177572-10	2020	We note that core TAMs evolve towards a pro-inflammatory state and identify a subpopulation of cells based on a gene program exhibiting strong, opposing correlation with Programmed cell Death-1 (PD-1) signaling, which may correlate to their response to PD-1 inhibition.	tams	18-22	programmed cell death 1	Homo sapiens	195-199
33177572-10	2020	We note that core TAMs evolve towards a pro-inflammatory state and identify a subpopulation of cells based on a gene program exhibiting strong, opposing correlation with Programmed cell Death-1 (PD-1) signaling, which may correlate to their response to PD-1 inhibition.	tams	18-22	programmed cell death 1	Homo sapiens	253-257
32933967-7	2020	Furthermore, resistance to immunotherapy (anti-PD-1 antibody) and chemotherapy (cisplatin) were both overcome by co-administration of the P2X7 inhibitors O-ATP, A-438079 hydrochloride and A-740003.	periodate-oxidized adenosine 5'-triphosphate	154-159	programmed cell death 1	Homo sapiens	47-51
32500232-11	2020	Induction of CD8+ PD-1+ tumor-infiltrating lymphocytes and PD-L1 expression in the TME by vaccination suggests S-588410 in combination with anti-PD-(L)1 antibodies may offer a clinically useful therapy.Trial registration UMIN-CTR registration identifier: UMIN000023324.	s-588410	111-119	programmed cell death 1	Homo sapiens	18-23
32529292-14	2020	Adoptive TIL therapy combined with PD-1 inhibitors might be promising for TNBC patients with residual tumors after NAC.	nac	115-118	programmed cell death 1	Homo sapiens	35-39
32933967-7	2020	Furthermore, resistance to immunotherapy (anti-PD-1 antibody) and chemotherapy (cisplatin) were both overcome by co-administration of the P2X7 inhibitors O-ATP, A-438079 hydrochloride and A-740003.	A 438079 hydrochloride	161-183	programmed cell death 1	Homo sapiens	47-51
32933967-7	2020	Furthermore, resistance to immunotherapy (anti-PD-1 antibody) and chemotherapy (cisplatin) were both overcome by co-administration of the P2X7 inhibitors O-ATP, A-438079 hydrochloride and A-740003.	(N-(1-(((cyanoimino)(5-quinolinylamino) methyl) amino)-2,2-dimethylpropyl)-2-(3,4-dimethoxyphenyl)acetamide)	188-196	programmed cell death 1	Homo sapiens	47-51
32748216-13	2020	In anti-PD-1-mAb-pretreated patients, PTCy-based GvHD prophylaxis may be effective.	ptcy	38-42	programmed cell death 1	Homo sapiens	8-12
32496569-0	2020	Advanced malignant melanoma successfully treated with dacarbazine following anti-PD-1/CTLA-4 treatment.	Dacarbazine	54-65	programmed cell death 1	Homo sapiens	81-85
33000216-0	2020	M2-TAM subsets altered by lactic acid promote T-cell apoptosis through the PD-L1/PD-1 pathway.	tam	3-6	programmed cell death 1	Homo sapiens	81-85
33154150-10	2020	CONCLUSION: We confirmed the association between baseline steroids administered for cancer-related indication, systemic antibiotics, PPIs and worse clinical outcomes with PD-1/PD-L1 checkpoint inhibitors, which can be assumed to have immune-modulating detrimental effects.	Steroids	58-66	programmed cell death 1	Homo sapiens	171-175
33158915-10	2020	By targeting the SOX2-JAK-STAT signaling, SAHA promoted the antitumor efficacy of IFNgamma or anti-PD-1 in vitro and in vivo.	Vorinostat	42-46	programmed cell death 1	Homo sapiens	99-103
33000216-0	2020	M2-TAM subsets altered by lactic acid promote T-cell apoptosis through the PD-L1/PD-1 pathway.	Lactic Acid	26-37	programmed cell death 1	Homo sapiens	81-85
33142805-7	2020	A significant link exists between altered lipid and glucose metabolism in different cells and the expression of PD-1/PD-L1 molecules, and its possible implications on vascular inflammation are justified.	Glucose	52-59	programmed cell death 1	Homo sapiens	112-116
32721947-6	2020	RESULTS: In glioma patients, the adenosine-CD73-CD39 immune suppressive pathway was most frequently expressed, followed by PD-1.	Adenosine	33-42	programmed cell death 1	Homo sapiens	123-127
33193362-8	2020	In co-culture, dMP-treated DCs (dMP-DCs) reduced allogeneic T cell receptor (TCR) signaling and proliferation, while increasing PD-1 expression, IL-10 production, and regulatory T cell (Treg) frequency.	dmp	15-18	programmed cell death 1	Homo sapiens	128-132
33193362-8	2020	In co-culture, dMP-treated DCs (dMP-DCs) reduced allogeneic T cell receptor (TCR) signaling and proliferation, while increasing PD-1 expression, IL-10 production, and regulatory T cell (Treg) frequency.	dmp	32-35	programmed cell death 1	Homo sapiens	128-132
32690363-6	2020	We found that hPD-1 can quench fluorescence of carboxytetramethylrhodamine labeled on its N-terminal and QPD-1 is a convenient tool to rapidly detect hPD-L1 with a limit of detection of 10 nM and detectable range of 10 nM-1000 nM.	carboxytetramethylrhodamine	47-74	programmed cell death 1	Homo sapiens	14-19
32984529-8	2020	Conclusion: Antifungal azole therapy is commonly used in oncology patients who may be co-treated with PD-1 inhibitors.	Azoles	23-28	programmed cell death 1	Homo sapiens	102-106
32868421-7	2020	[D. J. Nurnberg et al., Science 360, 1210-1213 (2018)], in which the primary electron donor is a FR-chlorophyll and the secondary donor is chlorophyll-a (PD1 of the central chlorophyll pair).	chlorophyll a	139-152	programmed cell death 1	Homo sapiens	154-157
32716739-1	2020	PURPOSE: The immunomodulatory effect of lenvatinib (a multikinase inhibitor) on tumor microenvironments may contribute to antitumor activity when combined with programmed death receptor-1 (PD-1) signaling inhibitors in hepatocellular carcinoma (HCC).	lenvatinib	40-50	programmed cell death 1	Homo sapiens	189-193
33098265-2	2020	Here, we explore the prognostic role of DDR alterations in advanced UC treated with anti-PD-1/PD-L1 agents.	ddr	40-43	programmed cell death 1	Homo sapiens	89-93
33194624-4	2020	However, all three patients responded to low-dose decitabine, an epigenetic drug, in combination with camrelizumab (anti-PD-1 antibody), with only controllable adverse events, indicating that low-dose decitabine can sensitize PD-1/PD-L1 inhibitors.	Decitabine	50-60	programmed cell death 1	Homo sapiens	226-230
33194624-4	2020	However, all three patients responded to low-dose decitabine, an epigenetic drug, in combination with camrelizumab (anti-PD-1 antibody), with only controllable adverse events, indicating that low-dose decitabine can sensitize PD-1/PD-L1 inhibitors.	Decitabine	201-211	programmed cell death 1	Homo sapiens	226-230
33194624-5	2020	Summary: We report a novel therapy with low-dose decitabine plus camrelizumab for advanced NSCLC on the basis of successful treatment of three patients, emphasizing the potential of epigenetic drugs to regulate PD-1/PD-L1 inhibitors in advanced NSCLC.	Decitabine	49-59	programmed cell death 1	Homo sapiens	211-215
33092011-2	2020	Alternatively, the potential impact of the lenvatinib in patients who showed tumor progression on PD-1/PD-L1 blockade is unknown.	lenvatinib	43-53	programmed cell death 1	Homo sapiens	98-102
33092011-4	2020	The outcome and safety of lenvatinib administered after PD-1/PD-L1 blockade failure was analyzed retrospectively in 36 patients.	lenvatinib	26-36	programmed cell death 1	Homo sapiens	56-60
33092011-10	2020	Lenvatinib demonstrated considerable antitumor effects with acceptable safety in patients with progressive and unresectable HCC when administered right after PD-1/PD-L1 blockade failure.	lenvatinib	0-10	programmed cell death 1	Homo sapiens	158-162
33150045-1	2020	Antibodies targeting the co-inhibitory receptor programmed cell death 1 (PDCD1, best known as PD-1) or its main ligand CD274 (best known as PD-L1) have shown some activity in patients with metastatic triple-negative breast cancer (TNBC), especially in a recent Phase III clinical trial combining PD-L1 blockade with taxane-based chemotherapy.	taxane	316-322	programmed cell death 1	Homo sapiens	48-71
33150045-1	2020	Antibodies targeting the co-inhibitory receptor programmed cell death 1 (PDCD1, best known as PD-1) or its main ligand CD274 (best known as PD-L1) have shown some activity in patients with metastatic triple-negative breast cancer (TNBC), especially in a recent Phase III clinical trial combining PD-L1 blockade with taxane-based chemotherapy.	taxane	316-322	programmed cell death 1	Homo sapiens	73-78
33150045-1	2020	Antibodies targeting the co-inhibitory receptor programmed cell death 1 (PDCD1, best known as PD-1) or its main ligand CD274 (best known as PD-L1) have shown some activity in patients with metastatic triple-negative breast cancer (TNBC), especially in a recent Phase III clinical trial combining PD-L1 blockade with taxane-based chemotherapy.	taxane	316-322	programmed cell death 1	Homo sapiens	94-98
33193355-11	2020	In adults, the loss of PD1 expression in naive Treg and naive Th cells was associated with cGvHD.	treg	47-51	programmed cell death 1	Homo sapiens	23-26
32964498-4	2020	Here, we show that inhibition of N6 -methyladenosine (m6 A) mRNA modification by depletion of methyltransferases, Mettl3 and Mettl14, enhanced response to anti-PD-1 treatment in pMMR-MSI-L CRC and melanoma.	N-methyladenosine	33-52	programmed cell death 1	Homo sapiens	160-164
33076303-7	2020	Among the sociologic factors, sex and race positively influenced the CPI effectiveness on account of increased effector T cell activity and increased PD-1 expression while ageing impaired CPI responsiveness by decreasing functional T cell and increased toxicity.	methyl 2-isocyano-2-methylpropanoate	69-72	programmed cell death 1	Homo sapiens	150-154
33055241-0	2020	Intratumoral nanoplexed poly I:C BO-112 in combination with systemic anti-PD-1 for patients with anti-PD-1-refractory tumors.	Poly I	24-30	programmed cell death 1	Homo sapiens	74-78
33055241-6	2020	In a fourth cohort of 28 patients with tumors that had primary resistance to anti-programmed cell death protein-1 (PD-1), the combination of intratumoral BO-112 with nivolumab or pembrolizumab was also well tolerated, and 3 patients (2 with melanoma and 1 with renal cell carcinoma) achieved partial responses, with 10 more patients having stable disease at 8 to 12 weeks.	bo-112	154-160	programmed cell death 1	Homo sapiens	82-113
33055241-7	2020	Thus, local BO-112 combined with a systemic anti-PD-1 agent might be a strategy to revert anti-PD-1 resistance.	bo-112	12-18	programmed cell death 1	Homo sapiens	49-53
33055241-7	2020	Thus, local BO-112 combined with a systemic anti-PD-1 agent might be a strategy to revert anti-PD-1 resistance.	bo-112	12-18	programmed cell death 1	Homo sapiens	95-99
33163408-1	2020	Background: The anti-programmed cell death protein-1 (PD-1) inhibitor is one of the second-line therapies for advanced hepatocellular carcinoma (HCC) after sorafenib failure.	Sorafenib	156-165	programmed cell death 1	Homo sapiens	21-52
33163408-1	2020	Background: The anti-programmed cell death protein-1 (PD-1) inhibitor is one of the second-line therapies for advanced hepatocellular carcinoma (HCC) after sorafenib failure.	Sorafenib	156-165	programmed cell death 1	Homo sapiens	54-58
32936638-0	2020	Di-bromo-Based Small-Molecule Inhibitors of the PD-1/PD-L1 Immune Checkpoint.	di-bromo	0-8	programmed cell death 1	Homo sapiens	48-52
32236803-0	2020	1H, 13C, 15N chemical shift assignments of SHP2 SH2 domains in complex with PD-1 immune-tyrosine motifs.	Hydrogen	0-2	programmed cell death 1	Homo sapiens	76-80
32236803-0	2020	1H, 13C, 15N chemical shift assignments of SHP2 SH2 domains in complex with PD-1 immune-tyrosine motifs.	13c	4-7	programmed cell death 1	Homo sapiens	76-80
32236803-0	2020	1H, 13C, 15N chemical shift assignments of SHP2 SH2 domains in complex with PD-1 immune-tyrosine motifs.	15n	9-12	programmed cell death 1	Homo sapiens	76-80
32236803-0	2020	1H, 13C, 15N chemical shift assignments of SHP2 SH2 domains in complex with PD-1 immune-tyrosine motifs.	Tyrosine	88-96	programmed cell death 1	Homo sapiens	76-80
32236803-4	2020	Activation of PD-1 leads to phosphorylation of two signaling motifs located in its cytoplasmic domain, the immune tyrosine inhibitory motif (ITIM) and immune tyrosine switch motif (ITSM), which recruit and activate protein tyrosine phosphatase SHP2.	Tyrosine	114-122	programmed cell death 1	Homo sapiens	14-18
32236803-4	2020	Activation of PD-1 leads to phosphorylation of two signaling motifs located in its cytoplasmic domain, the immune tyrosine inhibitory motif (ITIM) and immune tyrosine switch motif (ITSM), which recruit and activate protein tyrosine phosphatase SHP2.	Tyrosine	158-166	programmed cell death 1	Homo sapiens	14-18
32873605-3	2020	Here, we describe LY3434172, a bispecific IgG1 mAb with ablated Fc immune effector function that targets both human PD-1 and PD-L1.	ly3434172	18-27	programmed cell death 1	Homo sapiens	116-120
32873605-4	2020	LY3434172 fully inhibited the major inhibitory receptor-ligand interactions in the PD-1 pathway.	ly3434172	0-9	programmed cell death 1	Homo sapiens	83-87
32810392-8	2020	Oxysophocarpine sensitized the Lag-3 immunotherapy effect of CD8+ T cells against HCC in vivo and in vitro by decreasing Fibrinogen-like protein 1 (FGL1) expression through downregulating IL-6-mediated JAK2/STAT3 signaling, whereas Oxysophocarpine treatment had a little effect of CD8+ T cells cytotoxicity function against HCC with PD-1, Tim-3, or TIGIT blockade.	oxysophocarpine	0-15	programmed cell death 1	Homo sapiens	333-337
32474075-9	2020	The in vivo study demonstrates reduction of heart and kidney apoptosis with increased programmed cell death protein-1 (PD-1); as the major anticancer drug (doxorubicin) pathway is to release free radicals with decreased PD-1 levels and induction of apoptosis.	Doxorubicin	156-167	programmed cell death 1	Homo sapiens	86-117
32474075-9	2020	The in vivo study demonstrates reduction of heart and kidney apoptosis with increased programmed cell death protein-1 (PD-1); as the major anticancer drug (doxorubicin) pathway is to release free radicals with decreased PD-1 levels and induction of apoptosis.	Doxorubicin	156-167	programmed cell death 1	Homo sapiens	119-123
32474075-9	2020	The in vivo study demonstrates reduction of heart and kidney apoptosis with increased programmed cell death protein-1 (PD-1); as the major anticancer drug (doxorubicin) pathway is to release free radicals with decreased PD-1 levels and induction of apoptosis.	Doxorubicin	156-167	programmed cell death 1	Homo sapiens	220-224
31985048-0	2020	(Curcumin+sildenafil) enhances the efficacy of 5FU and anti-PD1 therapies in vivo.	Curcumin	1-20	programmed cell death 1	Homo sapiens	60-63
32747741-3	2020	By dispersing Pd atoms onto Cu nanomaterials with different exposed facets, Cu(111) and Cu(100), we demonstrate in this work that while the hydrogen spillover from Pd to Cu is facet independent, the spillover hydrogenation only occurs on Pd1/Cu(100), where the hydrogen atoms spilled from Pd are readily utilized for the semi-hydrogenation of alkynes.	Palladium	14-16	programmed cell death 1	Homo sapiens	238-241
32747741-3	2020	By dispersing Pd atoms onto Cu nanomaterials with different exposed facets, Cu(111) and Cu(100), we demonstrate in this work that while the hydrogen spillover from Pd to Cu is facet independent, the spillover hydrogenation only occurs on Pd1/Cu(100), where the hydrogen atoms spilled from Pd are readily utilized for the semi-hydrogenation of alkynes.	Hydrogen	140-148	programmed cell death 1	Homo sapiens	238-241
33131514-1	2020	Objective To investigate the clinical features and treatments of programmed death-1(PD-1)inhibitors-induced bullous pemphigoid(BP).Methods The clinicopathological and immunohistological data of patients with PD-1 inhibitors-induced BP from Peking Union Medical Collage Hospital and reported in the literature were retrospectively analyzed.Results Totally 21 cases(15 males and 6 females)were enrolled.The average age was(70.9+-9.7)years(56-86 years).The most common primary malignancies were melanoma(38.10%)and lung cancer(33.33%).The average duration from onset of PD-1 inhibitors treatment to diagnosis of BP was(49.1+-23.7)weeks.Typical dermatopathological features were sub-epidermal blisters(76.19%)with infiltration of eosinophils(88.24%).Direct immunofluorescence features were linear deposition of complement C3(95%)and IgG(75%)in the basement membrane zone.Anti-BP180-NC16A antibodies were positive in most cases(84.21%).Patients were mainly treated with systemic corticosteroids,whereas biologics such as rituximab and omazumab were also effective.Conclusions The risk of PD-1 inhibitors-induced BP should be recognized by dermatologists and oncologists.Early diagnosis and timely treatment of BP induced by PD-1 inhibitors are important to improve the prognosis.	DDP-BLM protocol	127-129	programmed cell death 1	Homo sapiens	84-88
32963251-0	2020	Publisher Correction: Phosphorylation of PD-1-Y248 is a marker of PD-1-mediated inhibitory function in human T cells.	y248	46-50	programmed cell death 1	Homo sapiens	41-45
32963251-0	2020	Publisher Correction: Phosphorylation of PD-1-Y248 is a marker of PD-1-mediated inhibitory function in human T cells.	y248	46-50	programmed cell death 1	Homo sapiens	66-70
31981371-8	2020	Coculture with human peripheral blood mononuclear cells (PBMCs) with poly I:C-activated hPDL cells was performed.	Poly I	69-75	programmed cell death 1	Homo sapiens	88-92
32947924-2	2020	The combination of PD-1/PD-L1 immune checkpoint inhibitors (ICIs) with first-line platinum-etoposide chemotherapy has been recently evaluated in randomized clinical trials.	Platinum	82-90	programmed cell death 1	Homo sapiens	19-23
32878822-0	2020	Recovery of the Sensitivity to Anti-PD-1 Antibody by Celecoxib in Lung Cancer.	Celecoxib	53-62	programmed cell death 1	Homo sapiens	36-40
32878822-1	2020	BACKGROUND/AIM: Experimental studies have shown that celecoxib is related to the downregulation of Tregs and an increase in the therapeutic efficacy of PD-1 inhibitors; however, such effect has not been shown in human cancers.	Celecoxib	53-62	programmed cell death 1	Homo sapiens	152-156
32878822-2	2020	Our report confirmed the synergistic effect of celecoxib with a PD-1 inhibitor.	Celecoxib	47-56	programmed cell death 1	Homo sapiens	64-68
32585229-8	2020	Targeting CD73-derived adenosine via small molecule inhibitor or monoclonal antibodies studies especially in combination with immune checkpoint blockers including PD-1 and CTLA-4 have shown desirable results for management of melanoma in preclinical studies and several clinical trials have recently been started to evaluate the therapeutic potential of CD73-derived adenosine targeting in solid tumors.	Adenosine	367-376	programmed cell death 1	Homo sapiens	163-167
31981371-13	2020	In co-culture experiments, poly I:C-activated hPDL cells inhibited PBMCs proliferation and increased mRNA expression of forkhead box P3 (FOXP3), a transcription factor which is a marker of regulatory T cells.	Poly I	27-33	programmed cell death 1	Homo sapiens	46-50
32820119-2	2020	We identified major histocompatibility complex (MHC) class I-binding epitopes in the tail length tape measure protein (TMP) of a prophage found in the genome of the bacteriophage Enterococcus hirae Mice bearing E. hirae harboring this prophage mounted a TMP-specific H-2Kb-restricted CD8+ T lymphocyte response upon immunotherapy with cyclophosphamide or anti-PD-1 antibodies.	tmp	119-122	programmed cell death 1	Homo sapiens	360-364
32843031-11	2020	Estimated TMB by the 23-gene panel was significantly associated with DFS and OS in patients with early-stage NSCLC and could serve as a predictive biomarker for anti-PD-1 and anti-PD-L1 treatment response.	1,2,4,5-tetramethoxybenzene	10-13	programmed cell death 1	Homo sapiens	166-170
32859050-7	2020	Furthermore, OCT LAR treatment induces a functional impairment of the remaining circulating Tregs, significantly decreasing the expression of PD1, CTLA4 and ENTPD1.	oct lar	13-20	programmed cell death 1	Homo sapiens	142-145
32820119-4	2020	In renal and lung cancer patients, the presence of the enterococcal prophage in stools and expression of a TMP-cross-reactive antigen by tumors correlated with long-term benefit of PD-1 blockade therapy.	tmp	107-110	programmed cell death 1	Homo sapiens	181-185
32719002-0	2020	Improved efficacy of taxanes and ramucirumab combination chemotherapy after exposure to anti-PD-1 therapy in advanced gastric cancer.	Taxoids	21-28	programmed cell death 1	Homo sapiens	93-97
32973816-14	2020	After plasma glucose is well controlled using insulin therapy, PD-1 inhibitor treatment might be continued, especially when the immunotherapy is effective.	Glucose	13-20	programmed cell death 1	Homo sapiens	63-67
32747553-0	2020	ALKBH5 regulates anti-PD-1 therapy response by modulating lactate and suppressive immune cell accumulation in tumor microenvironment.	Lactic Acid	58-65	programmed cell death 1	Homo sapiens	22-26
32875254-0	2020	Synthesis and Evaluation of Biphenyl-1,2,3-Triazol-Benzonitrile Derivatives as PD-1/PD-L1 Inhibitors.	biphenyl-1,2,3-triazol-benzonitrile	28-63	programmed cell death 1	Homo sapiens	79-83
32667799-0	2020	Discovery of Novel Resorcinol Dibenzyl Ethers Targeting the Programmed Cell Death-1/Programmed Cell Death-Ligand 1 Interaction As Potential Anticancer Agents.	resorcinol dibenzyl ethers	19-45	programmed cell death 1	Homo sapiens	60-114
32667799-1	2020	Novel small molecule compounds based on various scaffolds including chalcone, flavonoid, and resorcinol dibenzyl ether were designed and tested for their inhibitory activity against the Programmed Cell Death-1/Programmed Cell Death-Ligand 1 (PD-1/PD-L1) pathway.	1,3-Dibenzyloxybenzene	93-118	programmed cell death 1	Homo sapiens	186-240
32667799-1	2020	Novel small molecule compounds based on various scaffolds including chalcone, flavonoid, and resorcinol dibenzyl ether were designed and tested for their inhibitory activity against the Programmed Cell Death-1/Programmed Cell Death-Ligand 1 (PD-1/PD-L1) pathway.	1,3-Dibenzyloxybenzene	93-118	programmed cell death 1	Homo sapiens	242-246
32784389-3	2020	The anti-PD-1 checkpoint inhibitors nivolumab and pembrolizumab have been FDA approved as a second line treatment in patients who progressed or are intolerant to Sorafenib.	Sorafenib	162-171	programmed cell death 1	Homo sapiens	9-13
32764539-4	2020	Here, we report a novel entropy-driven strategy to stabilize Pd single-atom on the high-entropy fluorite oxides (CeZrHfTiLa)Ox (HEFO) as the support by a combination of mechanical milling with calcination at 900  C. Characterization results reveal that single Pd atoms are incorporated into HEFO (Pd1@HEFO) sublattice by forming stable Pd-O-M bonds (M = Ce/Zr/La).	Palladium	61-63	programmed cell death 1	Homo sapiens	297-305
32764539-4	2020	Here, we report a novel entropy-driven strategy to stabilize Pd single-atom on the high-entropy fluorite oxides (CeZrHfTiLa)Ox (HEFO) as the support by a combination of mechanical milling with calcination at 900  C. Characterization results reveal that single Pd atoms are incorporated into HEFO (Pd1@HEFO) sublattice by forming stable Pd-O-M bonds (M = Ce/Zr/La).	fluorite oxides	96-111	programmed cell death 1	Homo sapiens	297-305
32764539-4	2020	Here, we report a novel entropy-driven strategy to stabilize Pd single-atom on the high-entropy fluorite oxides (CeZrHfTiLa)Ox (HEFO) as the support by a combination of mechanical milling with calcination at 900  C. Characterization results reveal that single Pd atoms are incorporated into HEFO (Pd1@HEFO) sublattice by forming stable Pd-O-M bonds (M = Ce/Zr/La).	cezrhftila)ox	113-126	programmed cell death 1	Homo sapiens	297-305
32764539-4	2020	Here, we report a novel entropy-driven strategy to stabilize Pd single-atom on the high-entropy fluorite oxides (CeZrHfTiLa)Ox (HEFO) as the support by a combination of mechanical milling with calcination at 900  C. Characterization results reveal that single Pd atoms are incorporated into HEFO (Pd1@HEFO) sublattice by forming stable Pd-O-M bonds (M = Ce/Zr/La).	hefo	128-132	programmed cell death 1	Homo sapiens	297-305
32764539-5	2020	Compared to the traditional support stabilized catalysts such as Pd@CeO2, Pd1@HEFO affords the improved reducibility of lattice oxygen and the existence of stable Pd-O-M species, thus exhibiting not only higher low-temperature CO oxidation activity but also outstanding resistance to thermal and hydrothermal degradation.	Palladium	65-67	programmed cell death 1	Homo sapiens	74-82
32764539-5	2020	Compared to the traditional support stabilized catalysts such as Pd@CeO2, Pd1@HEFO affords the improved reducibility of lattice oxygen and the existence of stable Pd-O-M species, thus exhibiting not only higher low-temperature CO oxidation activity but also outstanding resistance to thermal and hydrothermal degradation.	Oxygen	128-134	programmed cell death 1	Homo sapiens	74-82
32224220-3	2020	Here, we evaluated whether activation of neuroimmune cells such as human macrophage, brain endothelial cells (hBECs), astrocytes, microglia, and neurons by non-toxic concentrations of ethanol (EtOH) exposure can alter PD-1/PD-L1 expression.	Ethanol	184-191	programmed cell death 1	Homo sapiens	218-222
32224220-3	2020	Here, we evaluated whether activation of neuroimmune cells such as human macrophage, brain endothelial cells (hBECs), astrocytes, microglia, and neurons by non-toxic concentrations of ethanol (EtOH) exposure can alter PD-1/PD-L1 expression.	Ethanol	193-197	programmed cell death 1	Homo sapiens	218-222
32224220-4	2020	Thus, the present study is limited to the screening of PD-1/PD-L1 alterations in neuroimmune cells following ethanol exposure.	Ethanol	109-116	programmed cell death 1	Homo sapiens	55-59
32224220-5	2020	We found that exposure of human macrophage or microglia to EtOH in primary culture immediately increased the levels of PD-L1 and gradually up-regulated PD-1 levels (beginning at 1-2 hours).	Ethanol	59-63	programmed cell death 1	Homo sapiens	152-156
32224220-6	2020	Similarly, ethanol exposure was able to induce PD-1/PD-L1 levels in hBECs and neuronal culture in a delayed process (occurring at 24 hours).	Ethanol	11-18	programmed cell death 1	Homo sapiens	47-51
32224220-7	2020	Astrocyte culture was the only cell type that showed endogenous levels of PD-1/PD-L1 that was decreased by EtOH exposure time-dependently.	Ethanol	107-111	programmed cell death 1	Homo sapiens	74-78
32224220-8	2020	We concluded that ethanol (alcohol) mediated the induction of PD-1/PD-L1 differentially in neuroimmune cells.	Ethanol	18-25	programmed cell death 1	Homo sapiens	62-66
32224220-8	2020	We concluded that ethanol (alcohol) mediated the induction of PD-1/PD-L1 differentially in neuroimmune cells.	Alcohols	27-34	programmed cell death 1	Homo sapiens	62-66
32224220-9	2020	Taken together, our findings suggest that up-regulation of PD-1/PD-L1 by chronic alcohol use may dampen the innate immune response of neuroimmune cells, thereby contributing to neuroinflammation and neurodegeneration.	Alcohols	81-88	programmed cell death 1	Homo sapiens	59-63
32599410-2	2020	With an expanding role of ICB in earlier lines of therapy, we assessed activity of cabozantinib in patients with metastatic ccRCC after progressing on anti-PD-1/PD-L1-based ICBs.	cabozantinib	83-95	programmed cell death 1	Homo sapiens	156-160
32894535-1	2020	OBJECTIVE: To assess associations between parameters derived from F-18 fluorodeoxyglucose (FDG) positron emission tomography (PET) and mRNA expression levels of immune checkpoint biomarkers such as programmed death receptor 1 (PD-1), programmed death-ligand 1 (PD-L1), cytotoxic T-lymphocyte antigen 4 (CTLA-4) as well as tumor mutation burden (TMB) in non-small cell lung cancer (NSCLC) patients.	Fluorodeoxyglucose F18	66-89	programmed cell death 1	Homo sapiens	227-231
32894535-1	2020	OBJECTIVE: To assess associations between parameters derived from F-18 fluorodeoxyglucose (FDG) positron emission tomography (PET) and mRNA expression levels of immune checkpoint biomarkers such as programmed death receptor 1 (PD-1), programmed death-ligand 1 (PD-L1), cytotoxic T-lymphocyte antigen 4 (CTLA-4) as well as tumor mutation burden (TMB) in non-small cell lung cancer (NSCLC) patients.	Fluorodeoxyglucose F18	91-94	programmed cell death 1	Homo sapiens	227-231
32508184-0	2020	15-hydroxy-6alpha,12-epoxy-7beta,10alphaH,11betaH-spiroax-4-ene-12-onesensitizesrectal tumor cells to anti-PD1 treatment through agonism of CD11b.	15-hydroxy-6alpha,12-epoxy-7beta	0-32	programmed cell death 1	Homo sapiens	107-110
32508184-0	2020	15-hydroxy-6alpha,12-epoxy-7beta,10alphaH,11betaH-spiroax-4-ene-12-onesensitizesrectal tumor cells to anti-PD1 treatment through agonism of CD11b.	10alphah	33-41	programmed cell death 1	Homo sapiens	107-110
32508184-0	2020	15-hydroxy-6alpha,12-epoxy-7beta,10alphaH,11betaH-spiroax-4-ene-12-onesensitizesrectal tumor cells to anti-PD1 treatment through agonism of CD11b.	11betah-spiroax-4-ene-12	42-66	programmed cell death 1	Homo sapiens	107-110
32508184-5	2020	CD11b is highly expressed on the myeloid cell surface with an important role in their trafficking and cellular functions.In this study, we demonstrated that activation of CD11b with 15-hydroxy-6alpha,12-epoxy-7beta,10alphaH,11betaH-spiroax-4-ene-12-one (HESEO) enhanced the therapeutic efficacy of anti-PD1 treatment in the tumor model.	15-hydroxy-6alpha,12-epoxy-7beta	182-214	programmed cell death 1	Homo sapiens	303-306
32508184-5	2020	CD11b is highly expressed on the myeloid cell surface with an important role in their trafficking and cellular functions.In this study, we demonstrated that activation of CD11b with 15-hydroxy-6alpha,12-epoxy-7beta,10alphaH,11betaH-spiroax-4-ene-12-one (HESEO) enhanced the therapeutic efficacy of anti-PD1 treatment in the tumor model.	10alphah	215-223	programmed cell death 1	Homo sapiens	303-306
32508184-5	2020	CD11b is highly expressed on the myeloid cell surface with an important role in their trafficking and cellular functions.In this study, we demonstrated that activation of CD11b with 15-hydroxy-6alpha,12-epoxy-7beta,10alphaH,11betaH-spiroax-4-ene-12-one (HESEO) enhanced the therapeutic efficacy of anti-PD1 treatment in the tumor model.	11betah-spiroax-4-ene-12-one	224-252	programmed cell death 1	Homo sapiens	303-306
32508184-5	2020	CD11b is highly expressed on the myeloid cell surface with an important role in their trafficking and cellular functions.In this study, we demonstrated that activation of CD11b with 15-hydroxy-6alpha,12-epoxy-7beta,10alphaH,11betaH-spiroax-4-ene-12-one (HESEO) enhanced the therapeutic efficacy of anti-PD1 treatment in the tumor model.	heseo	254-259	programmed cell death 1	Homo sapiens	303-306
32515012-0	2020	Rechallenge of programmed cell death 1 inhibitor after an interval with dacarbazine treatment may be effective for advanced malignant melanoma.	Dacarbazine	72-83	programmed cell death 1	Homo sapiens	15-38
32515012-9	2020	Even if the first PD-1 inhibitor proves to be ineffective, it is worth re-administrating PD-1 inhibitor following a bridging therapy with DTIC.	Dacarbazine	138-142	programmed cell death 1	Homo sapiens	89-93
32737343-0	2020	A nanoscale metal organic frameworks-based vaccine synergises with PD-1 blockade to potentiate anti-tumour immunity.	Metals	12-17	programmed cell death 1	Homo sapiens	67-71
32801879-9	2020	Conclusion: 18F-FDG PET/CT may potentially predict tumor PD-L1 expression and play a role in predicting prognosis of PD-L1/PD-1 immunotherapy in lung adenocarcinoma.	Fluorodeoxyglucose F18	12-19	programmed cell death 1	Homo sapiens	123-127
32677895-9	2020	Ghrelin and GH treatment reduced program death receptor-1 (PD-1) expression, increased human leukocyte antigen-DR (HLA-DR) expression, attenuated lymphopenia, and cleaved caspase-3 levels in the spleen of septic aged rats.	Ghrelin	0-7	programmed cell death 1	Homo sapiens	59-63
32754587-9	2020	Thus, miR-138-5p inhibits tumor growth and activates the immune system by down-regulating PD-1/PD-L1 and it is a promising therapeutic target for NSCLC.	mir-138-5p	6-16	programmed cell death 1	Homo sapiens	90-94
32670420-0	2020	Efficacy and safety of PD-1/PD-L1 inhibitors plus nab-paclitaxel for patients with non-small cell lung cancer who have progressed after platinum-based chemotherapy.	Platinum	136-144	programmed cell death 1	Homo sapiens	23-27
32670420-10	2020	Conclusion: PD-1/PD-L1 inhibitor plus nab-paclitaxel resulted in significantly longer OS and higher response versus ICI single agent in metastatic NSCLC patients who have progressed after platinum-based chemotherapy.	Platinum	188-196	programmed cell death 1	Homo sapiens	12-16
32620165-3	2020	N-linked glycosylation of PD-L1 maintains its protein stability and interaction with its cognate receptor, programmed cell death protein 1 (PD-1), and this in turn promotes evasion of T-cell immunity.	Nitrogen	0-1	programmed cell death 1	Homo sapiens	107-138
32620165-3	2020	N-linked glycosylation of PD-L1 maintains its protein stability and interaction with its cognate receptor, programmed cell death protein 1 (PD-1), and this in turn promotes evasion of T-cell immunity.	Nitrogen	0-1	programmed cell death 1	Homo sapiens	140-144
32620165-6	2020	Notably, the removal of N-linked glycosylation enhances PD-L1 detection in a variety of bioassays and more accurately predicts the therapeutic efficacy of PD-1/PD-L1 inhibitors, suggesting an important clinical implication of PD-L1 N-linked glycosylation.	Nitrogen	0-1	programmed cell death 1	Homo sapiens	155-159
32840510-5	2020	Further results revealed that the synergistic immune stimulatory effects of CTLA-4 and PD-1 blockades in the form of hSNPs were at least partly through regulating the immune suppressive function of both Tregs and TIM3+ exhausted-like CD8 T cells and allowing effector T cells to expand.	tregs	203-208	programmed cell death 1	Homo sapiens	87-91
32756500-8	2020	The expression of immune checkpoint molecules PD-1 and LAG-3 positively correlated with the M2-TAM density in melanoma tissue.	tam	95-98	programmed cell death 1	Homo sapiens	46-50
32319671-3	2020	However, their conclusion about anti-PD-1 antibody treatment effecting a decline of PD-1+ Tregs is misleading.	tregs	90-95	programmed cell death 1	Homo sapiens	37-41
32388281-1	2020	Novel resorcinol diphenyl ether-based PROTACs (PROteolysis TArgeting Chimeras) were designed and evaluated for their inhibitory activity against the programmed cell death-1/programmed cell death-ligand 1 (PD-1/PD-L1) pathway and their ability to degrade PD-L1 protein.	1,3-Diphenoxybenzene	6-31	programmed cell death 1	Homo sapiens	149-203
32639111-9	2020	ROC curve analysis showed that serum uric acid (SUA), PD-1 mRNA and both combined displayed higher diagnostic value in patients with PG, NAPPG and APPG compared to that in NCs and patients with non-PG arthritis (NPG).	pg	133-135	programmed cell death 1	Homo sapiens	54-58
32589866-2	2020	Lenvatinib, a multikinase inhibitor of VEGF receptors and other receptor tyrosine kinases, substantially decreased tumour-associated macrophages and increased infiltration of CD8 T cells, resulting in enhanced anti-tumour activity of PD-1 inhibitors in an in-vivo model.	lenvatinib	0-10	programmed cell death 1	Homo sapiens	234-238
32801749-9	2020	It follows that PD-1 antibody, chidamide, etoposide, and thalidomide (PCET) regimen may be a promising choice for patients with R/R ENKTL and warrants further investigation.	Etoposide	42-51	programmed cell death 1	Homo sapiens	16-20
32801749-9	2020	It follows that PD-1 antibody, chidamide, etoposide, and thalidomide (PCET) regimen may be a promising choice for patients with R/R ENKTL and warrants further investigation.	Thalidomide	57-68	programmed cell death 1	Homo sapiens	16-20
32801749-9	2020	It follows that PD-1 antibody, chidamide, etoposide, and thalidomide (PCET) regimen may be a promising choice for patients with R/R ENKTL and warrants further investigation.	pcet	70-74	programmed cell death 1	Homo sapiens	16-20
32579975-4	2020	Through genetic code expansion, a latent bioreactive amino acid fluorosulfate-L-tyrosine (FSY) was incorporated into human programmed cell death protein-1 (PD-1).	amino acid fluorosulfate-l-tyrosine	53-88	programmed cell death 1	Homo sapiens	123-154
32579975-4	2020	Through genetic code expansion, a latent bioreactive amino acid fluorosulfate-L-tyrosine (FSY) was incorporated into human programmed cell death protein-1 (PD-1).	amino acid fluorosulfate-l-tyrosine	53-88	programmed cell death 1	Homo sapiens	156-160
32579975-4	2020	Through genetic code expansion, a latent bioreactive amino acid fluorosulfate-L-tyrosine (FSY) was incorporated into human programmed cell death protein-1 (PD-1).	fevipiprant	90-93	programmed cell death 1	Homo sapiens	123-154
32579975-4	2020	Through genetic code expansion, a latent bioreactive amino acid fluorosulfate-L-tyrosine (FSY) was incorporated into human programmed cell death protein-1 (PD-1).	fevipiprant	90-93	programmed cell death 1	Homo sapiens	156-160
32579975-5	2020	Only when PD-1 interacts with PD-L1 did the FSY react with a proximal histidine of PD-L1 selectively, enabling irreversible binding of PD-1 to only PD-L1 in vitro and in vivo.	Histidine	70-79	programmed cell death 1	Homo sapiens	10-14
32579975-5	2020	Only when PD-1 interacts with PD-L1 did the FSY react with a proximal histidine of PD-L1 selectively, enabling irreversible binding of PD-1 to only PD-L1 in vitro and in vivo.	Histidine	70-79	programmed cell death 1	Homo sapiens	135-139
32400116-0	2020	The Synthesis and Anti-tumour Properties of Poly Ethoxy Ethyl Glycinamide (PEE-G) Scaffolds with Multiple PD-1 Peptides Attached.	poly ethoxy ethyl glycinamide	44-73	programmed cell death 1	Homo sapiens	106-110
32400116-0	2020	The Synthesis and Anti-tumour Properties of Poly Ethoxy Ethyl Glycinamide (PEE-G) Scaffolds with Multiple PD-1 Peptides Attached.	pee-g	75-80	programmed cell death 1	Homo sapiens	106-110
32793733-6	2020	Most of the studies reported that hepatitis resulting from PD-1 inhibitor was manifested as elevated liver enzymes and bilirubin.	Bilirubin	119-128	programmed cell death 1	Homo sapiens	59-63
32719002-10	2020	CONCLUSIONS: Prior anti-PD-1 therapy might increase tumour response to taxanes plus ramucirumab without unexpected adverse events, which warrants further investigations in a large cohort.	Taxoids	71-78	programmed cell death 1	Homo sapiens	24-28
32397849-0	2020	Bispecific anti-PD-1/LAG-3 antibodies for treatment of advanced or metastatic solid tumors: a patent evaluation of US2018326054.	us2018326054	115-127	programmed cell death 1	Homo sapiens	16-20
32397849-2	2020	The authors of US2018326054 patent propose a method to eradicate cancer by using bispecific anti-PD-1/LAG-3 antibodies.Areas covered: The US2018326054 patent describes anti-PD-1/LAG3 antibodies, pharmaceutical composition that contains it, and their application for cancer treatment, particularly pancreatic carcinoma.	us2018326054	15-27	programmed cell death 1	Homo sapiens	97-101
32397849-2	2020	The authors of US2018326054 patent propose a method to eradicate cancer by using bispecific anti-PD-1/LAG-3 antibodies.Areas covered: The US2018326054 patent describes anti-PD-1/LAG3 antibodies, pharmaceutical composition that contains it, and their application for cancer treatment, particularly pancreatic carcinoma.	us2018326054	15-27	programmed cell death 1	Homo sapiens	173-177
32902402-0	2020	The possible regulatory effect of the PD-1/PD-L1 signaling pathway on Tregs in ovarian cancer.	tregs	70-75	programmed cell death 1	Homo sapiens	38-42
32902402-1	2020	Aim of this study was to investigate the possible regulatory effect of the programmed death-1 (PD-1)/programmed death ligand-1 (PD-L1) signaling pathway on Tregs in ovarian cancer.	tregs	156-161	programmed cell death 1	Homo sapiens	75-93
32902402-1	2020	Aim of this study was to investigate the possible regulatory effect of the programmed death-1 (PD-1)/programmed death ligand-1 (PD-L1) signaling pathway on Tregs in ovarian cancer.	tregs	156-161	programmed cell death 1	Homo sapiens	95-99
32709713-9	2020	CONCLUSION: MTV is a strong prognostic and predictive factor in patients with NSCLC treated with PD1 inhibitors and can be easily determined from routine 18F-FDG PET/CT scans.	mtv	12-15	programmed cell death 1	Homo sapiens	97-100
32709713-9	2020	CONCLUSION: MTV is a strong prognostic and predictive factor in patients with NSCLC treated with PD1 inhibitors and can be easily determined from routine 18F-FDG PET/CT scans.	Fluorodeoxyglucose F18	154-161	programmed cell death 1	Homo sapiens	97-100
32388276-8	2020	CONCLUSIONS: dNLR might be the most important factor for predicting the efficacy in NSCLC patients treated with anti-PD-1 therapy.	dnlr	13-17	programmed cell death 1	Homo sapiens	117-121
32115801-6	2020	Interestingly, 2-DG/gefitinib-induced deglycosylation of PD-L1 decreased the expression level of PD-L1 protein as well as its binding with PD-1.	Deoxyglucose	15-19	programmed cell death 1	Homo sapiens	139-143
32115801-6	2020	Interestingly, 2-DG/gefitinib-induced deglycosylation of PD-L1 decreased the expression level of PD-L1 protein as well as its binding with PD-1.	Gefitinib	20-29	programmed cell death 1	Homo sapiens	139-143
32585901-8	2020	The combination of anti-PD1 and BRAFi and/or MEKi was a safe rescue line for advanced melanoma patients previously treated with ICI/TT.	6-thiotheophylline	132-134	programmed cell death 1	Homo sapiens	24-27
32612680-3	2020	Programmed cell death 1 (PD-1) inhibitors showed encouraging results in the second line treatment of HCC after sorafenib but it efficacy in HCC-ICC has never been reported.	Sorafenib	111-120	programmed cell death 1	Homo sapiens	25-29
32596460-5	2020	Here, we show that our unique poly(2-oxazoline)-based nanomicellar formulation (PM) of Resiquimod, an imidazoquinoline Toll-like receptor (TLR) 7/8 agonist, had a superior tumor inhibitory effect in a metastatic model of lung adenocarcinoma, relative to anti-PD-1 therapy or platinum-based chemotherapy.	poly(2-oxazoline)	30-47	programmed cell death 1	Homo sapiens	259-263
32596460-5	2020	Here, we show that our unique poly(2-oxazoline)-based nanomicellar formulation (PM) of Resiquimod, an imidazoquinoline Toll-like receptor (TLR) 7/8 agonist, had a superior tumor inhibitory effect in a metastatic model of lung adenocarcinoma, relative to anti-PD-1 therapy or platinum-based chemotherapy.	resiquimod	87-97	programmed cell death 1	Homo sapiens	259-263
32521140-0	2020	Tofacitinib for Refractory Immune-Related Colitis from PD-1 Therapy.	tofacitinib	0-11	programmed cell death 1	Homo sapiens	55-59
32401534-5	2020	Further combination of nanovaccine with anti-programmed death-1 (anti-PD-1) checkpoint blockade offers effective inhibition on the growth of already-established melanoma.	nanovaccine	23-34	programmed cell death 1	Homo sapiens	70-74
32391629-4	2020	Here, we report that methylene blue (MB), an FDA-approved chemical for treating methemoglobinemia, potently inhibits PD-1 signaling.	Methylene Blue	21-35	programmed cell death 1	Homo sapiens	117-121
32391629-4	2020	Here, we report that methylene blue (MB), an FDA-approved chemical for treating methemoglobinemia, potently inhibits PD-1 signaling.	Methylene Blue	37-39	programmed cell death 1	Homo sapiens	117-121
32391629-6	2020	Mechanistically, MB blocks interaction between Y248-phosphorylated immunoreceptor tyrosine-based switch motif (ITSM) of human PD-1 and SHP2.	y248	47-51	programmed cell death 1	Homo sapiens	126-130
32391629-6	2020	Mechanistically, MB blocks interaction between Y248-phosphorylated immunoreceptor tyrosine-based switch motif (ITSM) of human PD-1 and SHP2.	Tyrosine	82-90	programmed cell death 1	Homo sapiens	126-130
32304268-5	2020	High frequency eTreg infiltration into HNSCC tissues was observed and high expressions of CD25, FOXP3, stimulatory-ICMs (4-1BB, ICOS, OX40 and GITR), and inhibitory-ICMs (PD-1 and CTLA-4) were found on invasive eTregs.	etreg	15-20	programmed cell death 1	Homo sapiens	171-175
32324337-8	2020	Our work suggests that both CD279 ligands contribute to the interaction length between T cells and macrophages as a mechanism of maintaining Treg homeostasis.	treg	141-145	programmed cell death 1	Homo sapiens	28-33
31495293-4	2020	The primary objective of this study is to determine if the use of concomitant steroids impacts the efficacy of anti-PD1 therapy.	Steroids	78-86	programmed cell death 1	Homo sapiens	116-119
32606052-12	2020	Notably, both GMS and PD-L1 were independent predictors and demonstrated poorly correlated; inclusion of PD-L1 with GMS further improved the predictive capacity for PD-1 blockade immunotherapy.	gms	116-119	programmed cell death 1	Homo sapiens	165-169
31495293-8	2020	RESULTS: Twenty-seven of 55 patients (13 melanoma, 11 NSCLC, 3 renal cell carcinoma) required steroids during anti-PD1 therapy.	Steroids	94-102	programmed cell death 1	Homo sapiens	115-118
31495293-13	2020	CONCLUSION: High-dose steroids for long durations during anti-PD1 therapy may be associated with poorer survival outcomes.	Steroids	22-30	programmed cell death 1	Homo sapiens	62-65
32387683-0	2020	Addition of ramucirumab enhances docetaxel efficacy in patients who had received anti-PD-1/PD-L1 treatment.	Docetaxel	33-42	programmed cell death 1	Homo sapiens	86-90
32387683-1	2020	OBJECTIVES: Docetaxel (DTX) efficacy increases in patients with non-small cell lung cancer (NSCLC) who had received anti-programmed cell death-1/ligand 1 (anti-PD-1/L1) therapy.	Docetaxel	12-21	programmed cell death 1	Homo sapiens	160-164
31764435-2	2020	Acute cellular allograft rejection on initiation of PD-1 inhibitor was successfully reversed with methylprednisolone.	Methylprednisolone	98-116	programmed cell death 1	Homo sapiens	52-56
32387683-1	2020	OBJECTIVES: Docetaxel (DTX) efficacy increases in patients with non-small cell lung cancer (NSCLC) who had received anti-programmed cell death-1/ligand 1 (anti-PD-1/L1) therapy.	Docetaxel	23-26	programmed cell death 1	Homo sapiens	160-164
32387683-3	2020	Here, we aimed to evaluate the effect of Ram on DTX efficacy following anti-PD-1/L1 therapy.	Docetaxel	48-51	programmed cell death 1	Homo sapiens	76-80
32387683-14	2020	CONCLUSIONS: DTX efficacy following anti-PD-1/L1 therapy may be enhanced by Ram.	Docetaxel	13-16	programmed cell death 1	Homo sapiens	41-45
32477577-4	2020	We treated a head and neck cancer patient (a 50-year-old Japanese male) who suffered from corticosteroid-resistant hepatitis during treatment with nivolumab, an anti-PD-1 ICI, and that was recovered by mycophenolate mofetil salvage therapy.	Mycophenolic Acid	202-223	programmed cell death 1	Homo sapiens	166-170
32238919-2	2020	Reportedly, fluoro-D-glucose (FDG)-uptake alteration by anti-PD-1 antibody treatment depicts the response in patients with lung cancer.	fluoro-d-glucose	12-28	programmed cell death 1	Homo sapiens	61-65
32455628-0	2020	Preparation of Biphenyl-Conjugated Bromotyrosine for Inhibition of PD-1/PD-L1 Immune Checkpoint Interactions.	bromotyrosine	35-48	programmed cell death 1	Homo sapiens	67-71
32429929-9	2020	Within tumor samples, TILs, CD8+ T cells, and PD-L1/PD-1 expression decreased after NAC.	nac	84-87	programmed cell death 1	Homo sapiens	52-56
32429929-10	2020	Additionally, fewer tumor specimens were considered to be PD-L1/PD-1 positive post-NAC as compared to pre-NAC biopsy samples using a cutoff of 1% expression.	nac	83-86	programmed cell death 1	Homo sapiens	64-68
32430013-13	2020	Furthermore, sitagliptin may enhance the efficacy of anti-PD1 therapy in a subgroup of patients with HCC.	Sitagliptin Phosphate	13-24	programmed cell death 1	Homo sapiens	58-61
32406880-2	2020	In this article, we provide a comprehensive review of the preclinical and clinical activity of enfortumab vedotin, which has been recently approved in the U.S. for the treatment of adult patients with locally advanced or metastatic urothelial carcinoma who have previously received a programmed cell death protein 1 (PD-1)/programmed cell death 1 ligand 1 (PD-L1) inhibitor as well as platinum-containing chemotherapy in the neoadjuvant/adjuvant, locally advanced or metastatic setting.	vedotin	106-113	programmed cell death 1	Homo sapiens	284-315
32221038-0	2020	Metformin Enhances the Antitumor Activity of CD8+ T Lymphocytes via the AMPK-miR-107-Eomes-PD-1 Pathway.	Metformin	0-9	programmed cell death 1	Homo sapiens	91-95
32221038-5	2020	In addition, AMP-activated protein kinase (AMPK) activation decreased microRNA-107 expression, thus enhancing Eomesodermin expression, which suppressed the transcription of PDCD1 in metformin-treated CD8+ T cells.	Metformin	182-191	programmed cell death 1	Homo sapiens	173-178
32197264-3	2020	Especially, the TOF of Pt/@-La2O3/SBA-15 reached 2324h-1, 2.3-fold higher than the atomically dispersed catalyst(Pd1/TiO2, 1002 h-1) in the literature.	Platinum	23-25	programmed cell death 1	Homo sapiens	113-116
32197264-3	2020	Especially, the TOF of Pt/@-La2O3/SBA-15 reached 2324h-1, 2.3-fold higher than the atomically dispersed catalyst(Pd1/TiO2, 1002 h-1) in the literature.	lanthanum oxide	26-33	programmed cell death 1	Homo sapiens	113-116
32197264-3	2020	Especially, the TOF of Pt/@-La2O3/SBA-15 reached 2324h-1, 2.3-fold higher than the atomically dispersed catalyst(Pd1/TiO2, 1002 h-1) in the literature.	sba	34-37	programmed cell death 1	Homo sapiens	113-116
32365500-2	2020	Previous studies have shown that ginsenosides can regulate the expression of PD-1 and PD-L1 in target diseases; however, it remains unknown whether ginsenosides act as a blockade of PD-1/PD-L1 interactions.	Ginsenosides	33-45	programmed cell death 1	Homo sapiens	77-81
32365500-2	2020	Previous studies have shown that ginsenosides can regulate the expression of PD-1 and PD-L1 in target diseases; however, it remains unknown whether ginsenosides act as a blockade of PD-1/PD-L1 interactions.	Ginsenosides	148-160	programmed cell death 1	Homo sapiens	182-186
32365500-3	2020	In this study, we used competitive ELISA to investigate 12 ginsenosides for their ability to block PD-1/PD-L1 interactions.	Ginsenosides	59-71	programmed cell death 1	Homo sapiens	99-103
32365500-4	2020	In addition, we performed a protein-ligand docking simulation and examined the hydrophobic interactions and hydrogen bonds formed at the interfaces between the ginsenosides and PD-L1/PD-1.	Ginsenosides	160-172	programmed cell death 1	Homo sapiens	183-187
32365500-5	2020	Eight out of the 12 ginsenosides studied showed inhibition of PD-1/PD-L1 interactions at 35% at the maximum concentration (1 muM).	Ginsenosides	20-32	programmed cell death 1	Homo sapiens	62-66
32365500-7	2020	Rg3 and C-K were further identified for their interaction efficacy with PD-1/PD-L1, which supported our results demonstrating the blocking activity of these compounds against PD-1/PD-L1 binding interactions.	ginsenoside Rg3	0-3	programmed cell death 1	Homo sapiens	72-76
32365500-7	2020	Rg3 and C-K were further identified for their interaction efficacy with PD-1/PD-L1, which supported our results demonstrating the blocking activity of these compounds against PD-1/PD-L1 binding interactions.	ginsenoside Rg3	0-3	programmed cell death 1	Homo sapiens	175-179
32365500-8	2020	Collectively, our findings suggest that some ginsenosides, including Rg3 and C-K, inhibit PD-1/PD-L1 binding interactions.	Ginsenosides	45-57	programmed cell death 1	Homo sapiens	90-94
32365500-8	2020	Collectively, our findings suggest that some ginsenosides, including Rg3 and C-K, inhibit PD-1/PD-L1 binding interactions.	ginsenoside Rg3	69-72	programmed cell death 1	Homo sapiens	90-94
32365500-8	2020	Collectively, our findings suggest that some ginsenosides, including Rg3 and C-K, inhibit PD-1/PD-L1 binding interactions.	ginsenoside M1	77-80	programmed cell death 1	Homo sapiens	90-94
32490201-4	2020	We found that this carrier-free therapeutic system can serve as a reservoir for extended tumoral release of camptothecin and aPD1 antibody, resulting in an immune-stimulating tumor microenvironment for boosted PD-1 blockade immune response.	Camptothecin	108-120	programmed cell death 1	Homo sapiens	210-214
31980914-15	2020	In a preclinical study, adding anti-PD-1 monoclonal antibody to CHP-NY-ESO-1 and MIS416 induced significant tumor suppression.	chp-ny-eso-1	64-76	programmed cell death 1	Homo sapiens	36-40
31953314-10	2020	Finally, adenosine signaling is associated with reduced efficacy of anti-PD1 therapy in published cohorts (HR=0.29, p=0.00012).	Adenosine	9-18	programmed cell death 1	Homo sapiens	73-76
32341383-5	2020	An antitumor effect was observed in animals that received anti-PD-1 treatment, alone or in combination with cisplatin, likely due to a mechanism independent of T lymphocytes.	Cisplatin	108-117	programmed cell death 1	Homo sapiens	63-67
32337213-7	2020	The mean annual cost of treatment for the four EMA-approved indications of anti-PD-1 therapy was estimated to be $48.7 million in the control group and at $421.8 million in the immunotherapy group.	ema	47-50	programmed cell death 1	Homo sapiens	80-84
32337408-4	2020	In this study, we first investigated the impact of radioisotope chelators on the biodistribution of 64Cu-labeled anti-PD-1 and anti-PD-L1 antibodies and compared the distribution profiles of anti-PD-1 and anti-PD-L1 antibodies.	Copper-64	100-104	programmed cell death 1	Homo sapiens	118-122
31837940-13	2020	Treatment with PD-1/PD-L1 inhibitors should be prescribed with caution in patients with UC and creatinine above 1.2 mg/dL.	Creatinine	95-105	programmed cell death 1	Homo sapiens	15-19
32368175-5	2020	Based on results of phase ii trials, PD-1 inhibitors were approved in North America for use in PD-L1-positive chemorefractory gastric cancers, in hepatocellular carcinoma after sorafenib exposure, and in treatment-refractory deficient mismatch repair (dmmr) or high microsatellite instability (msi-h) tumours, regardless of tissue site.	Sorafenib	177-186	programmed cell death 1	Homo sapiens	37-41
32368175-6	2020	Combination use of PD-1 and ctla-4 inhibitors has been approved by the U.S. Food and Drug Administration for chemorefractory dmmr or msi-h colorectal cancer.	dmmr	125-129	programmed cell death 1	Homo sapiens	19-23
31797379-4	2020	In this study, we examined the cellular effects of resveratrol on human periodontal ligament (hPDL) cells and osteoblast-like (MC3T3-E1) cells and evaluated the bone-healing capacity of tooth extraction sockets in mice.	resveratrol	51-62	programmed cell death 1	Homo sapiens	94-98
31797379-5	2020	MATERIAL AND METHODS: Resveratrol was applied to hPDL and MC3T3-E1 cells to detect cell proliferation and alkaline phosphatase (ALP) activity, and qPCR was employed to understand the gene expression level in vitro.	resveratrol	22-33	programmed cell death 1	Homo sapiens	49-53
31797379-8	2020	RESULTS: Treatment of hPDL and MC3T3-E1 cells with resveratrol increased the cell proliferation and ALP activity and enhanced the expression of ALP, BMP-2, BMP-4, and OC genes.	resveratrol	51-62	programmed cell death 1	Homo sapiens	22-26
31797379-10	2020	CONCLUSION: These results suggest that resveratrol increases the cellular physiology of PDL and osteoblast including their proliferation and differentiation and may play an important role in bone-healing capacity after tooth extraction.	resveratrol	39-50	programmed cell death 1	Homo sapiens	88-91
30767115-9	2020	In the subgroup analysis of local recurrence between the NAC treated group and those who received surgery alone, high levels of PD-1 and PD-L1 expressions were significantly found in the former, but not in the latter group.	nac	57-60	programmed cell death 1	Homo sapiens	128-132
31843683-1	2020	INTRODUCTION: Blood-based tumor mutational burden (bTMB) has been studied to identify patients with NSCLC who would benefit from anti-programmed cell death protein 1 (anti-PD-1) or anti-programmed death ligand 1 (anti-PD-L1) therapies.	3,5-Bis(trimethylsilyl)benzoic acid	51-55	programmed cell death 1	Homo sapiens	134-165
32420079-10	2020	After recovering from DKA and controlling his blood glucose, his anti PD-1 therapy was continued and he still got some benefit.	Glucose	52-59	programmed cell death 1	Homo sapiens	70-74
32110280-4	2020	ICB therapy was defined as treatment with any CTLA-4, PD-1, and/or PD-L1 monoclonal antibody.	indole-2-carboxylic acid	0-3	programmed cell death 1	Homo sapiens	54-58
32308589-3	2020	In this report, we present a case with anti-PD1 Ab-resistant recurrent malignant melanoma of the nasal cavity successfully treated with nivolu-mab, ipilimumab plus denosumab combination therapy.	nivolu	136-142	programmed cell death 1	Homo sapiens	44-47
32760603-5	2020	Here we investigated the expression of PD-1 and its ligands, PD-L1 and PD-L2 in blood and skin from patients with L-CTCL.	l-ctcl	114-120	programmed cell death 1	Homo sapiens	39-43
32760603-9	2020	Our study sheds some light on the PD-1 axis in both peripheral blood and skin compartments in SS patients, which may be relevant for the treatment of L-CTCL with immune checkpoint inhibitor.	l-ctcl	150-156	programmed cell death 1	Homo sapiens	34-38
32178474-6	2020	The anti-PD-1/PD-L1 therapy enhanced T cell-mediated cytotoxicity of NSCLC cells treated with pemetrexed and expressing high levels of PD-L1 in comparison with untreated cells.	Pemetrexed	94-104	programmed cell death 1	Homo sapiens	9-13
31942578-2	2020	As a chemotherapeutic drug for NSCLC, docetaxel (DTX) can synergize with PD1/PD-L1 checkpoint inhibitors but increase haematoxicity and neurotoxicity.	docetaxel	38-47	programmed cell death 1	Homo sapiens	73-76
32180046-9	2020	Six patients of 10 patients continued to receive anti-PD-1 antibodies with corticosteroid hormone replacement after diagnosis.	corticosteroid hormone	75-97	programmed cell death 1	Homo sapiens	54-58
32315237-6	2020	Defective DNA repair, leading to microsatellite instability, is an endogenous mechanism for increased tumor TMB that augments response to anti-PD-1 blockade.	1,2,4,5-tetramethoxybenzene	108-111	programmed cell death 1	Homo sapiens	143-147
32048666-3	2020	The Pd1/TiO2-V catalyst is not suitable for the CO catalytic coupling reaction since CO is easily bound to the O atom on the surface of TiO2-V leading to the formation of CO2.	titanium dioxide	8-12	programmed cell death 1	Homo sapiens	4-7
32048666-3	2020	The Pd1/TiO2-V catalyst is not suitable for the CO catalytic coupling reaction since CO is easily bound to the O atom on the surface of TiO2-V leading to the formation of CO2.	N2,N6-bis(4-(2-aminoethoxy)quinolin-2-yl)-4-((4-fluorobenzyl)oxy)pyridine-2,6-dicarboxamide	171-174	programmed cell death 1	Homo sapiens	4-7
32154170-1	2020	Immune checkpoint blockade (ICB) therapies that target programmed cell death 1 (PD1) and PD1 ligand 1 (PDL1) have demonstrated promising benefits in lung adenocarcinoma (LUAD), and tumor mutational burden (TMB) is the most robust biomarker associated with the efficacy of PD-1-PD-L1 axis blockade in LUAD, but the assessment of TMB by whole-exome sequencing (WES) is rather expensive and time-consuming.	1,2,4,5-tetramethoxybenzene	206-209	programmed cell death 1	Homo sapiens	80-83
32154170-1	2020	Immune checkpoint blockade (ICB) therapies that target programmed cell death 1 (PD1) and PD1 ligand 1 (PDL1) have demonstrated promising benefits in lung adenocarcinoma (LUAD), and tumor mutational burden (TMB) is the most robust biomarker associated with the efficacy of PD-1-PD-L1 axis blockade in LUAD, but the assessment of TMB by whole-exome sequencing (WES) is rather expensive and time-consuming.	1,2,4,5-tetramethoxybenzene	328-331	programmed cell death 1	Homo sapiens	80-83
31729876-1	2020	In photosystem II (PSII), water oxidation occurs in the Mn4CaO5 cluster with the release of electrons via the redox-active tyrosine (TyrZ) to the reaction-center chlorophylls (PD1/PD2).	Manganese	56-63	programmed cell death 1	Homo sapiens	176-183
31761899-4	2020	METHODS: An international database of 439 patients who received post-platinum PD-1/L1 monotherapies was collected for validation.	Platinum	69-77	programmed cell death 1	Homo sapiens	78-82
31769560-5	2020	Human PDL cells were pretreated with the NF-kappaB inhibitor BAY 11-7082 or cytochalasin D, respectively, before exposure to vibration.	3-(4-methylphenylsulfonyl)-2-propenenitrile	61-72	programmed cell death 1	Homo sapiens	6-9
31769560-9	2020	Pretreatment with BAY 11-7082 significantly inhibited vibration-induced IL-6 and IL-8 mRNA and protein expression in hPDL cells.	3-(4-methylphenylsulfonyl)-2-propenenitrile	18-29	programmed cell death 1	Homo sapiens	117-121
31115691-8	2020	RESULTS: Endomethasone N decreased secretion of IL-6 and TNF-alpha from hPDL cells.	corticosteroid methanetriol mixture	9-22	programmed cell death 1	Homo sapiens	72-76
32038880-5	2020	Here we present three cases of dermal sarcomas with high TMB and PD-L1 expression and responses to anti-PD1 agents in two of them.	Trimedoxime	57-60	programmed cell death 1	Homo sapiens	104-107
31978106-3	2020	We asked in this study whether D1143 would stimulate the potency of an anti-human PD-1 monoclonal antibody (mAb) to reduce HIV loads in humanized mice.	N-benzhydryl-5-(2-(methylamino)propanamido)-3-(3-methylbutanoyl)-6-oxodecahydropyrrolo(1,2-a)(1,5)diazocine-8-carboxamide	31-36	programmed cell death 1	Homo sapiens	82-86
31580492-1	2020	BACKGROUND: Anti-programmed death protein 1 (anti-PD-1) agents have transformed the treatment of advanced melanoma and other cancers, but the rates of steroid-refractory toxicities and health care utilization are not well described.	Steroids	151-158	programmed cell death 1	Homo sapiens	50-54
31734021-0	2020	Discovery of the programmed cell death-1/programmed cell death-ligand 1 interaction inhibitors bearing an indoline scaffold.	indoline	106-114	programmed cell death 1	Homo sapiens	17-71
31770816-4	2020	The percentage of CpG methylation at the Pdcd1 locus was analyzed by bisulfite sequencing.	hydrogen sulfite	69-78	programmed cell death 1	Homo sapiens	41-46
31911600-3	2020	Here we present a synergistic function of single-atom palladium (Pd1) and nanoparticles (PdNPs) on TiO2 for highly efficient ketone/aldehydes hydrogenation to alcohols at room temperature.	Ketones	125-131	programmed cell death 1	Homo sapiens	65-68
31911600-3	2020	Here we present a synergistic function of single-atom palladium (Pd1) and nanoparticles (PdNPs) on TiO2 for highly efficient ketone/aldehydes hydrogenation to alcohols at room temperature.	Aldehydes	132-141	programmed cell death 1	Homo sapiens	65-68
31911600-3	2020	Here we present a synergistic function of single-atom palladium (Pd1) and nanoparticles (PdNPs) on TiO2 for highly efficient ketone/aldehydes hydrogenation to alcohols at room temperature.	Ethanol	159-167	programmed cell death 1	Homo sapiens	65-68
31911600-4	2020	Compared to simple but inferior Pd1/TiO2 and PdNPs/TiO2 catalysts, more than twice activity enhancement is achieved with the Pd1+NPs/TiO2 catalyst that integrates both Pd1 and Pd NPs on mesoporous TiO2 supports, obtained by a simple but large-scaled spray pyrolysis route.	Titanium	36-40	programmed cell death 1	Homo sapiens	32-35
31911600-4	2020	Compared to simple but inferior Pd1/TiO2 and PdNPs/TiO2 catalysts, more than twice activity enhancement is achieved with the Pd1+NPs/TiO2 catalyst that integrates both Pd1 and Pd NPs on mesoporous TiO2 supports, obtained by a simple but large-scaled spray pyrolysis route.	Titanium	36-40	programmed cell death 1	Homo sapiens	125-128
31911600-4	2020	Compared to simple but inferior Pd1/TiO2 and PdNPs/TiO2 catalysts, more than twice activity enhancement is achieved with the Pd1+NPs/TiO2 catalyst that integrates both Pd1 and Pd NPs on mesoporous TiO2 supports, obtained by a simple but large-scaled spray pyrolysis route.	Titanium	36-40	programmed cell death 1	Homo sapiens	125-128
31911600-4	2020	Compared to simple but inferior Pd1/TiO2 and PdNPs/TiO2 catalysts, more than twice activity enhancement is achieved with the Pd1+NPs/TiO2 catalyst that integrates both Pd1 and Pd NPs on mesoporous TiO2 supports, obtained by a simple but large-scaled spray pyrolysis route.	Titanium	51-55	programmed cell death 1	Homo sapiens	125-128
31911600-4	2020	Compared to simple but inferior Pd1/TiO2 and PdNPs/TiO2 catalysts, more than twice activity enhancement is achieved with the Pd1+NPs/TiO2 catalyst that integrates both Pd1 and Pd NPs on mesoporous TiO2 supports, obtained by a simple but large-scaled spray pyrolysis route.	Titanium	51-55	programmed cell death 1	Homo sapiens	125-128
31911600-4	2020	Compared to simple but inferior Pd1/TiO2 and PdNPs/TiO2 catalysts, more than twice activity enhancement is achieved with the Pd1+NPs/TiO2 catalyst that integrates both Pd1 and Pd NPs on mesoporous TiO2 supports, obtained by a simple but large-scaled spray pyrolysis route.	Titanium	51-55	programmed cell death 1	Homo sapiens	125-128
31911600-4	2020	Compared to simple but inferior Pd1/TiO2 and PdNPs/TiO2 catalysts, more than twice activity enhancement is achieved with the Pd1+NPs/TiO2 catalyst that integrates both Pd1 and Pd NPs on mesoporous TiO2 supports, obtained by a simple but large-scaled spray pyrolysis route.	Titanium	51-55	programmed cell death 1	Homo sapiens	125-128
31911600-4	2020	Compared to simple but inferior Pd1/TiO2 and PdNPs/TiO2 catalysts, more than twice activity enhancement is achieved with the Pd1+NPs/TiO2 catalyst that integrates both Pd1 and Pd NPs on mesoporous TiO2 supports, obtained by a simple but large-scaled spray pyrolysis route.	Titanium	51-55	programmed cell death 1	Homo sapiens	125-128
31911600-4	2020	Compared to simple but inferior Pd1/TiO2 and PdNPs/TiO2 catalysts, more than twice activity enhancement is achieved with the Pd1+NPs/TiO2 catalyst that integrates both Pd1 and Pd NPs on mesoporous TiO2 supports, obtained by a simple but large-scaled spray pyrolysis route.	Titanium	51-55	programmed cell death 1	Homo sapiens	125-128
31911600-5	2020	The synergistic function of Pd1 and PdNPs is assigned so that the partial Pd1 dispersion contributes enough sites for the activation of C=O group while PdNPs site boosts the dissociation of H2 molecules to H atoms.	Hydrogen	190-192	programmed cell death 1	Homo sapiens	28-31
31911600-5	2020	The synergistic function of Pd1 and PdNPs is assigned so that the partial Pd1 dispersion contributes enough sites for the activation of C=O group while PdNPs site boosts the dissociation of H2 molecules to H atoms.	Hydrogen	190-192	programmed cell death 1	Homo sapiens	74-77
31901900-4	2020	RSV was also predicted to interact with the inner surface of PD-L1 involved in the interaction with PD-1, almost perfectly occupying the target space of the small compound BMS-202 that binds to and induces dimerization of PD-L1.	Resveratrol	0-3	programmed cell death 1	Homo sapiens	100-104
31901900-7	2020	This unforeseen immunomodulating mechanism of RSV might illuminate new approaches to restore T-cell function by targeting the PD-1/PD-L1 immunologic checkpoint with natural polyphenols.	Resveratrol	46-49	programmed cell death 1	Homo sapiens	126-130
31901900-7	2020	This unforeseen immunomodulating mechanism of RSV might illuminate new approaches to restore T-cell function by targeting the PD-1/PD-L1 immunologic checkpoint with natural polyphenols.	Polyphenols	173-184	programmed cell death 1	Homo sapiens	126-130
31613799-0	2020	Targeting tumor-intrinsic hexosamine biosynthesis sensitizes pancreatic cancer to anti-PD1 therapy.	Hexosamines	26-36	programmed cell death 1	Homo sapiens	87-90
31613799-9	2020	Additionally, treatment with DON sensitized pancreatic tumors to anti-PD1 therapy resulting in tumor regression and prolonged survival.	3-acetyldeoxynivalenol	29-32	programmed cell death 1	Homo sapiens	70-73
31729876-1	2020	In photosystem II (PSII), water oxidation occurs in the Mn4CaO5 cluster with the release of electrons via the redox-active tyrosine (TyrZ) to the reaction-center chlorophylls (PD1/PD2).	Tyrosine	123-131	programmed cell death 1	Homo sapiens	176-183
31729876-1	2020	In photosystem II (PSII), water oxidation occurs in the Mn4CaO5 cluster with the release of electrons via the redox-active tyrosine (TyrZ) to the reaction-center chlorophylls (PD1/PD2).	tyrosyltyrosine	133-137	programmed cell death 1	Homo sapiens	176-183
31729876-1	2020	In photosystem II (PSII), water oxidation occurs in the Mn4CaO5 cluster with the release of electrons via the redox-active tyrosine (TyrZ) to the reaction-center chlorophylls (PD1/PD2).	Chlorophyll	162-174	programmed cell death 1	Homo sapiens	176-183
31756590-7	2020	Moreover, the role of NK cells and TAMs in efficient PD-1 blockade will be discussed.	tams	35-39	programmed cell death 1	Homo sapiens	53-57
31827263-0	2020	Correction to: Low-dose decitabine enhances the effect of PD-1 blockade in colorectal cancer with microsatellite stability by re-modulating the tumor microenvironment.	decitabine	24-34	programmed cell death 1	Homo sapiens	58-62
31527167-6	2020	Higher CDK4 levels were associated with endocrine resistance which was mitigated by the addition of palbociclib, while lower PD1 levels were associated with greater palbociclib plus letrozole benefit.	Letrozole	182-191	programmed cell death 1	Homo sapiens	125-128
31506751-2	2020	Recently, anti-PD-1 antibody therapy became a key treatment for stage IV NSCLC as the combination of immune checkpoint inhibitors (ICIs) and platinum doublet chemotherapy.	Platinum	141-149	programmed cell death 1	Homo sapiens	15-19
31731087-6	2020	It was found that the most common neurotoxicity per antibody class are as follows; Bi-specific T-cell engagers was headache 38% [35-40%; I2 0%]; anti-CD20, neuropathy, 16% [7-24%, I2 65%]; anti-CD30, neuropathy 57% [46-68%, I2 72%]; anti-CD52, neuropathy 5-15%; anti-CTL4, headache 12% [7-16%, I2 49%]; anti-EGFR, headache 25% [11-38%, I2 92%]; anti-Her2, neuropathy 33% [18-49%, I2 98%]; anti-PD1 and PDL1, headache 3% [2-5%, I2 85%]; and anti-VEGF, headache 25% [16-35%, I2 73%].	Bismuth	83-85	programmed cell death 1	Homo sapiens	394-397
32381854-11	2020	The expression of inhibitory receptors, such as PD-1 is decreased in tumor-infiltrating CD8 T cells cultured under glutamine-restricted conditions.	Glutamine	115-124	programmed cell death 1	Homo sapiens	48-52
31911600-3	2020	Here we present a synergistic function of single-atom palladium (Pd1) and nanoparticles (PdNPs) on TiO2 for highly efficient ketone/aldehydes hydrogenation to alcohols at room temperature.	Palladium	54-63	programmed cell death 1	Homo sapiens	65-68
31911600-3	2020	Here we present a synergistic function of single-atom palladium (Pd1) and nanoparticles (PdNPs) on TiO2 for highly efficient ketone/aldehydes hydrogenation to alcohols at room temperature.	Titanium	99-103	programmed cell death 1	Homo sapiens	65-68
31531785-5	2020	We aimed to determine whether AGR is a predictive biomarker of anti-PD-1 antibody response in patients with NSCLC.	alanylglycylarginine	30-33	programmed cell death 1	Homo sapiens	68-72
31531785-13	2020	CONCLUSION: Pretreatment serum AGR may be a useful predictor for DC and prognostic factor of anti-PD-1 antibody in patients with NSCLC.	alanylglycylarginine	31-34	programmed cell death 1	Homo sapiens	98-102
32642723-4	2020	As COX-2 modulates PD-L1 expression in cancer cells, we tested the hypothesis that the COX-2 inhibitor celecoxib potentiates anti-PD-1 antibody treatment via the downregulation of PD-L1.	Celecoxib	103-112	programmed cell death 1	Homo sapiens	130-134
31921686-8	2019	Conclusions: Patients with a history of radiation-induced pneumonitis and treated with sequential different PD-1/PD-L1 inhibitors have a relative high risk to develop high-grade or steroid-resistant pneumonitis, and additional immunosuppressive medications should be used earlier when severe pulmonary toxicity occurs.	Steroids	181-188	programmed cell death 1	Homo sapiens	108-112
31671550-2	2019	Nearly 10 years after the approval of cetuximab, anti-PD1/PD-L1 checkpoint inhibitors are the first drugs that have shown any survival benefit for the treatment on platinum-refractory recurrent/metastatic (R/M) HNSCC.	Platinum	164-172	programmed cell death 1	Homo sapiens	54-57
31701974-1	2019	A new family of ferrocenyl-palladacycle complexes Pd(L1)Cl (Pd1) and Pd(L2)Cl (Pd2) were synthesized and characterized by UV-visible, IR, ESI-MS, and NMR spectral studies.	biphosphinic palladacycle complex	16-39	programmed cell death 1	Homo sapiens	60-63
31679184-10	2019	Although the rates of these events were low, the risk was increased following ICI-based treatment, particularly for CTLA-4 inhibitors, which were associated with a higher incidence of pituitary-adrenal dysfunction than PD-1/PD-L1 inhibitors.	2-I-ICI-H	78-81	programmed cell death 1	Homo sapiens	219-223
31791080-3	2019	Inhibitory signaling pathways are interrupted by binding to CTLA-4 and PD-1 or PD-L1, which increases the activity of cytotoxic T lymphocytes and reduces the immunological tolerance to tumor cells.Diarrhea - a symptom of enterocolitis - is the most common side effect of ICPI therapy after dermatological phenomena.	icpi	271-275	programmed cell death 1	Homo sapiens	71-75
31200951-1	2019	CONTEXT: Several anti-programmed death-1 (anti-PD-1) and anti-programmed death ligand-1 (anti-PD-L1) antibodies have been approved by regulatory authorities for treatment of platinum-resistant metastatic urothelial cancer (mUC).	Platinum	174-182	programmed cell death 1	Homo sapiens	47-51
31200951-3	2019	OBJECTIVE: To determine the restricted mean survival time (RMST) of patients with platinum-resistant mUC treated with PD-1/PD-L1 inhibitors and to compare RMSTs in patients treated with PD-1 versus PD-L1 inhibitors.	Platinum	82-90	programmed cell death 1	Homo sapiens	118-122
31200951-4	2019	EVIDENCE ACQUISITION: We searched for phase 1, 2, and 3 clinical trials that assessed PD-1 or PD-L1 inhibition for patients with platinum-resistant mUC.	Platinum	129-137	programmed cell death 1	Homo sapiens	86-90
31627712-2	2019	Authors of WO2018202649 patent propose a method to eradicate cancer using a bispecific antibodies against OX40/CTLA-4.Areas covered: WO2018202649 patent describes several bispecific antibodies capable of specifically binding to OX40 and CTLA-4 that target regulatory T cells in the tumor microenvironment.Expert opinion: WO2018202649 patent demonstrates that bispecific antibodies against OX40/CTLA-4 have anti-tumor activity against colon, pancreatic and bladder cancer, and that there is a synergistic action with anti-PD-1 antibodies for the treatment of colon cancer.	wo2018202649	11-23	programmed cell death 1	Homo sapiens	521-525
31691624-0	2019	(3R)-5,6,7-trihydroxy-3-isopropyl-3-methylisochroman-1-one enhanced the therapeutic efficacy of anti-PD1 antibody through inhibiting PI3Kdelta/gamma.	7,8-dihydroxy-3-methylisochroman-4-one	0-58	programmed cell death 1	Homo sapiens	101-104
31691624-3	2019	In this study, we demonstrated that functional inhibition of MDSCs with (3 R)-5,6,7-trihydroxy-3-isopropyl-3-methylisochroman-1-one (TIMO), a potent PI3Kdelta/gamma inhibitor, enhanced the therapeutic efficacy of anti-PD1 antibody in the tumor model.Materials and methods: A syngeneic ovarian tumor model was established.	7,8-dihydroxy-3-methylisochroman-4-one	72-131	programmed cell death 1	Homo sapiens	218-221
31781109-4	2019	We found that the Treg expansion was strongly associated with markers of recent immune activation, including PD-1, plasma concentrations of IL-2 and the type I interferon biomarker soluble SIGLEC-1.	treg	18-22	programmed cell death 1	Homo sapiens	109-113
32002288-8	2020	More remarkably, hIL-2/TCB2c showed synergy with checkpoint inhibitors such as anti-CTLA-4 or PD1 antibodies, and resulted in almost complete regression of implanted tumors and resistance to secondary tumor challenge.	2,3,4-trimethoxy-4'-carbomethoxy-1,1'-biphenyl	23-28	programmed cell death 1	Homo sapiens	94-97
31711939-0	2019	Caffeine-enhanced anti-tumor activity of anti-PD1 monoclonal antibody.	Caffeine	0-8	programmed cell death 1	Homo sapiens	46-49
31711939-3	2019	The production of extracellular adenosine in solid tumors was recently identified as a major immunosuppressive pathway, targeting this pathway would enhance the therapeutic activity of anti-PD1 mAbs.	Adenosine	32-41	programmed cell death 1	Homo sapiens	190-193
31711939-11	2019	Our work suggests that administration of caffeine and anti-PD1 mAb harness the therapeutic potential of effector T cells in vivo possibly due to combined blockade of PD1 and adenosine-A2A receptor pathway.	Caffeine	41-49	programmed cell death 1	Homo sapiens	166-169
31805700-13	2019	A transient increase of CD8+ T-cell activation, TNF production, and poly-functionality resulted from PD-1 blockade.	poly If	68-72	programmed cell death 1	Homo sapiens	101-105
31470128-5	2019	We further show that combining low, non-cytotoxic doses of gemcitabine with SRA737 + anti-PD-L1/anti-PD-1 significantly increased antitumorigenic CD8+ cytotoxic T cells, dendritic cells, and M1 macrophage populations in an SCLC model.	gemcitabine	59-70	programmed cell death 1	Homo sapiens	101-105
31470128-5	2019	We further show that combining low, non-cytotoxic doses of gemcitabine with SRA737 + anti-PD-L1/anti-PD-1 significantly increased antitumorigenic CD8+ cytotoxic T cells, dendritic cells, and M1 macrophage populations in an SCLC model.	SRA737	76-82	programmed cell death 1	Homo sapiens	101-105
31780710-4	2019	Interface analysis reveals that N-glycosylation sites 49, 74 and 116 on PD-1 do not contact mAb059c; while N58 in the BC loop is recognized by mAb059c heavy chain CDR1 and CDR2.	Nitrogen	32-33	programmed cell death 1	Homo sapiens	72-76
31593831-1	2019	BACKGROUND: Nivolumab and pembrolizumab targeting programmed cell death protein 1 (PD-1) have recently been approved among patients with recurrent and/or metastatic head and neck squamous cell carcinoma (HNSCC) who failed platinum therapy.	Platinum	222-230	programmed cell death 1	Homo sapiens	50-81
31593831-1	2019	BACKGROUND: Nivolumab and pembrolizumab targeting programmed cell death protein 1 (PD-1) have recently been approved among patients with recurrent and/or metastatic head and neck squamous cell carcinoma (HNSCC) who failed platinum therapy.	Platinum	222-230	programmed cell death 1	Homo sapiens	83-87
31676812-0	2019	Quasi Pd1Ni single-atom surface alloy catalyst enables hydrogenation of nitriles to secondary amines.	Nitriles	72-80	programmed cell death 1	Homo sapiens	6-9
31676812-0	2019	Quasi Pd1Ni single-atom surface alloy catalyst enables hydrogenation of nitriles to secondary amines.	Imino Acids	84-100	programmed cell death 1	Homo sapiens	6-9
31676812-3	2019	Here we show that quasi atomic-dispersion of Pd within the outermost layer of Ni nanoparticles to form a Pd1Ni single-atom surface alloy structure maximizes the Pd utilization and breaks the strong metal-selectivity relations in benzonitrile hydrogenation, by prompting the yield of dibenzylamine drastically from ~5 to 97% under mild conditions (80  C; 0.6 MPa), and boosting an activity to about eight and four times higher than Pd and Pt standard catalysts, respectively.	Palladium	45-47	programmed cell death 1	Homo sapiens	105-108
31676812-3	2019	Here we show that quasi atomic-dispersion of Pd within the outermost layer of Ni nanoparticles to form a Pd1Ni single-atom surface alloy structure maximizes the Pd utilization and breaks the strong metal-selectivity relations in benzonitrile hydrogenation, by prompting the yield of dibenzylamine drastically from ~5 to 97% under mild conditions (80  C; 0.6 MPa), and boosting an activity to about eight and four times higher than Pd and Pt standard catalysts, respectively.	benzonitrile	229-241	programmed cell death 1	Homo sapiens	105-108
31676812-3	2019	Here we show that quasi atomic-dispersion of Pd within the outermost layer of Ni nanoparticles to form a Pd1Ni single-atom surface alloy structure maximizes the Pd utilization and breaks the strong metal-selectivity relations in benzonitrile hydrogenation, by prompting the yield of dibenzylamine drastically from ~5 to 97% under mild conditions (80  C; 0.6 MPa), and boosting an activity to about eight and four times higher than Pd and Pt standard catalysts, respectively.	dibenzylamine	283-296	programmed cell death 1	Homo sapiens	105-108
31676812-3	2019	Here we show that quasi atomic-dispersion of Pd within the outermost layer of Ni nanoparticles to form a Pd1Ni single-atom surface alloy structure maximizes the Pd utilization and breaks the strong metal-selectivity relations in benzonitrile hydrogenation, by prompting the yield of dibenzylamine drastically from ~5 to 97% under mild conditions (80  C; 0.6 MPa), and boosting an activity to about eight and four times higher than Pd and Pt standard catalysts, respectively.	Platinum	438-440	programmed cell death 1	Homo sapiens	105-108
31731492-2	2019	In this work, one peptide of PD-1 was used as the template for molecular imprinting to form magnetic peptide-imprinted poly(ethylene-co-vinyl alcohol) composite nanoparticles (MPIP NPs).	ethylene-vinyl alcohol copolymer	119-150	programmed cell death 1	Homo sapiens	29-33
31624262-2	2019	In a melanoma patient in whom programmed-death 1 (PD-1) blockade resulted in organ rejection and colitis, the addition of the mTOR inhibitor sirolimus resulted in ongoing anti-tumor efficacy while promoting allograft tolerance.	Sirolimus	141-150	programmed cell death 1	Homo sapiens	30-48
31624262-2	2019	In a melanoma patient in whom programmed-death 1 (PD-1) blockade resulted in organ rejection and colitis, the addition of the mTOR inhibitor sirolimus resulted in ongoing anti-tumor efficacy while promoting allograft tolerance.	Sirolimus	141-150	programmed cell death 1	Homo sapiens	50-54
31624262-5	2019	Interestingly, numbers of IFN-gamma+ CD4+ T cells and serum IFN-gamma levels increased with the addition of sirolimus treatment likely promoting ongoing anti-PD-1 efficacy.	Sirolimus	108-117	programmed cell death 1	Homo sapiens	158-162
31624262-6	2019	Thus, our results indicate that sirolimus has the potential to uncouple anti-PD-1 therapy toxicity and efficacy.	Sirolimus	32-41	programmed cell death 1	Homo sapiens	77-81
31276987-7	2019	A further analysis reveals that the free linear DS-I and DS-II peptides are highly flexible without protein context support, which would incur a large entropy penalty (unfavorable indirect readout effect) when rebinding to PD-1.	ds-ii	57-62	programmed cell death 1	Homo sapiens	223-227
31276987-9	2019	Several cyclized counterparts of linear DS-II peptide are designed and their affinities to PD-1 are determined using fluorescence polarization assays.	ds-ii	40-45	programmed cell death 1	Homo sapiens	91-95
31346755-0	2019	Prognostic and theranostic 18F-FDG PET biomarkers for anti-PD1 immunotherapy in metastatic melanoma: association with outcome and transcriptomics.	Fluorodeoxyglucose F18	27-34	programmed cell death 1	Homo sapiens	59-62
31235619-3	2019	Using two lymphoma models, we show that treatment of B-cell lymphomas refractory to PD1 blockade with both OKI-179 and anti-PD1 inhibited growth; furthermore, sensitivity to single or combined treatment required tumor-derived MHC class I, and positively correlated with MHC class II expression level.	oki-179	107-114	programmed cell death 1	Homo sapiens	84-87
31476119-5	2019	Such extraordinary electronic promotion was further demonstrated on Pd1/Co3O4 and in hydrogenation reactions, providing a new promising way to design advanced SACs with high activity and stability.	co3o4	72-77	programmed cell death 1	Homo sapiens	68-71
32055371-5	2019	We also demonstrate the proof-of-concept applications of PdII complexes (Pd-1 and Pd-3) encapsulated in silica nanoparticles, in both in vitro and in vivo bioimaging experiments without oxygen interference.	Palladium	57-61	programmed cell death 1	Homo sapiens	73-86
32055371-5	2019	We also demonstrate the proof-of-concept applications of PdII complexes (Pd-1 and Pd-3) encapsulated in silica nanoparticles, in both in vitro and in vivo bioimaging experiments without oxygen interference.	Silicon Dioxide	104-110	programmed cell death 1	Homo sapiens	73-86
31128215-0	2019	The anthelmintic flubendazole blocks human melanoma growth and metastasis and suppresses programmed cell death protein-1 and myeloid-derived suppressor cell accumulation.	flubendazole	17-29	programmed cell death 1	Homo sapiens	89-120
31128215-10	2019	Most surprisingly, flubendazole inhibited PD-1 levels within the tumors, but not PD-L1.	flubendazole	19-31	programmed cell death 1	Homo sapiens	42-46
31128215-13	2019	Further we found that flubendazole inhibited active (phospho-Tyr705) signal transducer and activator of transcription (STAT3), an upstream regulator of PD-1 expression.	flubendazole	22-34	programmed cell death 1	Homo sapiens	152-156
31128215-14	2019	These findings uncover that flubendazole is a novel small molecule inhibitor of not only melanoma growth and spread but also of PD-1 and MDSC.	flubendazole	28-40	programmed cell death 1	Homo sapiens	128-132
31238000-13	2019	In addition, A23187-treated hPDL fibroblasts also showed the suppression of osteogenic differentiation and mineralization.	Calcimycin	13-19	programmed cell death 1	Homo sapiens	28-32
31252292-10	2019	One-year OS was 61% for patients receiving RT before anti-PD-1 (95% CI: 46-76%), 78% for RT during anti-PD-1 (95% CI: 60-95%), and 58% for RT after anti-PD-1 (95% CI: 26-89%).	Osmium	9-11	programmed cell death 1	Homo sapiens	58-62
31217250-5	2019	Compared to the PD-1 or LAG-3 blockade alone, the combined blockade of PD-1 and LAG-3 appeared to have a synergistic effect in generating frequent polyfunctional Ki-67+, IFN-gamma+, CD107+, and CD8+ T cells.	ki-67+	162-168	programmed cell death 1	Homo sapiens	71-75
31686799-0	2019	Effect of PD-1 inhibitor on exhaled nitric oxide and pulmonary function in non-small cell lung cancer patients with and without COPD.	Nitric Oxide	36-48	programmed cell death 1	Homo sapiens	10-14
31496815-12	2019	Conclusion: EBV-induced up-regulation of PD-1-PD-L1 expression is associated with worse outcomes in CLL.	(2S)-2-amino-1-[(3aR,6aS)-5-[(5-chloro-1H-indol-3-yl)methyl]hexahydropyrrolo[3,4-c]pyrrol-2(1H)-yl]-3-(1H-indol-3-yl)propan-1-one	12-15	programmed cell death 1	Homo sapiens	41-45
31383016-12	2019	CONCLUSIONS: This study provided the first set of evidence for the effectiveness of SBRT and PD-1 blockade combined therapy in late-stage or recurrent ICC patients with low TMB, MSS, pMMR and negative PD-L1 expression, and potentially expanded the indications of the combined therapy to those patients who were previously not suitable for immunotherapy.	1,2,4,5-tetramethoxybenzene	173-176	programmed cell death 1	Homo sapiens	93-97
30865286-4	2019	MATERIALS AND METHODS: Fifth passage hPDL cells were mechanically loaded in the presence of the HSP70 inhibitor VER155008.	VER 155008	112-121	programmed cell death 1	Homo sapiens	37-41
30891778-8	2019	RESULTS: The dendritic Lys-PDA matrix well supported the hPDL cell growth and differentiation.	lys-pda	23-30	programmed cell death 1	Homo sapiens	57-61
30891778-11	2019	The electrospun PCL mat functionalized with Lys-PDA maintained the viability, morphology, and spreading of the hPDL cells.	lys-pda	44-51	programmed cell death 1	Homo sapiens	111-115
31353229-19	2019	CONCLUSIONS: PD-L1 and PD-1 were expressed in majority of MMR-deficient UEAC /DEAC cases.	ueac	72-76	programmed cell death 1	Homo sapiens	23-27
31353229-19	2019	CONCLUSIONS: PD-L1 and PD-1 were expressed in majority of MMR-deficient UEAC /DEAC cases.	deac	78-82	programmed cell death 1	Homo sapiens	23-27
31310752-0	2019	Caffeine-enhanced anti-tumor immune response through decreased expression of PD1 on infiltrated cytotoxic T lymphocytes.	Caffeine	0-8	programmed cell death 1	Homo sapiens	77-80
31424903-2	2019	Herein, Pd1-xAgx alloy electrocatalysts are investigated as a platform to uncover the electronic effects on the CO2RR.	co2rr	112-117	programmed cell death 1	Homo sapiens	8-11
31424903-4	2019	Experimental and theoretical analysis further evidence that varying the composition of Pd1-xAgx alloys can effectively alter the electronic configurations and consequently break the inherent scaling relationship of the binding energy of different intermediates (*COOH and *CO).	Carbonic Acid	263-267	programmed cell death 1	Homo sapiens	87-90
31413142-11	2019	Re-resection in five of five patients with suspected recurrence after Ad-RTS-hIL-12 revealed mostly pseudoprogression with increased tumor-infiltrating lymphocytes producing IFN-gamma and programmed cell death protein 1 (PD-1).	hil-12	77-83	programmed cell death 1	Homo sapiens	188-219
31327656-0	2019	Removal of N-Linked Glycosylation Enhances PD-L1 Detection and Predicts Anti-PD-1/PD-L1 Therapeutic Efficacy.	Nitrogen	11-12	programmed cell death 1	Homo sapiens	77-81
31235619-4	2019	We conclude that OKI-179 sensitizes lymphomas to PD1-blockade by enhancing tumor immunogenicity.	oki-179	17-24	programmed cell death 1	Homo sapiens	49-52
31310587-8	2019	These results suggest an IFNgamma-JAK-STAT-TET signaling pathway that mediates tumor response to anti-PD-L1/PD-1 therapy and is frequently disrupted in solid tumors.	tetramethylenedisulfotetramine	43-46	programmed cell death 1	Homo sapiens	108-112
31140644-0	2019	Hematopoietic stem cell mobilization following PD-1 blockade: Cytokine release syndrome after transplantation managed with ascorbic acid.	Ascorbic Acid	123-136	programmed cell death 1	Homo sapiens	47-51
31646079-2	2019	Several clinical trials now confirm that pretreatment with ICD-inducing anthracyclines sensitizes to immune checkpoint blockade targeting PD-1 and PD-L1 interaction.	Anthracyclines	72-86	programmed cell death 1	Homo sapiens	138-142
31310587-9	2019	Our findings also suggest TET activity as a biomarker for predicting the efficacy and patient response to anti-PD-1/PD-L1 therapy, and stimulating TET activity as an adjuvant immunotherapy of solid tumors.	tetramethylenedisulfotetramine	26-29	programmed cell death 1	Homo sapiens	111-115
31188590-1	2019	Herein, we report a novel carbothermal welding strategy to prepare atomically dispersed Pd sites anchored on a three-dimensional (3D) ZrO2 nanonet (Pd1@ZrO2) via two-step pyrolysis, which were evolved from isolated Pd sites anchored on linker-derived nitrogen-doped carbon (Pd1@NC/ZrO2).	zirconium oxide	152-156	programmed cell death 1	Homo sapiens	148-151
31188590-0	2019	Two-Step Carbothermal Welding To Access Atomically Dispersed Pd1 on Three-Dimensional Zirconia Nanonet for Direct Indole Synthesis.	zirconium oxide	86-94	programmed cell death 1	Homo sapiens	61-64
31188590-0	2019	Two-Step Carbothermal Welding To Access Atomically Dispersed Pd1 on Three-Dimensional Zirconia Nanonet for Direct Indole Synthesis.	direct indole	107-120	programmed cell death 1	Homo sapiens	61-64
31188590-1	2019	Herein, we report a novel carbothermal welding strategy to prepare atomically dispersed Pd sites anchored on a three-dimensional (3D) ZrO2 nanonet (Pd1@ZrO2) via two-step pyrolysis, which were evolved from isolated Pd sites anchored on linker-derived nitrogen-doped carbon (Pd1@NC/ZrO2).	Palladium	88-90	programmed cell death 1	Homo sapiens	148-151
31188590-1	2019	Herein, we report a novel carbothermal welding strategy to prepare atomically dispersed Pd sites anchored on a three-dimensional (3D) ZrO2 nanonet (Pd1@ZrO2) via two-step pyrolysis, which were evolved from isolated Pd sites anchored on linker-derived nitrogen-doped carbon (Pd1@NC/ZrO2).	Palladium	88-90	programmed cell death 1	Homo sapiens	274-277
31188590-1	2019	Herein, we report a novel carbothermal welding strategy to prepare atomically dispersed Pd sites anchored on a three-dimensional (3D) ZrO2 nanonet (Pd1@ZrO2) via two-step pyrolysis, which were evolved from isolated Pd sites anchored on linker-derived nitrogen-doped carbon (Pd1@NC/ZrO2).	zirconium oxide	134-138	programmed cell death 1	Homo sapiens	148-151
31031094-3	2019	Tumor tissues enriched with cholesterol and cholesterol content in tumor-infiltrating CD8+ T cells were positively and progressively associated with upregulated T cell expression of PD-1, 2B4, TIM-3, and LAG-3.	Cholesterol	28-39	programmed cell death 1	Homo sapiens	182-191
31031094-3	2019	Tumor tissues enriched with cholesterol and cholesterol content in tumor-infiltrating CD8+ T cells were positively and progressively associated with upregulated T cell expression of PD-1, 2B4, TIM-3, and LAG-3.	Cholesterol	44-55	programmed cell death 1	Homo sapiens	182-191
31383016-3	2019	However, it is currently believed that patients with low TMB, microsatellite stable (MSS), proficient mismatch repair (pMMR) or negative PD-L1 expression are less likely to benefit from PD-1 blockade.	1,2,4,5-tetramethoxybenzene	57-60	programmed cell death 1	Homo sapiens	186-190
31383016-4	2019	CASE PRESENTATION: Here we provide the first report on the therapeutic responses of ICC patients treated with combined PD-1 blockade with stereotactic body radiotherapy (SBRT) (Cyberknife) in the background of low TMB, MSS, pMMR and negative PD-L1 expression.	1,2,4,5-tetramethoxybenzene	214-217	programmed cell death 1	Homo sapiens	119-123
30947117-6	2019	More significantly, the nanovaccine shows excellent therapeutic effect to treat established B16-OVA melanoma when used in combination with the programmed cell death protein 1 (PD-1) checkpoint-blockade immunotherapy.	nanovaccine	24-35	programmed cell death 1	Homo sapiens	143-174
30947117-6	2019	More significantly, the nanovaccine shows excellent therapeutic effect to treat established B16-OVA melanoma when used in combination with the programmed cell death protein 1 (PD-1) checkpoint-blockade immunotherapy.	nanovaccine	24-35	programmed cell death 1	Homo sapiens	176-180
31074244-0	2019	Early experiences with PD-1 inhibitor treatment of platinum resistant epithelial ovarian cancer.	Platinum	51-59	programmed cell death 1	Homo sapiens	23-27
31240480-9	2019	Anti-PD-1 nivolumab and pembrolizumab are now approved for platinum refractory patients, providing prolonged survival in the case of response, and improvement in quality of life.	Platinum	59-67	programmed cell death 1	Homo sapiens	5-9
31196176-15	2019	PD-1 reprograms CD8+ T cell metabolism for efficient use of fatty acid oxidation; this mitochondrial phenotype might explain the long-lived phenotype of PD-1-engaged T cells.	Fatty Acids	60-70	programmed cell death 1	Homo sapiens	0-4
31244820-5	2019	Like several other barriers in the TME, such as the PD-1/PDL-1 axis, CTLA-4, and indoleamine 2,3-dioxygenase (IDO-1), adenosine plays important physiologic roles, but has been co-opted by tumors to promote their growth and impair immunity.	Adenosine	118-127	programmed cell death 1	Homo sapiens	52-56
31258783-4	2019	Following NACT, the overall median expression levels of CD4, CD8, PD1, PD-L1 and TIM3 were significantly increased (P = 0.008 for PD-L1 and P &lt; 0.001 for all the other markers), while the median FOXP3 expression level remained stable (P = 0.120).	nact	10-14	programmed cell death 1	Homo sapiens	66-69
30336201-2	2019	Since human periodontal ligament (hPDL) fibroblasts play a key role in orthodontic tooth movement (OTM) by expressing cytokines and chemokines, we wanted to clarify whether ethanol modulates the physiological activity and expression pattern of hPDL fibroblasts during static compressive force application.	Ethanol	173-180	programmed cell death 1	Homo sapiens	34-38
30336201-9	2019	Simultaneously, ethanol reduced the induction of IL-6 and increased prostaglandin E2 synthesis as well as hPDL-fibroblast-mediated osteoclastogenesis without affecting the RANK-L/OPG-system.	Ethanol	16-23	programmed cell death 1	Homo sapiens	106-110
30336201-10	2019	hPDL fibroblasts thus seem to be a cell type quite resistant to ethanol, as no cytotoxic effects or influence on cell viability were detected.	Ethanol	64-71	programmed cell death 1	Homo sapiens	0-4
30336201-12	2019	Ethanol at 0.179% also enhanced hPDL-induced osteoclastogenesis, indicating increased bone resorption and thus tooth movement velocity to be expected during orthodontic therapy.	Ethanol	0-7	programmed cell death 1	Homo sapiens	32-36
31188590-1	2019	Herein, we report a novel carbothermal welding strategy to prepare atomically dispersed Pd sites anchored on a three-dimensional (3D) ZrO2 nanonet (Pd1@ZrO2) via two-step pyrolysis, which were evolved from isolated Pd sites anchored on linker-derived nitrogen-doped carbon (Pd1@NC/ZrO2).	Nitrogen	251-259	programmed cell death 1	Homo sapiens	148-151
31188590-1	2019	Herein, we report a novel carbothermal welding strategy to prepare atomically dispersed Pd sites anchored on a three-dimensional (3D) ZrO2 nanonet (Pd1@ZrO2) via two-step pyrolysis, which were evolved from isolated Pd sites anchored on linker-derived nitrogen-doped carbon (Pd1@NC/ZrO2).	Carbon	266-272	programmed cell death 1	Homo sapiens	148-151
31188590-1	2019	Herein, we report a novel carbothermal welding strategy to prepare atomically dispersed Pd sites anchored on a three-dimensional (3D) ZrO2 nanonet (Pd1@ZrO2) via two-step pyrolysis, which were evolved from isolated Pd sites anchored on linker-derived nitrogen-doped carbon (Pd1@NC/ZrO2).	zirconium oxide	152-156	programmed cell death 1	Homo sapiens	148-151
31188590-3	2019	The NC supports can simultaneously reduce and anchor the Pd sites, forming isolated Pd1-N/C sites.	Palladium	57-59	programmed cell death 1	Homo sapiens	84-87
31188590-5	2019	Moreover, the reductive carbon will result in abundant oxygen (O*) defects, which could help to capture the migratory Pd1 species, leaving a sintering-resistant Pd1@ZrO2 catalyst via atom trapping.	Carbon	24-30	programmed cell death 1	Homo sapiens	118-121
31188590-5	2019	Moreover, the reductive carbon will result in abundant oxygen (O*) defects, which could help to capture the migratory Pd1 species, leaving a sintering-resistant Pd1@ZrO2 catalyst via atom trapping.	Carbon	24-30	programmed cell death 1	Homo sapiens	161-164
31188590-5	2019	Moreover, the reductive carbon will result in abundant oxygen (O*) defects, which could help to capture the migratory Pd1 species, leaving a sintering-resistant Pd1@ZrO2 catalyst via atom trapping.	Oxygen	55-61	programmed cell death 1	Homo sapiens	118-121
31188590-5	2019	Moreover, the reductive carbon will result in abundant oxygen (O*) defects, which could help to capture the migratory Pd1 species, leaving a sintering-resistant Pd1@ZrO2 catalyst via atom trapping.	Oxygen	55-61	programmed cell death 1	Homo sapiens	161-164
31188590-5	2019	Moreover, the reductive carbon will result in abundant oxygen (O*) defects, which could help to capture the migratory Pd1 species, leaving a sintering-resistant Pd1@ZrO2 catalyst via atom trapping.	zirconium oxide	165-169	programmed cell death 1	Homo sapiens	161-164
31188590-6	2019	This Pd1@ZrO2 nanonet can act as a semi-homogeneous catalyst to boost the direct synthesis of indole through hydrogenation and intramolecular condensation processes, with an excellent turnover frequency (1109.2 h-1) and 94% selectivity.	indole	94-100	programmed cell death 1	Homo sapiens	5-8
31141680-6	2019	EVTs also increased PD1HI Tregs that could be inhibited by HLA-C and CD3 antibodies, suggesting an antigen-specific induction.	evts	0-4	programmed cell death 1	Homo sapiens	20-23
30633591-7	2019	The expressions of co-inhibitory receptors (CTLA-4, PD-1, Tim-3, LAG-3 and TIGIT) on Tregs in FK506 + MMF group were significant higher than those in the FK506 group and control group.	Tacrolimus	94-99	programmed cell death 1	Homo sapiens	52-56
30633591-7	2019	The expressions of co-inhibitory receptors (CTLA-4, PD-1, Tim-3, LAG-3 and TIGIT) on Tregs in FK506 + MMF group were significant higher than those in the FK506 group and control group.	Mycophenolic Acid	102-105	programmed cell death 1	Homo sapiens	52-56
31182690-8	2019	There was a significant increase in the percentage of exhausted PD-1+(CD279) Tregs (p=0.035) in the PE group comparisons with the HP group.	histidylproline	130-132	programmed cell death 1	Homo sapiens	64-68
31182690-8	2019	There was a significant increase in the percentage of exhausted PD-1+(CD279) Tregs (p=0.035) in the PE group comparisons with the HP group.	histidylproline	130-132	programmed cell death 1	Homo sapiens	70-75
31086347-8	2019	Together, the clinical and translational data of this study indicate that short-term doxorubicin and cisplatin may induce a more favorable tumor microenvironment and increase the likelihood of response to PD-1 blockade in TNBC.	Doxorubicin	85-96	programmed cell death 1	Homo sapiens	205-209
31086347-8	2019	Together, the clinical and translational data of this study indicate that short-term doxorubicin and cisplatin may induce a more favorable tumor microenvironment and increase the likelihood of response to PD-1 blockade in TNBC.	Cisplatin	101-110	programmed cell death 1	Homo sapiens	205-209
31137694-6	2019	PD-1 expression and CTLA-4 expression were significantly associated with a worse OS and CSS in log rank survival analysis and univariate Cox regression analysis.	thiocysteine	88-91	programmed cell death 1	Homo sapiens	0-4
31137694-8	2019	Patients with combined CTLA-4 expression and PD-1-expression are at highest risk in OS and CSS.	thiocysteine	91-94	programmed cell death 1	Homo sapiens	45-49
31137694-9	2019	In RCC patients, PD-1 expression in TIMC and CTLA-4 expression in TIMC are associated with a worse OS and CSS.	Osmium	99-101	programmed cell death 1	Homo sapiens	17-21
31137694-9	2019	In RCC patients, PD-1 expression in TIMC and CTLA-4 expression in TIMC are associated with a worse OS and CSS.	thiocysteine	106-109	programmed cell death 1	Homo sapiens	17-21
30520137-0	2019	Brentuximab induced CD30+ cutaneous lymphoma responded to anti-PD1 treatment.	SGN-30 monoclonal antibody	0-11	programmed cell death 1	Homo sapiens	63-66
31191023-7	2019	OS was longer in patients who received PD-1 inhibitors (HR =0.71, 95% CI =0.62-0.74, P=0.000).	Osmium	0-2	programmed cell death 1	Homo sapiens	39-43
31109153-12	2019	In conclusion, PD-L1 expression by tumor cells is detectable in a sizeable subset of patients with BPDCN, suggesting that exploration of the effectiveness of therapeutic inhibition of the PD1/PD-L1 axis in patients with refractory or progressive BPDCN is warranted.	bpdcn	99-104	programmed cell death 1	Homo sapiens	188-191
31100059-7	2019	In coculture experiments, sorted pTfh did not support the B cell IgG production in VNRs and were predominantly an inflammatory T helper 1 (Th1)/T helper 17 (Th17) phenotype with lower ICOS and higher programmed cell death protein 1 (PD1) expression.	ptfh	33-37	programmed cell death 1	Homo sapiens	200-231
31100059-7	2019	In coculture experiments, sorted pTfh did not support the B cell IgG production in VNRs and were predominantly an inflammatory T helper 1 (Th1)/T helper 17 (Th17) phenotype with lower ICOS and higher programmed cell death protein 1 (PD1) expression.	ptfh	33-37	programmed cell death 1	Homo sapiens	233-236
31064408-10	2019	CONCLUSIONS: These two cases suggest that indels might be a new predictor of PD-1 blockade response for ICC patients beside PD-L1 expression, TMB, MSI, and dMMR, warranting further clinical investigation.	1,2,4,5-tetramethoxybenzene	142-145	programmed cell death 1	Homo sapiens	77-81
31064408-10	2019	CONCLUSIONS: These two cases suggest that indels might be a new predictor of PD-1 blockade response for ICC patients beside PD-L1 expression, TMB, MSI, and dMMR, warranting further clinical investigation.	dmmr	156-160	programmed cell death 1	Homo sapiens	77-81
30582240-1	2019	BACKGROUND: To evaluate the expression of programmed death-1 (PD-1) and programmed death-ligand 1 (PD-L1) by using immunohistochemistry analysis in locoregionally advanced nasopharyngeal carcinoma (NPC) patients receiving cisplatin, fluorouracil, and docetaxel followed by concurrent chemoradiotherapy.	Cisplatin	222-231	programmed cell death 1	Homo sapiens	42-60
30582240-1	2019	BACKGROUND: To evaluate the expression of programmed death-1 (PD-1) and programmed death-ligand 1 (PD-L1) by using immunohistochemistry analysis in locoregionally advanced nasopharyngeal carcinoma (NPC) patients receiving cisplatin, fluorouracil, and docetaxel followed by concurrent chemoradiotherapy.	Fluorouracil	233-245	programmed cell death 1	Homo sapiens	42-60
30582240-1	2019	BACKGROUND: To evaluate the expression of programmed death-1 (PD-1) and programmed death-ligand 1 (PD-L1) by using immunohistochemistry analysis in locoregionally advanced nasopharyngeal carcinoma (NPC) patients receiving cisplatin, fluorouracil, and docetaxel followed by concurrent chemoradiotherapy.	Docetaxel	251-260	programmed cell death 1	Homo sapiens	42-60
30892132-5	2019	The glycan modifications of PD-1 could be observed in three potential N-linked glycosylation sites, while no substantial influences were detected to the binding of toripalimab.	Polysaccharides	4-10	programmed cell death 1	Homo sapiens	28-32
30892132-5	2019	The glycan modifications of PD-1 could be observed in three potential N-linked glycosylation sites, while no substantial influences were detected to the binding of toripalimab.	Nitrogen	70-71	programmed cell death 1	Homo sapiens	28-32
31192153-13	2019	Anti-PD1 therapy appeared more effective in PD-L1-expressing than nonexpressing tumors, but the difference was diminished by the addition of sorafenib.	Sorafenib	141-150	programmed cell death 1	Homo sapiens	5-8
31002479-3	2019	PDL is a laser that emits yellow light using Rhodamine dye as it is lasing medium.	Rhodamines	45-54	programmed cell death 1	Homo sapiens	0-3
30920211-7	2019	The calculated adsorption energy, oxygen vacancy formation energy, and the free energy profiles show that the catalytic activity of Pd1/PTA, Rh1/PTA, and Pt1/PTA SACs is quite high, especially for Pt1/PTA and Pd1/PTA systems.	Oxygen	34-40	programmed cell death 1	Homo sapiens	132-135
30975201-10	2019	It is further demonstrated that ATOR-1015 induces tumor-specific and long-term immunological memory and enhances the response to PD-1 inhibition.	ator-1015	32-41	programmed cell death 1	Homo sapiens	129-133
30975201-13	2019	ATOR-1015 is also expected to act synergistically with anti-PD-1/PD-L1 therapy.	ator-1015	0-9	programmed cell death 1	Homo sapiens	60-64
30854842-1	2019	Two Pd(II) complexes based on tetradentate chelate ligands with either a 1,2,4-triazolyl (Pd1) or 1,2,3-triazolyl (Pd2) unit were synthesized, and their structure-property relationships were studied.	Polydioxanone	4-10	programmed cell death 1	Homo sapiens	90-93
30854842-2	2019	Both Pd1 and Pd2 are rare bright deep blue Pd(II) phosphors with contrasting properties.	Polydioxanone	43-49	programmed cell death 1	Homo sapiens	5-8
30854842-6	2019	In solution, the excimer emission of Pd1 shows a much greater sensitivity toward oxygen than the monomer emission with a very large Stern-Volmer constant ( Ksv) that is more than twice that of the monomer emission.	Oxygen	81-87	programmed cell death 1	Homo sapiens	37-40
30854842-6	2019	In solution, the excimer emission of Pd1 shows a much greater sensitivity toward oxygen than the monomer emission with a very large Stern-Volmer constant ( Ksv) that is more than twice that of the monomer emission.	(2R)-2,3-dihydroxypropyl ethyl hydrogen (S)-phosphate	156-159	programmed cell death 1	Homo sapiens	37-40
30854842-8	2019	Furthermore, Pd1 shows an excellent photostability, compared to the Pt(II) analogue, making it one of the best and highly robust oxygen sensors based on cyclometalated metal complexes.	Oxygen	129-135	programmed cell death 1	Homo sapiens	13-16
30854842-8	2019	Furthermore, Pd1 shows an excellent photostability, compared to the Pt(II) analogue, making it one of the best and highly robust oxygen sensors based on cyclometalated metal complexes.	Metals	158-163	programmed cell death 1	Homo sapiens	13-16
30940805-5	2019	Crizotinib plus cisplatin leads to an increase in the expression of PD-1 and PD-L1 in tumors, coupled to a strong sensitization of NSCLC to immunotherapy with PD-1 antibodies.	Crizotinib	0-10	programmed cell death 1	Homo sapiens	68-72
30940805-5	2019	Crizotinib plus cisplatin leads to an increase in the expression of PD-1 and PD-L1 in tumors, coupled to a strong sensitization of NSCLC to immunotherapy with PD-1 antibodies.	Crizotinib	0-10	programmed cell death 1	Homo sapiens	159-163
30940805-5	2019	Crizotinib plus cisplatin leads to an increase in the expression of PD-1 and PD-L1 in tumors, coupled to a strong sensitization of NSCLC to immunotherapy with PD-1 antibodies.	Cisplatin	16-25	programmed cell death 1	Homo sapiens	68-72
30940805-5	2019	Crizotinib plus cisplatin leads to an increase in the expression of PD-1 and PD-L1 in tumors, coupled to a strong sensitization of NSCLC to immunotherapy with PD-1 antibodies.	Cisplatin	16-25	programmed cell death 1	Homo sapiens	159-163
29622799-8	2019	The application of decitabine in PD-1 blockade-based immunotherapy may elicit more potent immune responses, which can provide clinical benefits to the colorectal cancer patients with low microsatellite instability or stable microsatellites.	Decitabine	19-29	programmed cell death 1	Homo sapiens	33-37
30873691-3	2019	Herein, the successful synthesis of atomically dispersed Pd single-atom catalysts on nitrogen-doped graphene (Pd1 /N-graphene) by a freeze-drying-assisted method is reported.	Palladium	57-59	programmed cell death 1	Homo sapiens	110-113
30873691-3	2019	Herein, the successful synthesis of atomically dispersed Pd single-atom catalysts on nitrogen-doped graphene (Pd1 /N-graphene) by a freeze-drying-assisted method is reported.	Nitrogen	85-93	programmed cell death 1	Homo sapiens	110-113
30873691-3	2019	Herein, the successful synthesis of atomically dispersed Pd single-atom catalysts on nitrogen-doped graphene (Pd1 /N-graphene) by a freeze-drying-assisted method is reported.	Graphite	100-108	programmed cell death 1	Homo sapiens	110-113
30873691-4	2019	The Pd1 /N-graphene catalyst exhibits outstanding activity and selectivity for the hydrogenation of C2 H2 with H2 in the presence of excess C2 H4 under photothermal heating (UV and visible-light irradiation from a Xe lamp), achieving 99% conversion of acetylene and 93.5% selectivity to ethylene at 125  C. This remarkable catalytic performance is attributed to the high concentration of Pd active sites on the catalyst surface and the weak adsorption energy of ethylene on isolated Pd atoms, which prevents C2 H4 hydrogenation.	Hydrogen	103-105	programmed cell death 1	Homo sapiens	4-7
30873691-4	2019	The Pd1 /N-graphene catalyst exhibits outstanding activity and selectivity for the hydrogenation of C2 H2 with H2 in the presence of excess C2 H4 under photothermal heating (UV and visible-light irradiation from a Xe lamp), achieving 99% conversion of acetylene and 93.5% selectivity to ethylene at 125  C. This remarkable catalytic performance is attributed to the high concentration of Pd active sites on the catalyst surface and the weak adsorption energy of ethylene on isolated Pd atoms, which prevents C2 H4 hydrogenation.	Acetylene	252-261	programmed cell death 1	Homo sapiens	4-7
30873691-4	2019	The Pd1 /N-graphene catalyst exhibits outstanding activity and selectivity for the hydrogenation of C2 H2 with H2 in the presence of excess C2 H4 under photothermal heating (UV and visible-light irradiation from a Xe lamp), achieving 99% conversion of acetylene and 93.5% selectivity to ethylene at 125  C. This remarkable catalytic performance is attributed to the high concentration of Pd active sites on the catalyst surface and the weak adsorption energy of ethylene on isolated Pd atoms, which prevents C2 H4 hydrogenation.	ethylene	287-295	programmed cell death 1	Homo sapiens	4-7
30873691-4	2019	The Pd1 /N-graphene catalyst exhibits outstanding activity and selectivity for the hydrogenation of C2 H2 with H2 in the presence of excess C2 H4 under photothermal heating (UV and visible-light irradiation from a Xe lamp), achieving 99% conversion of acetylene and 93.5% selectivity to ethylene at 125  C. This remarkable catalytic performance is attributed to the high concentration of Pd active sites on the catalyst surface and the weak adsorption energy of ethylene on isolated Pd atoms, which prevents C2 H4 hydrogenation.	ethylene	462-470	programmed cell death 1	Homo sapiens	4-7
30873691-4	2019	The Pd1 /N-graphene catalyst exhibits outstanding activity and selectivity for the hydrogenation of C2 H2 with H2 in the presence of excess C2 H4 under photothermal heating (UV and visible-light irradiation from a Xe lamp), achieving 99% conversion of acetylene and 93.5% selectivity to ethylene at 125  C. This remarkable catalytic performance is attributed to the high concentration of Pd active sites on the catalyst surface and the weak adsorption energy of ethylene on isolated Pd atoms, which prevents C2 H4 hydrogenation.	Palladium	388-390	programmed cell death 1	Homo sapiens	4-7
30873691-5	2019	Importantly, the Pd1 /N-graphene catalyst exhibits excellent durability at the optimal reaction temperature of 125  C, which is explained by the strong local coordination of Pd atoms by nitrogen atoms, which suppresses the Pd aggregation.	Nitrogen	186-194	programmed cell death 1	Homo sapiens	17-20
30873691-5	2019	Importantly, the Pd1 /N-graphene catalyst exhibits excellent durability at the optimal reaction temperature of 125  C, which is explained by the strong local coordination of Pd atoms by nitrogen atoms, which suppresses the Pd aggregation.	Palladium	174-176	programmed cell death 1	Homo sapiens	17-20
30638266-9	2019	In Tcons , ATV at 10 microM decreased PD-1 and CD45RO expression.	Atorvastatin	11-14	programmed cell death 1	Homo sapiens	38-42
30322329-1	2019	Programmed death 1 (PD-1) blocking antibodies now represent a major advance in the treatment of patients with classical Hodgkin lymphoma (cHL) who relapse after autologous stem cell transplantation (ASCT) and pre- and/or post-ASCT brentuximab vedotin or after at least three lines of therapy.	asct	199-203	programmed cell death 1	Homo sapiens	0-18
30322329-1	2019	Programmed death 1 (PD-1) blocking antibodies now represent a major advance in the treatment of patients with classical Hodgkin lymphoma (cHL) who relapse after autologous stem cell transplantation (ASCT) and pre- and/or post-ASCT brentuximab vedotin or after at least three lines of therapy.	asct	199-203	programmed cell death 1	Homo sapiens	20-24
30322329-1	2019	Programmed death 1 (PD-1) blocking antibodies now represent a major advance in the treatment of patients with classical Hodgkin lymphoma (cHL) who relapse after autologous stem cell transplantation (ASCT) and pre- and/or post-ASCT brentuximab vedotin or after at least three lines of therapy.	asct brentuximab vedotin	226-250	programmed cell death 1	Homo sapiens	0-18
30322329-1	2019	Programmed death 1 (PD-1) blocking antibodies now represent a major advance in the treatment of patients with classical Hodgkin lymphoma (cHL) who relapse after autologous stem cell transplantation (ASCT) and pre- and/or post-ASCT brentuximab vedotin or after at least three lines of therapy.	asct brentuximab vedotin	226-250	programmed cell death 1	Homo sapiens	20-24
30952089-6	2019	Glycosylation modifications of PD-1 could be observed in three of the four potential N-linked glycosylation sites.	Nitrogen	85-86	programmed cell death 1	Homo sapiens	31-35
30952089-7	2019	However, the binding of GY-5 and GY-14 to PD-1 was not affected by glycosylation.	glycyltyrosine	24-26	programmed cell death 1	Homo sapiens	42-46
30952089-7	2019	However, the binding of GY-5 and GY-14 to PD-1 was not affected by glycosylation.	glycyltyrosine	33-35	programmed cell death 1	Homo sapiens	42-46
30991766-4	2019	A water-soluble polysaccharide, PD1-1, was successfully obtained from dandelion through ultrasonic-assisted extraction and purification using diethylaminoethyl (DEAE)-Sepharose fast flow and Sephadex G-75 columns.	Water	2-7	programmed cell death 1	Homo sapiens	32-37
30991766-4	2019	A water-soluble polysaccharide, PD1-1, was successfully obtained from dandelion through ultrasonic-assisted extraction and purification using diethylaminoethyl (DEAE)-Sepharose fast flow and Sephadex G-75 columns.	Polysaccharides	16-30	programmed cell death 1	Homo sapiens	32-37
30991766-4	2019	A water-soluble polysaccharide, PD1-1, was successfully obtained from dandelion through ultrasonic-assisted extraction and purification using diethylaminoethyl (DEAE)-Sepharose fast flow and Sephadex G-75 columns.	diethylaminoethyl	142-159	programmed cell death 1	Homo sapiens	32-37
30991766-4	2019	A water-soluble polysaccharide, PD1-1, was successfully obtained from dandelion through ultrasonic-assisted extraction and purification using diethylaminoethyl (DEAE)-Sepharose fast flow and Sephadex G-75 columns.	2-diethylaminoethanol	161-165	programmed cell death 1	Homo sapiens	32-37
30991766-4	2019	A water-soluble polysaccharide, PD1-1, was successfully obtained from dandelion through ultrasonic-assisted extraction and purification using diethylaminoethyl (DEAE)-Sepharose fast flow and Sephadex G-75 columns.	Sepharose	167-176	programmed cell death 1	Homo sapiens	32-37
30991766-4	2019	A water-soluble polysaccharide, PD1-1, was successfully obtained from dandelion through ultrasonic-assisted extraction and purification using diethylaminoethyl (DEAE)-Sepharose fast flow and Sephadex G-75 columns.	sephadex	191-199	programmed cell death 1	Homo sapiens	32-37
30991766-5	2019	The results showed that PD1-1 is an inulin-type polysaccharide with a molecular weight of 2.6 kDa and is composed of glucose (52.39%), and mannose (45.41%).	Polysaccharides	48-62	programmed cell death 1	Homo sapiens	24-29
30991766-5	2019	The results showed that PD1-1 is an inulin-type polysaccharide with a molecular weight of 2.6 kDa and is composed of glucose (52.39%), and mannose (45.41%).	Glucose	117-124	programmed cell death 1	Homo sapiens	24-29
30991766-5	2019	The results showed that PD1-1 is an inulin-type polysaccharide with a molecular weight of 2.6 kDa and is composed of glucose (52.39%), and mannose (45.41%).	Mannose	139-146	programmed cell death 1	Homo sapiens	24-29
30991766-7	2019	A physicochemical analysis indicated that PD1-1 has a triple helix structure and exhibits important properties, including good swelling, water-holding, and oil-holding capacities.	Water	137-142	programmed cell death 1	Homo sapiens	42-47
30991766-7	2019	A physicochemical analysis indicated that PD1-1 has a triple helix structure and exhibits important properties, including good swelling, water-holding, and oil-holding capacities.	Oils	156-159	programmed cell death 1	Homo sapiens	42-47
30991766-8	2019	Furthermore, PD1-1 showed good antioxidant activities in DPPH and hydroxyl free radical scavenging abilities, with IC50 values of 0.23 mg/mL and 0.25 mg/mL, respectively, and good hypoglycemic activities in alpha-amylase and alpha-glucosidase inhibition, with IC50 values of 0.53 mg/mL and 0.40 mg/mL, respectively, in a concentration-dependent manner.	1,1-diphenyl-2-picrylhydrazyl	57-61	programmed cell death 1	Homo sapiens	13-18
30991766-8	2019	Furthermore, PD1-1 showed good antioxidant activities in DPPH and hydroxyl free radical scavenging abilities, with IC50 values of 0.23 mg/mL and 0.25 mg/mL, respectively, and good hypoglycemic activities in alpha-amylase and alpha-glucosidase inhibition, with IC50 values of 0.53 mg/mL and 0.40 mg/mL, respectively, in a concentration-dependent manner.	hydroxyl free radical	66-87	programmed cell death 1	Homo sapiens	13-18
30856290-3	2019	Here, a dual bioresponsive gel depot that can respond to the acidic pH and reactive oxygen species (ROS) within the tumor microenvironment (TME) for codelivery of anti-PD1 antibody (aPD1) and Zebularine (Zeb), an HMA, is engineered.	Reactive Oxygen Species	75-98	programmed cell death 1	Homo sapiens	168-171
30856290-3	2019	Here, a dual bioresponsive gel depot that can respond to the acidic pH and reactive oxygen species (ROS) within the tumor microenvironment (TME) for codelivery of anti-PD1 antibody (aPD1) and Zebularine (Zeb), an HMA, is engineered.	Reactive Oxygen Species	100-103	programmed cell death 1	Homo sapiens	168-171
30885328-16	2019	CONCLUSIONS: Abx treatment was significantly associated with attenuated clinical outcomes derived from anti-PD-1-based ICIs in a Chinese cohort of patients with advanced NSCLC.	CHEMBL369125	13-16	programmed cell death 1	Homo sapiens	108-112
30925928-8	2019	In co-culture systems of B-lymphoma cells with immune cells, miR155 induced Fas-mediated apoptosis of CD8+T cells, which could be targeted by anti-PD-1 and anti-PD-L1 antibodies.	ammonium ferrous sulfate	76-79	programmed cell death 1	Homo sapiens	147-151
30984621-4	2019	The PD-1 inhibitor pembrolizumab is approved as monotherapy or in combination with platinum + pemetrexed for most newly diagnosed patients with metastatic NSCLC, excluding those with a targetable oncogene such as ALK and EGFR.	Pemetrexed	94-104	programmed cell death 1	Homo sapiens	4-8
30857561-3	2019	Here we explore the role of human DNT cells in targeting late-stage established lung cancer either alone or in combination with Nivolumab (anti-PD-1 antibody) and describe underlying mechanisms.	2,6-dinitrotoluene	34-37	programmed cell death 1	Homo sapiens	144-148
30857561-9	2019	Healthy donor-derived DNT cells significantly inhibited the growth of late-stage lung cancer xenografts, which was further augmented by anti-PD-1 through increased DNT cell tumor infiltration.	2,6-dinitrotoluene	22-25	programmed cell death 1	Homo sapiens	141-145
30983880-3	2019	In this in vitro study, we investigated possible side effects of two clinically relevant etoricoxib concentrations on the expression pattern of mechanically strained hPDL fibroblasts and associated osteoclastogenesis in a model of simulated orthodontic compressive strain occurring during orthodontic tooth movement.	Etoricoxib	89-99	programmed cell death 1	Homo sapiens	166-170
30325236-0	2019	Expression of programmed death-1 (PD-1) and its ligand PD-L1 is upregulated in endometriosis and promoted by 17beta-estradiol.	Estradiol	109-125	programmed cell death 1	Homo sapiens	14-32
30325236-0	2019	Expression of programmed death-1 (PD-1) and its ligand PD-L1 is upregulated in endometriosis and promoted by 17beta-estradiol.	Estradiol	109-125	programmed cell death 1	Homo sapiens	34-38
33014516-2	2019	Pembrolizumab and nivolumab, which are classified as immune checkpoint inhibitors of programmed cell death protein 1, have shown clinically significant activity in patients who progressed on or after platinum-based regimens, and these agents are now US Food and Drug Administration approved for this indication.	Platinum	200-208	programmed cell death 1	Homo sapiens	85-116
30609280-0	2019	Indirubin modulates CD4+ T-cell homeostasis via PD1/PTEN/AKT signalling pathway in immune thrombocytopenia.	indirubin	0-9	programmed cell death 1	Homo sapiens	48-51
30543161-6	2019	RESULTS: We demonstrate the utility of the Pyrite Shrink-Wrap Laminate for the chemical generation of hydroxyl radicals by mapping the surface of the T-cell co-stimulatory protein Programmed Death - 1 (PD-1) and the interface of the complex with its ligand PD-L1.	Hydroxyl Radical	102-119	programmed cell death 1	Homo sapiens	180-200
30778080-5	2019	Conversely, PD-1 blockade with the monoclonal antibody pembrolizumab enhances HIV production in combination with the latency reversing agent bryostatin without increasing T cell activation.	Bryostatins	141-151	programmed cell death 1	Homo sapiens	12-16
30642453-5	2019	Based on this case report, we discuss the literature regarding the efficacy of inhibitors of programmed death-1 protein (PD-1) in L-LCNEC and their use in association with radiotherapy and in the neoadjuvant setting.	l-lcnec	130-137	programmed cell death 1	Homo sapiens	93-119
30642453-5	2019	Based on this case report, we discuss the literature regarding the efficacy of inhibitors of programmed death-1 protein (PD-1) in L-LCNEC and their use in association with radiotherapy and in the neoadjuvant setting.	l-lcnec	130-137	programmed cell death 1	Homo sapiens	121-125
30500923-20	2019	In addition, PD-1 blockade promoted macrophage glycolysis (P &lt; 0.01) and inhibited fatty acid oxidation (P &lt; 0.05).	Fatty Acids	86-96	programmed cell death 1	Homo sapiens	13-17
30783096-5	2019	PD-L1 signaling, which is associated with activation of the MAPK pathway and increased mitochondrial oxygen consumption, is reversed by PD-1 blockade.	Oxygen	101-107	programmed cell death 1	Homo sapiens	136-140
30338648-1	2019	AIM: To study the influence of total glucosides of paeony (TGP) on the expression of peripheral blood programmed cell death protein 1 (PD-1) and its ligand (PD-L1) in patients with primary Sjogren"s syndrome (pSS).	Glucosides	37-47	programmed cell death 1	Homo sapiens	102-133
30338648-1	2019	AIM: To study the influence of total glucosides of paeony (TGP) on the expression of peripheral blood programmed cell death protein 1 (PD-1) and its ligand (PD-L1) in patients with primary Sjogren"s syndrome (pSS).	Glucosides	37-47	programmed cell death 1	Homo sapiens	135-139
30338648-5	2019	RESULTS: The PD-1 expression on the surface of CD4+ T and CD8+ T lymphocytes in the peripheral blood of patients with pSS were significantly higher than in the control group (P &lt; 0.001).	pss	118-121	programmed cell death 1	Homo sapiens	13-17
30253189-5	2019	Therefore, we analyzed the role of HSP70 and its frequently used inhibitor VER155008 in the regulation of physiological hPDL cell functions and immune cell interaction.	VER 155008	75-84	programmed cell death 1	Homo sapiens	120-124
30565086-8	2019	In cases of progression after platinum-based therapy, PD-1/PD-L1 inhibitors are standard alternatives.	Platinum	30-38	programmed cell death 1	Homo sapiens	54-58
30565086-9	2019	Vinflunine is another option when anti-PD-1/PD-L1 therapy is not possible.	vinflunine	0-10	programmed cell death 1	Homo sapiens	39-43
31727250-5	2019	In this chapter, we describe the methods for efficient production of extracellular domain of human immune checkpoint receptors and Fv fragments of ICI therapeutic antibodies in milligram quantities sufficient for structural studies, taking examples of the PD-1/pembrolizumab Fv and CTLA-4-ipilimumab Fv complexes.	2-I-ICI-H	147-150	programmed cell death 1	Homo sapiens	256-260
29762725-13	2019	This study highlights a rare but serious adverse event of anti-PD-1 antibodies and we recommend, in addition to electrolytes panel, routine calcium monitoring.	Calcium	140-147	programmed cell death 1	Homo sapiens	63-67
30366100-11	2019	Bryostatin and both BET inhibitors downregulated the expression of CD279 on CD8+ T cells without affecting their activation.	Bryostatins	0-10	programmed cell death 1	Homo sapiens	67-72
30543161-6	2019	RESULTS: We demonstrate the utility of the Pyrite Shrink-Wrap Laminate for the chemical generation of hydroxyl radicals by mapping the surface of the T-cell co-stimulatory protein Programmed Death - 1 (PD-1) and the interface of the complex with its ligand PD-L1.	Hydroxyl Radical	102-119	programmed cell death 1	Homo sapiens	202-206
30583461-8	2018	The median tumor mutational burden (TMB) was low (1.7 alterations/megabase); 12% of patients had intermediate or high TMB (higher TMB correlates with favorable response to anti-PD1/PDL1 inhibition in solid tumors).	1,2,4,5-tetramethoxybenzene	118-121	programmed cell death 1	Homo sapiens	177-180
30583461-8	2018	The median tumor mutational burden (TMB) was low (1.7 alterations/megabase); 12% of patients had intermediate or high TMB (higher TMB correlates with favorable response to anti-PD1/PDL1 inhibition in solid tumors).	1,2,4,5-tetramethoxybenzene	118-121	programmed cell death 1	Homo sapiens	177-180
30546030-6	2018	We also observed that PD-1 expression by TMCs was associated with metastatic disease at diagnosis, and the levels of circulating PD-1+ PBMCs were associated with progressive disease upon follow-ups.	trimethylchlorosilane	41-45	programmed cell death 1	Homo sapiens	22-26
30482243-2	2018	Based on the mechanisms of CSCC carcinogenesis has been postulated that these tumors may be amenable to PD-1/PD-L1 blockade.This case illustrates a patient with CSCC with nodal involvement and pulmonary metastases, refractory to two lines of platinum-based regimens and salvage surgery, for whom treatment with nivolumab was recommended.	Platinum	242-250	programmed cell death 1	Homo sapiens	104-108
30603725-7	2018	Nivolumab, an immunotherapeutic agent to block programmed cell death protein 1 (PD-1), showed high efficacy potential for patients progressed with sorafenib and granted accelerated approval by the US Food and Drug Administration (FDA) recently.	Sorafenib	147-156	programmed cell death 1	Homo sapiens	80-84
30388448-3	2018	report that lipophilic statins or biphosphonates, targeting the mevalonate pathway, act as efficient vaccine adjuvants and synergize with anti-PD1 against cancer.	Diphosphonates	34-48	programmed cell death 1	Homo sapiens	143-146
30388448-3	2018	report that lipophilic statins or biphosphonates, targeting the mevalonate pathway, act as efficient vaccine adjuvants and synergize with anti-PD1 against cancer.	Mevalonic Acid	64-74	programmed cell death 1	Homo sapiens	143-146
29746927-1	2018	Indoleamine 2,3-dioxygenase 1 (IDO1), involved in the catabolism of tryptophan (Trp) to kynurenine (Kyn) is an important regulator of tumor-mediated immunosuppression implicated in resistance to anti-PD1 immunotherapy.	Tryptophan	68-78	programmed cell death 1	Homo sapiens	200-203
30204048-7	2018	We found that the PBMCs-CDX model was more accurate in evaluating PD-L1/PD-1 targeted immunotherapies.	Cefadroxil	24-27	programmed cell death 1	Homo sapiens	72-76
30019319-8	2018	In terms of summary toxic events, PD-1/PD-L1 inhibitors had a significantly lower risk of any all-grade AEs (66.20 vs. 86.08%; RR 0.77) and high-grade AEs (14.26 vs. 43.53%; RR 0.32), treatment discontinuation (5.94 vs. 13.92%; RR 0.44), and toxic deaths (0.48 vs. 1.12%; RR 0.45) than chemotherapy.	alanylglutamic acid	104-107	programmed cell death 1	Homo sapiens	34-38
30019319-8	2018	In terms of summary toxic events, PD-1/PD-L1 inhibitors had a significantly lower risk of any all-grade AEs (66.20 vs. 86.08%; RR 0.77) and high-grade AEs (14.26 vs. 43.53%; RR 0.32), treatment discontinuation (5.94 vs. 13.92%; RR 0.44), and toxic deaths (0.48 vs. 1.12%; RR 0.45) than chemotherapy.	alanylglutamic acid	151-154	programmed cell death 1	Homo sapiens	34-38
29920293-3	2018	We show that PL120131 is capable of inhibiting PD-1 mediated apoptotic signaling pathway and rescuing Jurkat cells and primary lymphocytes from apoptosis.	pl120131	13-21	programmed cell death 1	Homo sapiens	47-51
28913556-9	2018	Multivariate factor analysis discriminated between pre- and post-vitamin D supplementation with a combined increased qPCR expression of PD1, PD-L1, TGF-beta, IL-10, CD80, CD86, FOXP3, NFATc2 and cathelicidin.	Vitamin D	65-74	programmed cell death 1	Homo sapiens	136-139
30018132-8	2018	KEY POINTS: PD-1/PD-L1 inhibitor-induced bullous pemphigoid (BP) is a rare but potentially serious dermatologic toxicity associated with checkpoint inhibitorsIn patients with pruritus or rash that is refractory to topical steroids, physicians should have a greater index of suspicion for higher-grade cutaneous immune-related adverse events.There is no standardized treatment algorithm for management of PD-1/PD-L1 inhibitor-induced BP, but patients frequently require topical and systemic steroids.	Steroids	222-230	programmed cell death 1	Homo sapiens	12-16
30018132-8	2018	KEY POINTS: PD-1/PD-L1 inhibitor-induced bullous pemphigoid (BP) is a rare but potentially serious dermatologic toxicity associated with checkpoint inhibitorsIn patients with pruritus or rash that is refractory to topical steroids, physicians should have a greater index of suspicion for higher-grade cutaneous immune-related adverse events.There is no standardized treatment algorithm for management of PD-1/PD-L1 inhibitor-induced BP, but patients frequently require topical and systemic steroids.	Steroids	490-498	programmed cell death 1	Homo sapiens	12-16
30275703-7	2018	Results: The approved checkpoint inhibitors (PD1 and PDL1 inhibitors) have similar efficacy and safety profiles in metastatic platinum-refractory bladder cancer, but they vary in dose and frequency and cost burden.	Platinum	126-134	programmed cell death 1	Homo sapiens	45-48
30063143-6	2018	Furthermore, when a low dose of cyclophosphamide (CP) was loaded into PD-1-expressing platelets to deplete regulatory T cells (Tregs), an increased frequency of reinvigorated CD8+ lymphocyte cells was observed within the postsurgery tumor microenvironment, directly preventing tumor relapse.	Cyclophosphamide	32-48	programmed cell death 1	Homo sapiens	70-74
30176946-3	2018	CASE PRESENTATION: Here, we report the successful treatment of a mycophenolate-resistant organizing pneumonia (OP) with infliximab in a patient with metastatic melanoma after PD-1 blockade.	Mycophenolic Acid	65-78	programmed cell death 1	Homo sapiens	175-179
30176946-8	2018	CONCLUSION: This case describes a not well-studied situation, in which a mycophenolate-resistant PD-1 blocker-associated pneumonitis was successfully treated with a TNFalpha neutralizing antibody.	Mycophenolic Acid	73-86	programmed cell death 1	Homo sapiens	97-101
30181171-1	2018	Overexpression of CD38 after PD-1/PD-L1 blockade increases extracellular adenosine levels and may contribute to acquired resistance to anti-PD-1/PD-L1 therapy.	Adenosine	73-82	programmed cell death 1	Homo sapiens	29-33
29746927-1	2018	Indoleamine 2,3-dioxygenase 1 (IDO1), involved in the catabolism of tryptophan (Trp) to kynurenine (Kyn) is an important regulator of tumor-mediated immunosuppression implicated in resistance to anti-PD1 immunotherapy.	Tryptophan	80-83	programmed cell death 1	Homo sapiens	200-203
29746927-1	2018	Indoleamine 2,3-dioxygenase 1 (IDO1), involved in the catabolism of tryptophan (Trp) to kynurenine (Kyn) is an important regulator of tumor-mediated immunosuppression implicated in resistance to anti-PD1 immunotherapy.	Kynurenine	88-98	programmed cell death 1	Homo sapiens	200-203
29746927-1	2018	Indoleamine 2,3-dioxygenase 1 (IDO1), involved in the catabolism of tryptophan (Trp) to kynurenine (Kyn) is an important regulator of tumor-mediated immunosuppression implicated in resistance to anti-PD1 immunotherapy.	Kynurenine	100-103	programmed cell death 1	Homo sapiens	200-203
29844001-0	2018	Docetaxel Down-Regulates PD-1 Expression via STAT3 in T Lymphocytes.	Docetaxel	0-9	programmed cell death 1	Homo sapiens	25-29
29844001-10	2018	In vitro assay showed that docetaxel reduced the expression of PD-1 on T-cell subsets without altering cell death.	Docetaxel	27-36	programmed cell death 1	Homo sapiens	63-67
29844001-11	2018	Further tests in Jurkat T cells demonstrated that docetaxel activated signal transduction and activator of transcription 3 (STAT3) signaling to suppress PD-1 expression, whereas STAT3 inhibition reversed the down-regulation of PD-1.	Docetaxel	50-59	programmed cell death 1	Homo sapiens	153-157
29761497-0	2018	Vibration enhances PGE2 , IL-6, and IL-8 expression in compressed hPDL cells via cyclooxygenase pathway.	Dinoprostone	19-23	programmed cell death 1	Homo sapiens	66-70
29965858-7	2018	Here we report a case of severe, steroid refractory, lymphocytic myocarditis that occurred after the first cycle of combination immunotherapy with the programmed cell death protein-1 inhibitor, nivolumab, and the cytotoxic T-lymphocyte-associated protein 4 blocker, ipilimumab, for metastatic melanoma.	Steroids	33-40	programmed cell death 1	Homo sapiens	151-182
30129176-0	2018	PD-1 Blockade for Improving the Antitumor Efficiency of Polymer-Doxorubicin Nanoprodrug.	polymer-doxorubicin	56-75	programmed cell death 1	Homo sapiens	0-4
30129176-2	2018	Here, a strategy involving blocking programmed cell death protein 1 (PD-1) to enhance the chemotherapeutic effect of a doxorubicin nanoprodrug HA-Psi-DOX is proposed and the synergetic mechanism between them is further studied.	Doxorubicin	119-130	programmed cell death 1	Homo sapiens	36-67
30129176-2	2018	Here, a strategy involving blocking programmed cell death protein 1 (PD-1) to enhance the chemotherapeutic effect of a doxorubicin nanoprodrug HA-Psi-DOX is proposed and the synergetic mechanism between them is further studied.	Doxorubicin	119-130	programmed cell death 1	Homo sapiens	69-73
30129176-2	2018	Here, a strategy involving blocking programmed cell death protein 1 (PD-1) to enhance the chemotherapeutic effect of a doxorubicin nanoprodrug HA-Psi-DOX is proposed and the synergetic mechanism between them is further studied.	Doxorubicin	150-153	programmed cell death 1	Homo sapiens	36-67
30129176-2	2018	Here, a strategy involving blocking programmed cell death protein 1 (PD-1) to enhance the chemotherapeutic effect of a doxorubicin nanoprodrug HA-Psi-DOX is proposed and the synergetic mechanism between them is further studied.	Doxorubicin	150-153	programmed cell death 1	Homo sapiens	69-73
30129176-7	2018	The results suggest that the therapeutic efficiency of HA-Psi-DOX nanoparticles is significantly improved when combined with checkpoint inhibitors anti-PD-1 antibody (alpha-PD1) due to the neutralization of immunosuppression by blocking the interaction between PD-L1 and PD-1.	Doxorubicin	62-65	programmed cell death 1	Homo sapiens	152-156
30129176-7	2018	The results suggest that the therapeutic efficiency of HA-Psi-DOX nanoparticles is significantly improved when combined with checkpoint inhibitors anti-PD-1 antibody (alpha-PD1) due to the neutralization of immunosuppression by blocking the interaction between PD-L1 and PD-1.	Doxorubicin	62-65	programmed cell death 1	Homo sapiens	271-275
30126243-4	2018	A DNA fragmentation test in the HL-60 cell line has indicated that Pd1 causes comparable proapoptotic effects with regard to cisplatin but at substantially higher concentrations.	Cisplatin	125-134	programmed cell death 1	Homo sapiens	67-70
30126243-5	2018	Pd1 and cisplatin form intra-strand guanine bis-adducts as the palladium complex is less capable of forming DNA adducts.	Guanine	36-43	programmed cell death 1	Homo sapiens	0-3
30126243-5	2018	Pd1 and cisplatin form intra-strand guanine bis-adducts as the palladium complex is less capable of forming DNA adducts.	Palladium	63-72	programmed cell death 1	Homo sapiens	0-3
30126243-7	2018	The test for efficient removal of DNA-adducts by the NER synthesis after modification of pBS plasmids with either cisplatin or Pd1 has manifested that the lesions induced by cisplatin are far better recognized and repaired compared those of Pd1.	Lead	89-92	programmed cell death 1	Homo sapiens	127-130
30126243-7	2018	The test for efficient removal of DNA-adducts by the NER synthesis after modification of pBS plasmids with either cisplatin or Pd1 has manifested that the lesions induced by cisplatin are far better recognized and repaired compared those of Pd1.	Lead	89-92	programmed cell death 1	Homo sapiens	241-244
30126243-7	2018	The test for efficient removal of DNA-adducts by the NER synthesis after modification of pBS plasmids with either cisplatin or Pd1 has manifested that the lesions induced by cisplatin are far better recognized and repaired compared those of Pd1.	Cisplatin	114-123	programmed cell death 1	Homo sapiens	241-244
30126243-7	2018	The test for efficient removal of DNA-adducts by the NER synthesis after modification of pBS plasmids with either cisplatin or Pd1 has manifested that the lesions induced by cisplatin are far better recognized and repaired compared those of Pd1.	Cisplatin	174-183	programmed cell death 1	Homo sapiens	127-130
30126243-7	2018	The test for efficient removal of DNA-adducts by the NER synthesis after modification of pBS plasmids with either cisplatin or Pd1 has manifested that the lesions induced by cisplatin are far better recognized and repaired compared those of Pd1.	Cisplatin	174-183	programmed cell death 1	Homo sapiens	241-244
30104397-10	2018	Soluble PD-1 ligands reduced T-cell proliferation, phosphorylated extracellular signal-regulated kinase and cyclin A levels, mitochondrial adenosine triphosphate production, and spare respiratory capacity.	Adenosine Triphosphate	139-161	programmed cell death 1	Homo sapiens	8-12
30078154-7	2018	High-dose steroid monotherapy may be associated with clinical deterioration in some patients with PD-1 inhibitor-associated myasthenia gravis, immune-mediated myopathies, or Guillain-Barre syndrome.	Steroids	10-17	programmed cell death 1	Homo sapiens	98-102
30078154-9	2018	Although steroid monotherapy is commonly used in non-neuromuscular autoimmune disorders triggered by anti-PD-1 therapy, this may lead to unfavorable outcomes in some patients with PD-1 inhibitor-associated neuromuscular complications.	Steroids	9-16	programmed cell death 1	Homo sapiens	106-110
30078154-9	2018	Although steroid monotherapy is commonly used in non-neuromuscular autoimmune disorders triggered by anti-PD-1 therapy, this may lead to unfavorable outcomes in some patients with PD-1 inhibitor-associated neuromuscular complications.	Steroids	9-16	programmed cell death 1	Homo sapiens	180-184
29679556-1	2018	Check point inhibitor anti-PD1 antibody produced some efficacy in Hepatocellular Carcinoma (HCC) patients previously treated with sorafenib.	Sorafenib	130-139	programmed cell death 1	Homo sapiens	27-30
30151257-5	2018	Furthermore, we explore the ability to quantify TMB as a potential predictive biomarker of PD1/PD-L1 therapy in CRC.	1,2,4,5-tetramethoxybenzene	48-51	programmed cell death 1	Homo sapiens	91-94
29859415-6	2018	After treatment with Chidamide combined with chemotherapy, MFI of PD-1 significantly decreased (P &lt; 0.05).	N-(2-amino-5-fluorobenzyl)-4-(N-(pyridine-3-acrylyl)aminomethyl)benzamide	21-30	programmed cell death 1	Homo sapiens	66-70
29761497-6	2018	To demonstrate whether the expression of PGE2 , IL-6, and IL-8 was in the COX-dependent pathway, the hPDL cells were treated with indomethacin.	Indomethacin	130-142	programmed cell death 1	Homo sapiens	101-105
29761497-10	2018	In addition, exogenous PGE2 increased IL-6 and IL-8 mRNA and protein expressions in hPDL cells.	Dinoprostone	23-27	programmed cell death 1	Homo sapiens	84-88
29553121-1	2018	This study evaluated the influence in the biocompatibility of human periodontal ligament (hPDL) mesenchymal stromal cell onto poly lactic-acid (PLA) films and PLA fiber membrane.	poly(lactide)	126-142	programmed cell death 1	Homo sapiens	90-94
29884406-8	2018	High tumor mutational burden (TMB) (median 11.3 vs. 5.0) and unique mutational signatures were noted between unrelated and related donor groups - with a strong correlation between infiltrating PD-1+ lymphocytes and TMB (R = 0.98, p < 0.01).	1,2,4,5-tetramethoxybenzene	215-218	programmed cell death 1	Homo sapiens	193-197
29799520-7	2018	Together, our results are the first to show that GC-derived exosomes can effectively induce PD1+ TAM generation, and these cells can produce a large number of IL-10, impair CD8+ T-cell function, and thereby create conditions that promote GC progression.	tam	97-100	programmed cell death 1	Homo sapiens	92-95
29657128-2	2018	Using whole-exome sequencing to examine non-small-cell lung cancer (NSCLC) treated with PD-1 plus CTLA-4 blockade, we found that high tumor mutation burden (TMB) predicted improved objective response, durable benefit, and progression-free survival.	1,2,4,5-tetramethoxybenzene	157-160	programmed cell death 1	Homo sapiens	88-92
30293334-7	2018	Meanwhile, the expression of ICOS and PD-1 on cTfh in patient group was markedly more intensive (59.6+-10.0 vs.49.2+-6.9, P&lt;0.001 and 532.6+-104.2 vs. 485.1+-73.4, P=0.025, respectively).	ctfh	46-50	programmed cell death 1	Homo sapiens	38-42
30293334-10	2018	Nevertheless, the expression of PD-1 on cTfh was only positively correlated with the ratio of PD-1(+) Tfh (r=0.473, P=0.003).	ctfh	40-44	programmed cell death 1	Homo sapiens	32-36
30293334-10	2018	Nevertheless, the expression of PD-1 on cTfh was only positively correlated with the ratio of PD-1(+) Tfh (r=0.473, P=0.003).	ctfh	40-44	programmed cell death 1	Homo sapiens	94-98
29520784-1	2018	BACKGROUND: Asiaticoside is a compound isolated from Herb Centella asiatica, which has been shown to promote osteogenic differentiation of human periodontal ligament (hPDL) cells.	asiaticoside	12-24	programmed cell death 1	Homo sapiens	167-171
29520784-2	2018	This study investigated the molecular mechanism underlying the asiaticoside-induced osteogenic differentiation of hPDL cells.	asiaticoside	63-75	programmed cell death 1	Homo sapiens	114-118
29520784-3	2018	METHODS: hPDL cells were incubated with various concentrations of asiaticoside to test cell viability by MTT assay.	asiaticoside	66-78	programmed cell death 1	Homo sapiens	9-13
29520784-14	2018	CONCLUSION: The data demonstrate that asiaticoside induces osteogenic differentiation of hPDL cells by activating the Wnt/beta-catenin signaling pathway.	asiaticoside	38-50	programmed cell death 1	Homo sapiens	89-93
29605290-0	2018	Responses in patients receiving sequential paclitaxel post progression on PD1 inhibitors.	Paclitaxel	43-53	programmed cell death 1	Homo sapiens	74-77
29650143-3	2018	The introduction of anti-programmed cell death protein 1/programmed death-ligand 1(PD1/PD-L1) checkpoint inhibitors has redefined the therapeutic landscape for platinum-resistant urothelial cancers; their clinical efficacy and favorable toxicity render these agents attractive therapeutic options either as monotherapy or in combination with other agents in earlier disease states, including muscle-invasive disease.	Platinum	160-168	programmed cell death 1	Homo sapiens	83-86
29651624-8	2018	The positive correlation observed between expression of BRAF V600E and PD-L1/PD-1 suggests that immunotherapies targeting PD-L1/PD-1 might be effective for PTC patients with the BRAF V600E mutation, which are refractory to radioiodine therapy.	Iodine-131	223-234	programmed cell death 1	Homo sapiens	77-81
29651624-8	2018	The positive correlation observed between expression of BRAF V600E and PD-L1/PD-1 suggests that immunotherapies targeting PD-L1/PD-1 might be effective for PTC patients with the BRAF V600E mutation, which are refractory to radioiodine therapy.	Iodine-131	223-234	programmed cell death 1	Homo sapiens	128-132
29449276-9	2018	An in vitro functional model of TAM-like monocytes suppressed activation of PD-1hi NK cells, which was reversed by PD-1 blockade.	tam	32-35	programmed cell death 1	Homo sapiens	76-80
29615063-11	2018	CONCLUSIONS: PD-1 and PD-L1 expressions may be useful as biomarkers to predict treatment responses to NAC in breast cancer.	nac	102-105	programmed cell death 1	Homo sapiens	13-17
29464839-2	2018	Herein, using a stoichiometrically precise synthetic method, we prepare atomically dispersed palladium-cerium oxide (Pd1 /CeO2 ) and hexapalladium cluster-cerium oxide (Pd6 /CeO2 ), as confirmed by spherical-aberration-corrected transmission electron microscopy and X-ray absorption fine structure spectroscopy.	palladium-cerium oxide	93-115	programmed cell death 1	Homo sapiens	117-120
29464839-3	2018	For aerobic alcohol oxidation, Pd1 /CeO2 shows extremely high catalytic activity with a TOF of 6739 h-1 and satisfactory selectivity (almost 100 % for benzaldehyde), while Pd6 /CeO2 is inactive, indicating that the true active species are single Pd atoms.	Alcohols	12-19	programmed cell death 1	Homo sapiens	31-34
29464839-3	2018	For aerobic alcohol oxidation, Pd1 /CeO2 shows extremely high catalytic activity with a TOF of 6739 h-1 and satisfactory selectivity (almost 100 % for benzaldehyde), while Pd6 /CeO2 is inactive, indicating that the true active species are single Pd atoms.	benzaldehyde	151-163	programmed cell death 1	Homo sapiens	31-34
29617441-4	2018	Expressions of PD-1 and PD-L1 were detected immunohistochemically in 25 formalin-fixed, paraffin-embedded tumor specimens from 24 patients with intracranial germinoma consisting of 22 primary and 3 recurrent tumors.	Formaldehyde	72-80	programmed cell death 1	Homo sapiens	15-19
29617441-4	2018	Expressions of PD-1 and PD-L1 were detected immunohistochemically in 25 formalin-fixed, paraffin-embedded tumor specimens from 24 patients with intracranial germinoma consisting of 22 primary and 3 recurrent tumors.	Paraffin	88-96	programmed cell death 1	Homo sapiens	15-19
28770269-3	2018	The aim of this study was to evaluate the frequencies of PD-1-positive and PD-ligand 1 (PD-L1)-positive T and B lymphocytes in patients with NPGN and PGN in relation to clinical parameters for the first time.	pgn	142-145	programmed cell death 1	Homo sapiens	57-61
28770269-7	2018	The frequencies of CD4+/PD1+ T lymphocytes, CD8+/PD1+ T lymphocytes, and CD19+/PD-1+ B lymphocytes in the PGN group exceeded values obtained both in the NPGN group, and the control group.	pgn	106-109	programmed cell death 1	Homo sapiens	79-83
28770269-8	2018	Alteration of PD-1/PD-L1 pathway may be involved in poorer prognosis, as patients with PGN are characterized by higher frequencies of PD-1-positive and PD-L1-positive T and B lymphocytes than patients with NPGN.	pgn	87-90	programmed cell death 1	Homo sapiens	14-18
28770269-8	2018	Alteration of PD-1/PD-L1 pathway may be involved in poorer prognosis, as patients with PGN are characterized by higher frequencies of PD-1-positive and PD-L1-positive T and B lymphocytes than patients with NPGN.	pgn	87-90	programmed cell death 1	Homo sapiens	134-138
29407748-7	2018	hPDL alkaline phosphatase (ALP) enzymatic activity and mineral deposition were examined using an ALP assay and Alizarin Red S staining, respectively.	Alizarin Red S	111-125	programmed cell death 1	Homo sapiens	0-4
29325739-1	2018	Immunotherapy with programmed cell death 1/ligand 1 (PD-1/PD-L1) checkpoint inhibitors has expanded a previously limited pool of effective treatment options for patients with metastatic urothelial carcinoma, particularly those with recurring or refractory disease and those who are ineligible for cisplatin.	Cisplatin	297-306	programmed cell death 1	Homo sapiens	53-57
29325739-8	2018	Anti-PD-1/PD-L1 antibodies have shown favorable clinical activity and tolerability in patients with metastatic urothelial carcinoma refractory to platinum-based therapy or who are ineligible for cisplatin.	Platinum	146-154	programmed cell death 1	Homo sapiens	5-9
29325739-8	2018	Anti-PD-1/PD-L1 antibodies have shown favorable clinical activity and tolerability in patients with metastatic urothelial carcinoma refractory to platinum-based therapy or who are ineligible for cisplatin.	Cisplatin	195-204	programmed cell death 1	Homo sapiens	5-9
29325739-9	2018	The activity of PD-1/PD-L1 inhibitors is now also being studied as first-line monotherapy in cisplatin-eligible patients in combination with chemotherapy as maintenance therapy after first-line chemotherapy, and in earlier disease states, such as muscle-invasive and non-muscle-invasive bladder cancer.	Cisplatin	93-102	programmed cell death 1	Homo sapiens	16-20
29642147-1	2018	PURPOSE: Using bibliometrics, we analyzed the research status of immune checkpoint blockade (ICB, a popular tumor immunotherapy method represented by antibodies targeted CTLA-4 and PD-1/PD-L1) in tumor immunotherapy in China during the past 2 decades.	indole-2-carboxylic acid	93-96	programmed cell death 1	Homo sapiens	181-185
29089607-3	2018	Despite initial success, durable response rates in patients with advanced-stage MIBC treated with novel inhibitory antibodies targeting programmed cell death protein 1 (PD-1) or its endogenous ligand programmed cell death 1 ligand 1 (PD-L1) remain low.	4-METHYL-2-PENTANOL	80-84	programmed cell death 1	Homo sapiens	136-167
29525632-11	2018	Collectively, tumor with TH is closely associated with CLEC1Blow &amp; PD-L1high expression, which may imply high response of PD-L1/PD-1 immune checkpoint therapies.	Adenosine Monophosphate	66-69	programmed cell death 1	Homo sapiens	132-136
29502288-3	2018	The anti PD1 agent, nivolumab, was recently approved by the FDA as a standard of care regimen for patients with platinum refractory recurrent/metastatic (R/M) HNSCC.	Platinum	112-120	programmed cell death 1	Homo sapiens	9-12
29359792-4	2018	The aims of this study were to clarify the influence of PDCD1 and CTLA4 SNPs on the risk of developing cITP and its clinical features.	citp	103-107	programmed cell death 1	Homo sapiens	56-61
29359792-6	2018	Patients with cITP had a significantly higher frequency of the PDCD1 +7209 TT genotype compared with healthy controls.	citp	14-18	programmed cell death 1	Homo sapiens	63-68
29359792-8	2018	Moreover, the PDCD1 -606 AA genotype and +63379 TT genotype were significantly associated with a lower number of patients who achieved a complete response to prednisolone treatment.	Prednisolone	158-170	programmed cell death 1	Homo sapiens	14-19
29435074-4	2018	Therefore, the present study investigated whether and how the PD-1/PD-L1 axis is involved in regulating the sensitivity of CRL2631, a DLBCL cell line, to the CHOP (Cyclophosphamide, Hydroxydaunorubicin/adriamycin, Oncovin/vincristine and Prednisone) chemotherapeutic regimen.	crl2631	123-130	programmed cell death 1	Homo sapiens	62-66
28963773-4	2018	Peripheral blood mononuclear cells (PBMC) from healthy donors (HD) and primary breast cancer patients (PBC) were treated in vitro with pembrolizumab, which effectively reduced PD-1 expression in both cohorts.	potassium bicarbonate	103-106	programmed cell death 1	Homo sapiens	176-180
29308884-1	2018	The monomeric (PdL 2H2O) and dimeric (Pd2L2 7H2O) palladium(II) complexes of N,N"-bis(2-aminoethyl)oxamide (H2L) were isolated, and their structures were established by single-crystal X-ray diffraction.	N,N'-bis(2-aminoethyl)oxamide	77-106	programmed cell death 1	Homo sapiens	15-18
29308884-7	2018	Cyclic voltammetry of PdL in perchlorate-, chloride-, and sulfate-containing electrolytes revealed two-electron oxidation of the palladium center.	perchlorate	29-40	programmed cell death 1	Homo sapiens	22-25
29308884-7	2018	Cyclic voltammetry of PdL in perchlorate-, chloride-, and sulfate-containing electrolytes revealed two-electron oxidation of the palladium center.	Chlorides	43-51	programmed cell death 1	Homo sapiens	22-25
29308884-7	2018	Cyclic voltammetry of PdL in perchlorate-, chloride-, and sulfate-containing electrolytes revealed two-electron oxidation of the palladium center.	Sulfates	58-65	programmed cell death 1	Homo sapiens	22-25
29308884-7	2018	Cyclic voltammetry of PdL in perchlorate-, chloride-, and sulfate-containing electrolytes revealed two-electron oxidation of the palladium center.	Palladium	129-138	programmed cell death 1	Homo sapiens	22-25
29423118-7	2018	In addition, the anti-PD-1/PD-L1 antibody therapy had fewer treatment-related adverse events (AEs) (OR = 0.33, 95% CI 0.28-0.39, P &lt; 0.05) than docetaxel, especially the grade &gt;=3 AEs (OR = 0.18, 95% CI 0.12-0.28, P &lt; 0.001).	aes	94-97	programmed cell death 1	Homo sapiens	22-26
29282323-9	2018	Mechanistically, SAP opposed PD-1 function by acting as a molecular shield of key tyrosine residues that are targets for the tyrosine phosphatase SHP2, which mediates PD-1 inhibitory properties.	Tyrosine	82-90	programmed cell death 1	Homo sapiens	29-33
29282323-9	2018	Mechanistically, SAP opposed PD-1 function by acting as a molecular shield of key tyrosine residues that are targets for the tyrosine phosphatase SHP2, which mediates PD-1 inhibitory properties.	Tyrosine	82-90	programmed cell death 1	Homo sapiens	167-171
29467945-11	2018	High PD-L1 positivity in TCs, especially in SqCCs, indicated that PD-1/PD-L1 targeted therapy may be a promising therapeutic approach.	9-ethyl-N-(3,4,5-trimethoxyphenyl)carbazole-3-sulfonamide	25-28	programmed cell death 1	Homo sapiens	66-70
29159455-3	2018	A positive monotonic and significant correlation was indicated between P in the topsoil determined by the double lactate method (P DL) and the yearly flow-weight total (TP) concentrations in leachates with Spearman rank correlations r s (r s &gt; 0.183) and probability (p) &lt; 0.05.	Lactic Acid	113-120	programmed cell death 1	Homo sapiens	129-133
29150026-10	2018	Correlation analysis reinforced that PD1 and CD95L are efficient apoptosis" pathway that decreased levels of Tregs in the NI and PB groups.	pladienolide B	129-131	programmed cell death 1	Homo sapiens	37-40
29312350-6	2017	Focusing on hMDDC, we could partially reverse effects mediated by PD-1 blockade by neutralizing TNFalpha but not by neutralizing IFNgamma.	HMddC	12-17	programmed cell death 1	Homo sapiens	66-70
29312358-3	2017	In a cohort of AML patients, undergoing combined daunorubicin and cytarabine chemotherapy, a population of T regulatory cells (Tregs) with suppressive phenotype, expressing the immune checkpoint programmed cell death protein 1 (PD-1), was significantly increased.	Cytarabine	66-76	programmed cell death 1	Homo sapiens	195-226
29338562-2	2018	In this research, rituximab-conjugated and doxorubicin-loaded microbubbles (RDMs) were designed for exploring a combination approach of targeted microbubbles with ultrasound (US) irradiation and PD-1 inhibitor to overcome obstacles mentioned above.	Doxorubicin	43-54	programmed cell death 1	Homo sapiens	195-199
29087505-1	2018	We have developed an animal model of amodiaquine-induced liver injury that has characteristics very similar to idiosyncratic drug-induced liver injury (IDILI) in humans by impairing immune tolerance using a PD1-/- mouse and cotreatment with anti-CTLA-4.	Amodiaquine	37-48	programmed cell death 1	Homo sapiens	207-210
29262678-5	2018	The coupling between iodobenzene and phenylacetylene on Pd1/TiO2 exhibits a turnover rate of 51.0 diphenylacetylene molecules per anchored Pd atom per minute at 60  C, with a low apparent activation barrier of 28.9 kJ/mol and no cost of catalyst separation.	iodobenzene	21-32	programmed cell death 1	Homo sapiens	56-59
29262678-5	2018	The coupling between iodobenzene and phenylacetylene on Pd1/TiO2 exhibits a turnover rate of 51.0 diphenylacetylene molecules per anchored Pd atom per minute at 60  C, with a low apparent activation barrier of 28.9 kJ/mol and no cost of catalyst separation.	phenylacetylene	37-52	programmed cell death 1	Homo sapiens	56-59
29262678-5	2018	The coupling between iodobenzene and phenylacetylene on Pd1/TiO2 exhibits a turnover rate of 51.0 diphenylacetylene molecules per anchored Pd atom per minute at 60  C, with a low apparent activation barrier of 28.9 kJ/mol and no cost of catalyst separation.	titanium dioxide	60-64	programmed cell death 1	Homo sapiens	56-59
29262678-5	2018	The coupling between iodobenzene and phenylacetylene on Pd1/TiO2 exhibits a turnover rate of 51.0 diphenylacetylene molecules per anchored Pd atom per minute at 60  C, with a low apparent activation barrier of 28.9 kJ/mol and no cost of catalyst separation.	biphenylacetylene	98-115	programmed cell death 1	Homo sapiens	56-59
29262678-7	2018	This coupling of phenyl adsorbed on Pd1 and phenylacetylenyl bound to Oad of TiO2 forms the product molecule, diphenylacetylene.	titanium dioxide	77-81	programmed cell death 1	Homo sapiens	36-39
29262678-7	2018	This coupling of phenyl adsorbed on Pd1 and phenylacetylenyl bound to Oad of TiO2 forms the product molecule, diphenylacetylene.	biphenylacetylene	110-127	programmed cell death 1	Homo sapiens	36-39
29358573-3	2018	Recently, a subset of patients with locally advanced or metastatic UBC have responded to checkpoint blockade immunotherapy against the programmed cell death 1 protein (PD-1) or its ligand (PD-L1) or the cytotoxic T-lymphocyte antigen 4 that releases the inhibition of T cells, the remarkable clinical efficacy on UBC has brought total five checkpoint inhibitors approved by the FDA in the last 2 years, and this is revolutionizing treatment of advanced UBC.	1-(2-amino-2-carboxyethyl)-3-(2-carboxybenzyl)pyrimidine-2,4-dione	67-70	programmed cell death 1	Homo sapiens	135-166
29358573-3	2018	Recently, a subset of patients with locally advanced or metastatic UBC have responded to checkpoint blockade immunotherapy against the programmed cell death 1 protein (PD-1) or its ligand (PD-L1) or the cytotoxic T-lymphocyte antigen 4 that releases the inhibition of T cells, the remarkable clinical efficacy on UBC has brought total five checkpoint inhibitors approved by the FDA in the last 2 years, and this is revolutionizing treatment of advanced UBC.	1-(2-amino-2-carboxyethyl)-3-(2-carboxybenzyl)pyrimidine-2,4-dione	67-70	programmed cell death 1	Homo sapiens	168-172
29358573-3	2018	Recently, a subset of patients with locally advanced or metastatic UBC have responded to checkpoint blockade immunotherapy against the programmed cell death 1 protein (PD-1) or its ligand (PD-L1) or the cytotoxic T-lymphocyte antigen 4 that releases the inhibition of T cells, the remarkable clinical efficacy on UBC has brought total five checkpoint inhibitors approved by the FDA in the last 2 years, and this is revolutionizing treatment of advanced UBC.	1-(2-amino-2-carboxyethyl)-3-(2-carboxybenzyl)pyrimidine-2,4-dione	313-316	programmed cell death 1	Homo sapiens	135-166
29358573-3	2018	Recently, a subset of patients with locally advanced or metastatic UBC have responded to checkpoint blockade immunotherapy against the programmed cell death 1 protein (PD-1) or its ligand (PD-L1) or the cytotoxic T-lymphocyte antigen 4 that releases the inhibition of T cells, the remarkable clinical efficacy on UBC has brought total five checkpoint inhibitors approved by the FDA in the last 2 years, and this is revolutionizing treatment of advanced UBC.	1-(2-amino-2-carboxyethyl)-3-(2-carboxybenzyl)pyrimidine-2,4-dione	313-316	programmed cell death 1	Homo sapiens	168-172
29358573-3	2018	Recently, a subset of patients with locally advanced or metastatic UBC have responded to checkpoint blockade immunotherapy against the programmed cell death 1 protein (PD-1) or its ligand (PD-L1) or the cytotoxic T-lymphocyte antigen 4 that releases the inhibition of T cells, the remarkable clinical efficacy on UBC has brought total five checkpoint inhibitors approved by the FDA in the last 2 years, and this is revolutionizing treatment of advanced UBC.	1-(2-amino-2-carboxyethyl)-3-(2-carboxybenzyl)pyrimidine-2,4-dione	313-316	programmed cell death 1	Homo sapiens	135-166
29358573-3	2018	Recently, a subset of patients with locally advanced or metastatic UBC have responded to checkpoint blockade immunotherapy against the programmed cell death 1 protein (PD-1) or its ligand (PD-L1) or the cytotoxic T-lymphocyte antigen 4 that releases the inhibition of T cells, the remarkable clinical efficacy on UBC has brought total five checkpoint inhibitors approved by the FDA in the last 2 years, and this is revolutionizing treatment of advanced UBC.	1-(2-amino-2-carboxyethyl)-3-(2-carboxybenzyl)pyrimidine-2,4-dione	313-316	programmed cell death 1	Homo sapiens	168-172
29358573-4	2018	We discuss the rationale for immunotherapy in bladder cancer, progress with blocking the PD-1/PD-L1 pathway for UBC treatment, and ongoing clinical trials.	1-(2-amino-2-carboxyethyl)-3-(2-carboxybenzyl)pyrimidine-2,4-dione	112-115	programmed cell death 1	Homo sapiens	89-93
29330552-0	2018	Dosimetry Prediction for Clinical Translation of 64Cu-Pembrolizumab ImmunoPET Targeting Human PD-1 Expression.	Copper-64	49-53	programmed cell death 1	Homo sapiens	94-98
29330552-9	2018	In summary, we validated the 64Cu-pembrolizumab tracer"s specific hPD-1 receptor targeting and predicted human dosimetry.	Copper-64	29-33	programmed cell death 1	Homo sapiens	66-71
29304116-0	2018	The sorafenib anti-relapse effect after alloHSCT is associated with heightened alloreactivity and accumulation of CD8+PD-1+ (CD279+) lymphocytes in marrow.	Sorafenib	4-13	programmed cell death 1	Homo sapiens	118-122
29304116-0	2018	The sorafenib anti-relapse effect after alloHSCT is associated with heightened alloreactivity and accumulation of CD8+PD-1+ (CD279+) lymphocytes in marrow.	Sorafenib	4-13	programmed cell death 1	Homo sapiens	125-130
29045547-10	2018	Duration of steroid taper, severity of initial irAEs and use of additional immunosuppressants did not predict for toxicity on rechallenge, although patients remaining on steroid therapy at anti-PD-1 resumption had higher rates of toxicities (55% versus 31%, P = 0.03).	Steroids	170-177	programmed cell death 1	Homo sapiens	194-198
29126881-8	2018	In this review, we will illustrate the activity of TAMs and associated molecules in TNBC, focusing on their role in modulating the expression of PD-1/PD-L1 and on the emerging TAM-tailored strategies for TNBC patients.	tams	51-55	programmed cell death 1	Homo sapiens	145-149
28547570-14	2018	In conclusion, iloprost promoted mRNA and protein expression of VEGF and COL1, but not of bFGF in hPDL cells.	Iloprost	15-23	programmed cell death 1	Homo sapiens	98-102
28994323-3	2017	Atezolizumab is an engineered humanized anti-PD-L1 monoclonal antibody that inhibits PD-L1 binding to PD-1 and B7.1, enhancing immune-mediated tumor killing and is currently approved as second-line treatment after failure of platinum-based chemotherapy as well as first-line in cisplatin-ineligible patients.	Cisplatin	278-287	programmed cell death 1	Homo sapiens	102-115
28601918-0	2017	Osimertinib reactivated immune-related colitis after treatment with anti-PD1 antibody for non-small cell lung cancer.	osimertinib	0-11	programmed cell death 1	Homo sapiens	73-76
29310385-11	2017	CONCLUSIONS: Our meta-analysis has demonstrated that the use of PD-1 inhibitors is associated with an increased risk of colitis compared with chemotherapy or everolimus.	Everolimus	158-168	programmed cell death 1	Homo sapiens	64-68
28639391-10	2017	RESULTS: Memory Tfh cells with the CD4+ CXCR5+ PD1+ CCR7- and CD4+ CXCR5+ PD-1+ ICOS+ phenotypes showed a significant increase in RSA patients compared to women with a normal pregnancy who had chosen termination.	rabbit sperm membrane autoantigen	130-133	programmed cell death 1	Homo sapiens	47-50
29152831-8	2017	Vascular lasers like PDL, Nd:YAG, and argon are the most studied and of these, PDL offers the safest side effect profile.	Argon	38-43	programmed cell death 1	Homo sapiens	79-82
28978557-2	2017	The PD-1 inhibitor is approved for patients who cannot tolerate sorafenib and those whose disease progressed despite treatment with the multikinase inhibitor.	Sorafenib	64-73	programmed cell death 1	Homo sapiens	4-8
28400429-7	2017	Finally, we demonstrate high expression of PD1 mRNA and correlation of PD1 and CD8A in the TS subgroup.Conclusions: Molecular subtyping of TETs is associated with disease-free and overall survival.	tetramethylenedisulfotetramine	139-143	programmed cell death 1	Homo sapiens	43-46
28881302-3	2017	The smallest nanoparticles had a diameter of 212+-11nm which was achieved with LMW-PDL dissolved with 0.1M NaCl at pH 7 and a mass ratio of 2.0 (BSA: PDL).	Sodium Chloride	107-111	programmed cell death 1	Homo sapiens	83-86
28881302-9	2017	The curcumin loaded BSA:LMW-PDL nanoparticles were pretty stable over a period of 21days.	Curcumin	4-12	programmed cell death 1	Homo sapiens	28-31
28939757-6	2017	We found that unlike other coinhibitory molecules (CTLA-4, LAG-3, TIM-3), PD-1 was highly expressed by subdominant TCD8, which correlated with their propensity to favorably respond to PD-1/PD-1 ligand-1 (PD-L1)-blocking Abs.	tcd8	115-119	programmed cell death 1	Homo sapiens	74-78
28783138-5	2017	We found that, among the 11 cell surface or intracellular antigen markers investigated, CD3e, CD79A, LAT, PD-1, and PAX5 could be successfully labeled after antigen retrieval in Tris-EDTA buffer (pH 8.0) at 65  C for 60 min, and 1.8-2.7 mug DNA per million cells could be extracted after sorting with DNA quality similar to that of tissue without staining or sorting.	tris-edta	178-187	programmed cell death 1	Homo sapiens	106-110
28812167-1	2017	The aim of this study was to compare the efficacy and adverse effects of a 595-nm pulsed dye laser therapy alone (PDL alone) with a 5-aminolevulinic (5-ALA) local application followed by a 595-nm PDL (5-ALA PDL) in the treatment of superficial hemangioma (SH).	Aminolevulinic Acid	201-206	programmed cell death 1	Homo sapiens	196-199
28812167-1	2017	The aim of this study was to compare the efficacy and adverse effects of a 595-nm pulsed dye laser therapy alone (PDL alone) with a 5-aminolevulinic (5-ALA) local application followed by a 595-nm PDL (5-ALA PDL) in the treatment of superficial hemangioma (SH).	Aminolevulinic Acid	201-206	programmed cell death 1	Homo sapiens	196-199
28888058-9	2017	Additionally, the percentage of PD-1+ Tregs correlated positively with lactate levels as well as the Acute Physiology and Chronic Health Evaluation II and Sequential Organ Failure Assessment scores in patients with sepsis.	Lactic Acid	71-78	programmed cell death 1	Homo sapiens	32-36
29049359-9	2017	Children, whose mothers had received antenatal steroids, presented higher absolute numbers of non-classical monocytes with PD-1 expression.	Steroids	47-55	programmed cell death 1	Homo sapiens	123-127
29049359-14	2017	Antenatal steroid administration seems to induce PD-1 receptor expression in the non-classical monocytes.	Steroids	10-17	programmed cell death 1	Homo sapiens	49-53
28797844-0	2017	PD-1/PD-L1 blockade enhances the efficacy of SA-GM-CSF surface-modified tumor vaccine in prostate cancer.	2-chloro-10-(4'(N-beta-hydroxyethyl)piperazinyl-1')acetylphenothiazine	45-47	programmed cell death 1	Homo sapiens	0-4
28063224-4	2017	Such NAbs have gained substantial attention because several of them, including their recombinant forms, have therapeutic potential (e.g., programmed cell death-1 [PD-1, Pdcd1], which some of its inhibitors have been approved by FDA for cancer therapy).	nabs	5-9	programmed cell death 1	Homo sapiens	169-174
28734141-4	2017	Reactions of Pd1 with Tu, l-Met and l-Cys were followed by decomposition of complexes, while structures of dinuclear complexes were preserved during the substitution with nitrogen donors.	Thiourea	22-24	programmed cell death 1	Homo sapiens	13-16
28734141-4	2017	Reactions of Pd1 with Tu, l-Met and l-Cys were followed by decomposition of complexes, while structures of dinuclear complexes were preserved during the substitution with nitrogen donors.	Methionine	26-31	programmed cell death 1	Homo sapiens	13-16
28734141-4	2017	Reactions of Pd1 with Tu, l-Met and l-Cys were followed by decomposition of complexes, while structures of dinuclear complexes were preserved during the substitution with nitrogen donors.	Cysteine	36-41	programmed cell death 1	Homo sapiens	13-16
28734141-4	2017	Reactions of Pd1 with Tu, l-Met and l-Cys were followed by decomposition of complexes, while structures of dinuclear complexes were preserved during the substitution with nitrogen donors.	Nitrogen	171-179	programmed cell death 1	Homo sapiens	13-16
29147629-2	2017	Although considerable attention persists around the inhibition of cytotoxic T lymphocyte-associated protein 4 (CTLA4) and programmed cell death 1 (PDCD1, best known as PD-1) signaling, several other co-inhibitory T-cell receptors are being evaluated as potential targets for the development of novel ICBs.	icbs	300-304	programmed cell death 1	Homo sapiens	168-172
28400429-7	2017	Finally, we demonstrate high expression of PD1 mRNA and correlation of PD1 and CD8A in the TS subgroup.Conclusions: Molecular subtyping of TETs is associated with disease-free and overall survival.	tetramethylenedisulfotetramine	139-143	programmed cell death 1	Homo sapiens	71-74
28801607-5	2017	In contrast, we observed that the expression of PD-1 in NK cells was induced after co-culture with cisplatin-resistant cells.	Cisplatin	99-108	programmed cell death 1	Homo sapiens	48-52
28801607-6	2017	We also observed increased susceptibility of cisplatin-resistant cells to NK cell cytotoxicity when neutralizing antibody of PD-1 or PD-L1 was added.	Cisplatin	45-54	programmed cell death 1	Homo sapiens	125-129
28848559-1	2017	The programmed death-1 (PD-1) and its ligand PD-L1 (B7-H1) signaling pathway has been the focus of much enthusiasm in the fields of tumor immunology and oncology with recent FDA approval of the anti-PD-1 antibodies pembrolizumab and nivolumab and the anti-PD-L1 antibodies durvalumab, atezolimuab, and avelumab.	atezolimuab	285-296	programmed cell death 1	Homo sapiens	24-28
28848559-1	2017	The programmed death-1 (PD-1) and its ligand PD-L1 (B7-H1) signaling pathway has been the focus of much enthusiasm in the fields of tumor immunology and oncology with recent FDA approval of the anti-PD-1 antibodies pembrolizumab and nivolumab and the anti-PD-L1 antibodies durvalumab, atezolimuab, and avelumab.	atezolimuab	285-296	programmed cell death 1	Homo sapiens	199-203
28848559-1	2017	The programmed death-1 (PD-1) and its ligand PD-L1 (B7-H1) signaling pathway has been the focus of much enthusiasm in the fields of tumor immunology and oncology with recent FDA approval of the anti-PD-1 antibodies pembrolizumab and nivolumab and the anti-PD-L1 antibodies durvalumab, atezolimuab, and avelumab.	atezolimuab	285-296	programmed cell death 1	Homo sapiens	4-22
28629373-1	2017	BACKGROUND: T cell immunoglobulin and immunoreceptor tyrosine-based inhibitory motif (ITIM) domain (TIGIT) and programmed cell death protein 1 (PD-1) are important inhibitory receptors that associate with T cell exhaustion in acute myeloid leukemia (AML).	Tyrosine	53-61	programmed cell death 1	Homo sapiens	111-142
28327438-9	2017	High glucose augmented LPS-induced hPDL cell apoptosis and cell proliferation inhibition.	Glucose	5-12	programmed cell death 1	Homo sapiens	35-39
28641100-7	2017	Furthermore, based on its molecular activity and safety, ibrutinib has been considered as a partner for treatment combination with PI3K/AKT/mTOR inhibitors or with immune-checkpoint inhibitors, inhibiting immunosuppressive signals from the tumor microenvironment, and overcoming the immune resistance to current anti-PD1/PDL1 immunotherapeutic drugs by the CXCR4/CXCL2 pathway regulation.	ibrutinib	57-66	programmed cell death 1	Homo sapiens	317-320
28629373-1	2017	BACKGROUND: T cell immunoglobulin and immunoreceptor tyrosine-based inhibitory motif (ITIM) domain (TIGIT) and programmed cell death protein 1 (PD-1) are important inhibitory receptors that associate with T cell exhaustion in acute myeloid leukemia (AML).	Tyrosine	53-61	programmed cell death 1	Homo sapiens	144-148
28636292-3	2017	Indeed, in a recent phase 3 study, the PD1 inhibitor nivolumab has recently demonstrated a significant improvement in overall survival for platin-resistant recurrent and/or metastatic HNSCC.	Platinum	139-145	programmed cell death 1	Homo sapiens	39-42
28819582-7	2017	Thus, it is very likely that cisplatin resistance will lead to high expression of PD-L1/PD-1 which makes them vulnerable to anti PD-1 or anti PD-L1 antibody treatment.	Cisplatin	29-38	programmed cell death 1	Homo sapiens	88-92
28819582-7	2017	Thus, it is very likely that cisplatin resistance will lead to high expression of PD-L1/PD-1 which makes them vulnerable to anti PD-1 or anti PD-L1 antibody treatment.	Cisplatin	29-38	programmed cell death 1	Homo sapiens	129-133
28938692-9	2017	Furthermore, less AEs were observed in the PD-1/PD-L1 inhibitor groups than the control groups.	aes	18-21	programmed cell death 1	Homo sapiens	43-47
27686004-0	2017	Increased PD-1/STAT1 ratio may account for the survival benefit in decitabine therapy for lower risk myelodysplastic syndrome.	Decitabine	67-77	programmed cell death 1	Homo sapiens	10-14
28302724-2	2017	Significant positive-charge localization on one of the Chl constituents, PD1 or PD2, in P680+ has been proposed to contribute to this high Em To identify the Chl molecule on which the charge is mainly localized, we genetically introduced a hydrogen bond to the 131-keto C=O group of PD1 and PD2 by changing the nearby D1-Val-157 and D2-Val-156 residues to His, respectively.	Hydrogen	240-248	programmed cell death 1	Homo sapiens	73-76
28302724-2	2017	Significant positive-charge localization on one of the Chl constituents, PD1 or PD2, in P680+ has been proposed to contribute to this high Em To identify the Chl molecule on which the charge is mainly localized, we genetically introduced a hydrogen bond to the 131-keto C=O group of PD1 and PD2 by changing the nearby D1-Val-157 and D2-Val-156 residues to His, respectively.	Hydrogen	240-248	programmed cell death 1	Homo sapiens	283-286
28302724-2	2017	Significant positive-charge localization on one of the Chl constituents, PD1 or PD2, in P680+ has been proposed to contribute to this high Em To identify the Chl molecule on which the charge is mainly localized, we genetically introduced a hydrogen bond to the 131-keto C=O group of PD1 and PD2 by changing the nearby D1-Val-157 and D2-Val-156 residues to His, respectively.	Valine	321-324	programmed cell death 1	Homo sapiens	73-76
28302724-3	2017	Successful hydrogen bond formation at PD1 and PD2 in the obtained D1-V157H and D2-V156H mutants, respectively, was monitored by detecting 131-keto C=O vibrations in Fourier transfer infrared (FTIR) difference spectra upon oxidation of P680 and the symmetrically located redox-active tyrosines YZ and YD, and they were simulated by quantum-chemical calculations.	Hydrogen	11-19	programmed cell death 1	Homo sapiens	38-41
28302724-3	2017	Successful hydrogen bond formation at PD1 and PD2 in the obtained D1-V157H and D2-V156H mutants, respectively, was monitored by detecting 131-keto C=O vibrations in Fourier transfer infrared (FTIR) difference spectra upon oxidation of P680 and the symmetrically located redox-active tyrosines YZ and YD, and they were simulated by quantum-chemical calculations.	Tyrosine	283-292	programmed cell death 1	Homo sapiens	38-41
28302724-6	2017	These results, together with the previous results for the mutants of the His ligands of PD1 and PD2, lead to a definite conclusion that a charge is mainly localized to PD1 in P680&lt;sup/&gt;.	Histidine	73-76	programmed cell death 1	Homo sapiens	88-91
28302724-6	2017	These results, together with the previous results for the mutants of the His ligands of PD1 and PD2, lead to a definite conclusion that a charge is mainly localized to PD1 in P680&lt;sup/&gt;.	Histidine	73-76	programmed cell death 1	Homo sapiens	168-171
28327740-5	2017	Results show that the moderate stability of intramolecular hydrogen bonds between SER71 and THR120 allows the CC" loop to sample both the open and closed states in apo-PD-1.	Hydrogen	59-67	programmed cell death 1	Homo sapiens	168-172
28282342-10	2017	SUMMARY: PD-1/PD-L1 inhibition can be regarded as new first-line therapy for patients with mMCC not amendable by surgery and/or radiation.	mmcc	91-95	programmed cell death 1	Homo sapiens	9-13
28730785-0	2017	PDCD1 strengthens the sensitivity of ovarian cancer to cisplatin chemotherapy by promoting apoptosis.	Cisplatin	55-64	programmed cell death 1	Homo sapiens	0-5
28730785-8	2017	The CAOV3 and OVCAR3 cells with high expression of PDCD1 were more sensitive to cisplatin.	Cisplatin	80-89	programmed cell death 1	Homo sapiens	51-56
28730785-9	2017	The SKOV3 and 3AO cells with low expression of PDCD1 were less sensitive to cisplatin.	Cisplatin	76-85	programmed cell death 1	Homo sapiens	47-52
28730785-15	2017	PDCD1 strengthens the sensitivity of ovarian cancer to cisplatin by promoting cisplatin-induced apoptosis.	Cisplatin	55-64	programmed cell death 1	Homo sapiens	0-5
28730785-15	2017	PDCD1 strengthens the sensitivity of ovarian cancer to cisplatin by promoting cisplatin-induced apoptosis.	Cisplatin	78-87	programmed cell death 1	Homo sapiens	0-5
28475007-7	2017	Both the PD-1-TIM-3+ and PD-1+TIM-3+ CD8+ T cells responded to Treg-mediated and galectin 9-mediated suppression, whereas the PD-1+TIM-3- CD8+ T cells only responded to Treg-mediated suppression.	treg	63-67	programmed cell death 1	Homo sapiens	9-13
28475007-7	2017	Both the PD-1-TIM-3+ and PD-1+TIM-3+ CD8+ T cells responded to Treg-mediated and galectin 9-mediated suppression, whereas the PD-1+TIM-3- CD8+ T cells only responded to Treg-mediated suppression.	treg	63-67	programmed cell death 1	Homo sapiens	25-29
28475007-7	2017	Both the PD-1-TIM-3+ and PD-1+TIM-3+ CD8+ T cells responded to Treg-mediated and galectin 9-mediated suppression, whereas the PD-1+TIM-3- CD8+ T cells only responded to Treg-mediated suppression.	treg	63-67	programmed cell death 1	Homo sapiens	25-29
28494544-7	2017	In AIH patients, the positive rate of PD-1 in liver tissue was positively correlated with the levels of total bilirubin, alanine aminotransferase, aspartate aminotransferase, and IgG (r = 0.665, 0.721, 0.711, and 0.813, all P &lt; 0.01).	Bilirubin	110-119	programmed cell death 1	Homo sapiens	38-42
28515795-2	2017	Inspired by the recent experimental discovery of a highly efficient single-atom catalyst Pd1/gamma-Al2O3, we conducted a comprehensive DFT study on geometries, stabilities and CO oxidation catalytic activities of M1/gamma-Al2O3 (M=Pd, Fe, Co, and Ni) by using slab-model.	m1	213-215	programmed cell death 1	Homo sapiens	89-92
28515795-2	2017	Inspired by the recent experimental discovery of a highly efficient single-atom catalyst Pd1/gamma-Al2O3, we conducted a comprehensive DFT study on geometries, stabilities and CO oxidation catalytic activities of M1/gamma-Al2O3 (M=Pd, Fe, Co, and Ni) by using slab-model.	gamma-al2o3	216-227	programmed cell death 1	Homo sapiens	89-92
28515795-3	2017	One of the most important results here is that Ni1/Al2O3 catalyst exhibits higher activity in CO oxidation than Pd1/Al2O3.	ni1	47-50	programmed cell death 1	Homo sapiens	112-115
28515795-3	2017	One of the most important results here is that Ni1/Al2O3 catalyst exhibits higher activity in CO oxidation than Pd1/Al2O3.	Aluminum Oxide	51-56	programmed cell death 1	Homo sapiens	112-115
28515795-3	2017	One of the most important results here is that Ni1/Al2O3 catalyst exhibits higher activity in CO oxidation than Pd1/Al2O3.	Aluminum Oxide	116-121	programmed cell death 1	Homo sapiens	112-115
28199990-0	2017	Activation of NK cells and disruption of PD-L1/PD-1 axis: two different ways for lenalidomide to block myeloma progression.	Lenalidomide	81-93	programmed cell death 1	Homo sapiens	47-51
28199990-7	2017	This occurs since Lenalidomide acts on several critical points: stimulates T cell proliferation and cytokine secretion; decreases the expression of the immune check-point inhibitor Programmed Death-1 (PD-1) on both T and NK cells in MM patients; decreases the expression of both PD-1 and PD-L1 on MM cells; promotes MM cell death and abrogates MM/stromal microenvironment cross-talk, a process known to promote the MM cell survival and proliferation.	Lenalidomide	18-30	programmed cell death 1	Homo sapiens	201-205
28199990-7	2017	This occurs since Lenalidomide acts on several critical points: stimulates T cell proliferation and cytokine secretion; decreases the expression of the immune check-point inhibitor Programmed Death-1 (PD-1) on both T and NK cells in MM patients; decreases the expression of both PD-1 and PD-L1 on MM cells; promotes MM cell death and abrogates MM/stromal microenvironment cross-talk, a process known to promote the MM cell survival and proliferation.	Lenalidomide	18-30	programmed cell death 1	Homo sapiens	279-283
28199990-9	2017	Given the importance of an effective immune response to counteract the MM progression and the promising approaches using anti-PD-1/PD-L1 strategies, we will discuss in this review how Lenalidomide could represent an adequate approach to re-establish the recognition against MM by exhausted NK cell.	Lenalidomide	184-196	programmed cell death 1	Homo sapiens	126-130
28044198-8	2017	By inhibiting prostaglandin synthesis, meloxicam seems to downregulate hPDL-mediated inflammation, RANKL-induced osteoclastogenesis and, consequently, tooth movement velocity by about 50%, thus limiting its suitability for analgesia during orthodontic therapy.	Meloxicam	39-48	programmed cell death 1	Homo sapiens	71-75
27808592-0	2017	PD1 and PDL1 upregulation and survival after decitabine treatment in lower risk MDS.	Decitabine	45-55	programmed cell death 1	Homo sapiens	0-3
27686004-8	2017	Thus, our results suggest that the effect mechanism of decitabine toward lower risk MDS may be the moderate increase of PD-1/STAT1, which contributes to hematopoietic improvement.	Decitabine	55-65	programmed cell death 1	Homo sapiens	120-124
27926587-2	2017	Few data are available on anti-PD1 safety in patients who develop IPI-related severe adverse events (AEs) (grade&gt;=3).	diprotin A	66-69	programmed cell death 1	Homo sapiens	31-34
27926587-3	2017	The aim of this study was to compare the anti-PD1 safety and efficacy in patients with previous severe toxicity to IPI versus in those showing moderate and no previous IPI-related AEs.	diprotin A	115-118	programmed cell death 1	Homo sapiens	46-49
27816392-7	2017	A combined low S-PD-L1 and T-PD-1 was associated with poor survival in all patients (DSS: hazard ratio [HR], 1.81; 95% confidence interval [CI], 1.37-2.40; P &lt; .001) at both centers and for all pathologic stages.	dss	85-88	programmed cell death 1	Homo sapiens	29-33
27599705-0	2017	Osimertinib-induced interstitial lung disease after treatment with anti-PD1 antibody.	osimertinib	0-11	programmed cell death 1	Homo sapiens	72-75
27599705-2	2017	The patient was treated with osimertinib, a third-generation EGFR tyrosine kinase inhibitor (EGFR-TKI) following treatment with nivolumab, an anti-Programmed Cell Death 1 (anti-PD1) antibody.	osimertinib	29-40	programmed cell death 1	Homo sapiens	177-180
27599705-5	2017	Therefore we diagnosed the patient with osimertinib-induced interstitial lung disease (ILD) after treatment with anti-PD1 antibody.	osimertinib	40-51	programmed cell death 1	Homo sapiens	118-121
28203344-3	2017	To date, two main pathways, the cytotoxic T-lymphocyte-associated protein 4 (CTLA-4) and programmed death 1 (PD-1), have emerged as key targets of CBT demonstrating unprecedented activity particularly in heavily pretreated relapsed/refractory Hodgkin lymphoma and some forms of non-Hodgkin disease.	N,N-BIS(4-CHLOROBENZYL)-1H-1,2,3,4-TETRAAZOL-5-AMINE	147-150	programmed cell death 1	Homo sapiens	89-107
27859479-4	2017	Review of published reports of the DT to immunotherapy revealed patients receiving anti-CTCLA-4 antibody or anti-PD-1/PD-L1 antibody often develop a DT of any type and grade.	Thymidine	35-37	programmed cell death 1	Homo sapiens	113-117
27859479-4	2017	Review of published reports of the DT to immunotherapy revealed patients receiving anti-CTCLA-4 antibody or anti-PD-1/PD-L1 antibody often develop a DT of any type and grade.	Thymidine	149-151	programmed cell death 1	Homo sapiens	113-117
27859479-7	2017	Lichenoid dermatitis and bullous pemphigoid appear to be DT more associated with anti-PD-1/PD-L1 antibody.	Thymidine	57-59	programmed cell death 1	Homo sapiens	86-90
28203344-3	2017	To date, two main pathways, the cytotoxic T-lymphocyte-associated protein 4 (CTLA-4) and programmed death 1 (PD-1), have emerged as key targets of CBT demonstrating unprecedented activity particularly in heavily pretreated relapsed/refractory Hodgkin lymphoma and some forms of non-Hodgkin disease.	N,N-BIS(4-CHLOROBENZYL)-1H-1,2,3,4-TETRAAZOL-5-AMINE	147-150	programmed cell death 1	Homo sapiens	109-113
27470968-0	2017	PD-1/PD-L1 Blockade Enhances T-cell Activity and Antitumor Efficacy of Imatinib in Gastrointestinal Stromal Tumors.	Imatinib Mesylate	71-79	programmed cell death 1	Homo sapiens	0-4
27799536-10	2016	These findings suggest that a CpG oligonucleotide given intratumorally may increase the response of cancer patients to PD-1 blockade, increasing the quantity and the quality of tumor-specific CD8+ T cells.	CPG-oligonucleotide	30-49	programmed cell death 1	Homo sapiens	119-123
27910704-2	2017	ICBs targeting the programmed cell death receptor-1 (PD-1) have recently been investigated in a number of advanced tumors, including non-small cell lung cancer (NSCLC).	icbs	0-4	programmed cell death 1	Homo sapiens	53-57
27829019-6	2016	The expression of PD-1 and PD-L1 was higher on Gag-specific CD8+ T cells as compared to CEF-specific CD8+ T cells, and the expression of these markers did not change significantly after Treg depletion or co-culture with Treg/HIV-, unlike on CEF-specific CD8+ T cells.	Glycosaminoglycans	47-50	programmed cell death 1	Homo sapiens	18-22
27723142-3	2016	By maneuvering the Pd/Ag ratio, we found that the as-prepared Pd1 Ag3 hollow nanoflower catalysts had the optimized performance for catalytic activity toward ethanol oxidation reaction.	Palladium	19-21	programmed cell death 1	Homo sapiens	62-65
27723142-3	2016	By maneuvering the Pd/Ag ratio, we found that the as-prepared Pd1 Ag3 hollow nanoflower catalysts had the optimized performance for catalytic activity toward ethanol oxidation reaction.	Ethanol	158-165	programmed cell death 1	Homo sapiens	62-65
27689240-1	2016	In this work, the electroreductive removal of bromate by a Pd1-In4/Al2O3 catalyst in a three-dimensional electrochemical reactor was investigated.	Bromates	46-53	programmed cell death 1	Homo sapiens	59-62
27689240-1	2016	In this work, the electroreductive removal of bromate by a Pd1-In4/Al2O3 catalyst in a three-dimensional electrochemical reactor was investigated.	Aluminum Oxide	67-72	programmed cell death 1	Homo sapiens	59-62
27689240-3	2016	On the basis of the characterization results and kinetics analysis, a synergistic effect of Pd and In was observed, and Pd1-In4/Al2O3 had the highest reaction rate constant of 0.1275 min-1 (vs 0.0413, 0.0328, and 0.0253 min-1 for In/Al2O3, Pd/Al2O3, and Al2O3).	Palladium	92-94	programmed cell death 1	Homo sapiens	120-123
27689240-3	2016	On the basis of the characterization results and kinetics analysis, a synergistic effect of Pd and In was observed, and Pd1-In4/Al2O3 had the highest reaction rate constant of 0.1275 min-1 (vs 0.0413, 0.0328, and 0.0253 min-1 for In/Al2O3, Pd/Al2O3, and Al2O3).	Aluminum Oxide	128-133	programmed cell death 1	Homo sapiens	120-123
27689240-3	2016	On the basis of the characterization results and kinetics analysis, a synergistic effect of Pd and In was observed, and Pd1-In4/Al2O3 had the highest reaction rate constant of 0.1275 min-1 (vs 0.0413, 0.0328, and 0.0253 min-1 for In/Al2O3, Pd/Al2O3, and Al2O3).	Aluminum Oxide	233-238	programmed cell death 1	Homo sapiens	120-123
27689240-3	2016	On the basis of the characterization results and kinetics analysis, a synergistic effect of Pd and In was observed, and Pd1-In4/Al2O3 had the highest reaction rate constant of 0.1275 min-1 (vs 0.0413, 0.0328, and 0.0253 min-1 for In/Al2O3, Pd/Al2O3, and Al2O3).	Aluminum Oxide	233-238	programmed cell death 1	Homo sapiens	120-123
27689240-3	2016	On the basis of the characterization results and kinetics analysis, a synergistic effect of Pd and In was observed, and Pd1-In4/Al2O3 had the highest reaction rate constant of 0.1275 min-1 (vs 0.0413, 0.0328, and 0.0253 min-1 for In/Al2O3, Pd/Al2O3, and Al2O3).	Aluminum Oxide	233-238	programmed cell death 1	Homo sapiens	120-123
27689240-5	2016	Moreover, the introduction of In could increase the zeta potential of Pd1-In4/Al2O3, facilitating bromate adsorption and its subsequent reduction on the catalyst.	Aluminum Oxide	78-83	programmed cell death 1	Homo sapiens	70-73
27689240-5	2016	Moreover, the introduction of In could increase the zeta potential of Pd1-In4/Al2O3, facilitating bromate adsorption and its subsequent reduction on the catalyst.	Bromates	98-105	programmed cell death 1	Homo sapiens	70-73
27689240-6	2016	Finally, a reaction mechanism for bromate reduction by Pd1-In4/Al2O3 was proposed based on all the experimental results.	Bromates	34-41	programmed cell death 1	Homo sapiens	55-58
27689240-6	2016	Finally, a reaction mechanism for bromate reduction by Pd1-In4/Al2O3 was proposed based on all the experimental results.	Aluminum Oxide	63-68	programmed cell death 1	Homo sapiens	55-58
28123879-5	2016	Meanwhile, ibrutinib drove Th1-selective pressure in T lymphocytes, thus, reducing the PD-1 and PDL-1 expression.	ibrutinib	11-20	programmed cell death 1	Homo sapiens	87-91
27717086-0	2016	Low-Temperature Transformation of Methane to Methanol on Pd1 O4 Single Sites Anchored on the Internal Surface of Microporous Silicate.	Methane	34-41	programmed cell death 1	Homo sapiens	57-60
27717086-0	2016	Low-Temperature Transformation of Methane to Methanol on Pd1 O4 Single Sites Anchored on the Internal Surface of Microporous Silicate.	Methanol	45-53	programmed cell death 1	Homo sapiens	57-60
27717086-0	2016	Low-Temperature Transformation of Methane to Methanol on Pd1 O4 Single Sites Anchored on the Internal Surface of Microporous Silicate.	Silicates	125-133	programmed cell death 1	Homo sapiens	57-60
27717086-2	2016	Pd1 O4 single-sites anchored on the internal surface of micropores of a microporous silicate exhibit high selectivity and activity in transforming CH4 to CH3 OH at 50-95  C in aqueous phase through partial oxidation of CH4 with H2 O2 .	Silicates	84-92	programmed cell death 1	Homo sapiens	0-3
27717086-2	2016	Pd1 O4 single-sites anchored on the internal surface of micropores of a microporous silicate exhibit high selectivity and activity in transforming CH4 to CH3 OH at 50-95  C in aqueous phase through partial oxidation of CH4 with H2 O2 .	Hydrogen Peroxide	228-233	programmed cell death 1	Homo sapiens	0-3
27717086-3	2016	The selectivity for methanol production remains at 86.4 %, while the activity for methanol production at 95  C is about 2.78 molecules per Pd1 O4 site per second when 2.0 wt % CuO is used as a co-catalyst with the Pd1 O4 @ZSM-5.	Methanol	82-90	programmed cell death 1	Homo sapiens	139-142
27717086-3	2016	The selectivity for methanol production remains at 86.4 %, while the activity for methanol production at 95  C is about 2.78 molecules per Pd1 O4 site per second when 2.0 wt % CuO is used as a co-catalyst with the Pd1 O4 @ZSM-5.	Methanol	82-90	programmed cell death 1	Homo sapiens	214-217
27734966-5	2016	Here, we present the independently determined crystal structure of the Fv fragment of pembrolizumab (PemFv) in complex with the PD-1ECD at a resolution of 2.15 A.	pemfv	101-106	programmed cell death 1	Homo sapiens	128-135
27734966-6	2016	This high-resolution structure allows the accurate mapping of the interaction including water-mediated hydrogen bonds and provides, for the first time, a coherent explanation of PD-1 antagonism by pembrolizumab.	Water	88-93	programmed cell death 1	Homo sapiens	178-182
27734966-6	2016	This high-resolution structure allows the accurate mapping of the interaction including water-mediated hydrogen bonds and provides, for the first time, a coherent explanation of PD-1 antagonism by pembrolizumab.	Hydrogen	103-111	programmed cell death 1	Homo sapiens	178-182
27503244-3	2016	A recent phase III clinical trial (Checkmate 141) demonstrated an improved overall survival in head and neck cancer patients treated with anti-PD-1 monotherapy as compared to standard of care for recurrent and/or metastatic disease, which raises questions on how best to incorporate immunotherapy in the context of standard of care.	checkmate 141	35-48	programmed cell death 1	Homo sapiens	143-147
27506249-8	2016	While Pd1 catalysts showed promising activity at low temperature in a methanol decomposition reaction, 14 cycle TiO2 protected Pd1 was less active at high temperature.	titanium dioxide	112-116	programmed cell death 1	Homo sapiens	127-130
27429197-0	2016	Early evidence of anti-PD-1 activity in enzalutamide-resistant prostate cancer.	enzalutamide	40-52	programmed cell death 1	Homo sapiens	23-27
27470968-7	2017	PD-1 expression on T cells was highest in imatinib-treated human GISTs.	Imatinib Mesylate	42-50	programmed cell death 1	Homo sapiens	0-4
27470968-11	2017	PD-1 and PD-L1 blockade in vivo each had no efficacy alone but enhanced the antitumor effects of imatinib by increasing T-cell effector function in the presence of KIT and IDO inhibition.	Imatinib Mesylate	97-105	programmed cell death 1	Homo sapiens	0-4
27941003-0	2017	Efficacy of PD-1 Blockade Is Potentiated by Metformin-Induced Reduction of Tumor Hypoxia.	Metformin	44-53	programmed cell death 1	Homo sapiens	12-16
27978870-3	2016	METHODS: The expressions of PD-1 and PD-L1 in 20 cases of PC paraffin-embedded tissue specimens were detected through immunohistochemistry.	pc	58-60	programmed cell death 1	Homo sapiens	28-32
27978870-3	2016	METHODS: The expressions of PD-1 and PD-L1 in 20 cases of PC paraffin-embedded tissue specimens were detected through immunohistochemistry.	Paraffin	61-69	programmed cell death 1	Homo sapiens	28-32
27941630-3	2016	All complexes Pd1-Pd5 are revealed highly efficient catalyst in methyl acrylate (MA) polymerization as well as methyl acrylate/norbornene (MA/NB) copolymerization.	methyl acrylate	64-79	programmed cell death 1	Homo sapiens	14-17
27941630-3	2016	All complexes Pd1-Pd5 are revealed highly efficient catalyst in methyl acrylate (MA) polymerization as well as methyl acrylate/norbornene (MA/NB) copolymerization.	methyl acrylate/norbornene	111-137	programmed cell death 1	Homo sapiens	14-17
27941630-3	2016	All complexes Pd1-Pd5 are revealed highly efficient catalyst in methyl acrylate (MA) polymerization as well as methyl acrylate/norbornene (MA/NB) copolymerization.	Niobium	142-144	programmed cell death 1	Homo sapiens	14-17
27737562-4	2016	The potential impact of the approval of the programmed death receptor-1 (PD-1)-blocking antibody nivolumab or pembrolizumab on the use of ramucirumab plus docetaxel in advanced NSCLC patient population is uncertain in clinical practice.	Docetaxel	155-164	programmed cell death 1	Homo sapiens	73-77
28033249-13	2016	CONCLUSION: The PD-1/PD-L1 therapy significantly prolonged the OS and improved the ORR, simultaneously lowering the treatment-related adverse effect events versus docetaxel.	Docetaxel	163-172	programmed cell death 1	Homo sapiens	16-20
28033288-5	2016	The expressions of PD-1 and TIM-3 in tumor tissues, tumor adjacent tissues, and cirrhotic tissues were significantly associated with PD1 and TIM3 polymorphisms, with genotype AA of PD1 rs10204525 and genotypes GT+TT of TIM3 rs10053538 being associated with significantly increased PD-1 and TIM-3 expression, respectively.These findings support the potential to improve the efficiency of immune checkpoint-targeted therapy and reduce resistance to the therapy by blocking both PD-1 and TIM-3 and suggest the potential to apply the genotype determination of PD1 rs10204525 and TIM3 rs10053538 as biomarkers of immune checkpoint-directed therapies.	gt+tt	210-215	programmed cell death 1	Homo sapiens	19-23
28105229-5	2016	MTT was used to detect the effect of PD-1 signals on T-cell proliferation.	monooxyethylene trimethylolpropane tristearate	0-3	programmed cell death 1	Homo sapiens	37-41
27459735-12	2016	When T cells were co-cultured with TAMs, expression levels of Tim-3, PD-1 and CTLA-4 were significantly higher than controls, whereas levels of IFN-gamma and Granzyme B were significantly decreased, in a dose-dependent manner (p &lt; 0.05).	tams	35-39	programmed cell death 1	Homo sapiens	69-73
27799536-0	2016	Intratumoral injection of a CpG oligonucleotide reverts resistance to PD-1 blockade by expanding multifunctional CD8+ T cells.	Oligonucleotides	32-47	programmed cell death 1	Homo sapiens	70-74
27799536-4	2016	We show that intratumoral injection of a highly interferogenic TLR9 agonist, SD-101, in anti-PD-1 nonresponders led to a complete, durable rejection of essentially all injected tumors and a majority of uninjected, distant-site tumors.	sd-101	77-83	programmed cell death 1	Homo sapiens	93-97
28197370-9	2017	Immunofluorescence staining of CAS samples revealed that PD-L1-positive cells were adjacent to PD-1-positive cells and/or tumor stroma with high IFNgamma expression.	cas	31-34	programmed cell death 1	Homo sapiens	95-99
28197370-11	2017	Our results suggest that PD-1/PD-L1 expression is related to CAS progression, and the treatment with anti-PD-1 antibodies could be a new therapeutic option for CAS.	cas	61-64	programmed cell death 1	Homo sapiens	25-29
28197370-11	2017	Our results suggest that PD-1/PD-L1 expression is related to CAS progression, and the treatment with anti-PD-1 antibodies could be a new therapeutic option for CAS.	cas	61-64	programmed cell death 1	Homo sapiens	106-110
27610620-0	2016	Elevated Cellular PD1/PD-L1 Expression Confers Acquired Resistance to Cisplatin in Small Cell Lung Cancer Cells.	Cisplatin	70-79	programmed cell death 1	Homo sapiens	18-21
27610620-3	2016	Here we report that cell-intrinsic expression of PD1 and PD-L1, two immune checkpoints, is required for sustained expansion of SCLC cells under cisplatin selection.	Cisplatin	144-153	programmed cell death 1	Homo sapiens	49-52
27610620-4	2016	Indeed, PD1 and PD-L1 were expressed at a higher level in lung cancer cell lines, tumor tissues, and importantly, in SCLC cells resistant to cisplatin (H69R, H82R), when compared to respective controls.	Cisplatin	141-150	programmed cell death 1	Homo sapiens	8-11
27610620-8	2016	Thus, cell intrinsic PD1/PD-L1 signaling may be a predictor for poor efficacy of cisplatin treatment, and targeting the cellular PD1/PD-L1 axis may improve chemosensitization of aggressive SCLC.	Cisplatin	81-90	programmed cell death 1	Homo sapiens	21-24
27506249-5	2016	In situ infrared spectroscopy and Pd K-edge X-ray absorption spectroscopy (XAS) revealed that the Pd1 was anchored on the surface through chlorine sites.	Chlorine	138-146	programmed cell death 1	Homo sapiens	98-101
27506249-8	2016	While Pd1 catalysts showed promising activity at low temperature in a methanol decomposition reaction, 14 cycle TiO2 protected Pd1 was less active at high temperature.	Methanol	70-78	programmed cell death 1	Homo sapiens	6-9
26880074-1	2016	While the invariant natural killer T (iNKT)-cell response to primary stimulation with the glycolipid, alpha-galactosylceramide (alphaGalCer), is robust, the secondary response to this stimulus is muted resulting in a hyporesponsive state characterized by anti-inflammatory interleukin-10 (IL-10) production and high expression of programmed cell death 1 (PD1) and neuropilin 1 (NRP1).	alpha-galactosylceramide	102-126	programmed cell death 1	Homo sapiens	355-358
26880074-1	2016	While the invariant natural killer T (iNKT)-cell response to primary stimulation with the glycolipid, alpha-galactosylceramide (alphaGalCer), is robust, the secondary response to this stimulus is muted resulting in a hyporesponsive state characterized by anti-inflammatory interleukin-10 (IL-10) production and high expression of programmed cell death 1 (PD1) and neuropilin 1 (NRP1).	Glycolipids	90-100	programmed cell death 1	Homo sapiens	355-358
27356741-4	2016	Furthermore, NK cells expanded in the presence of a blocking antibody (exNK+PD1-blockage) against programmed cell death protein-1 (PD1), a key counteracting molecule for NK and T cell activity, demonstrated more potent cytolytic activity against the RPMI8226 than the exNK cells without PD1 blocking.	rpmi8226	250-258	programmed cell death 1	Homo sapiens	76-79
27356741-4	2016	Furthermore, NK cells expanded in the presence of a blocking antibody (exNK+PD1-blockage) against programmed cell death protein-1 (PD1), a key counteracting molecule for NK and T cell activity, demonstrated more potent cytolytic activity against the RPMI8226 than the exNK cells without PD1 blocking.	rpmi8226	250-258	programmed cell death 1	Homo sapiens	98-129
27356741-4	2016	Furthermore, NK cells expanded in the presence of a blocking antibody (exNK+PD1-blockage) against programmed cell death protein-1 (PD1), a key counteracting molecule for NK and T cell activity, demonstrated more potent cytolytic activity against the RPMI8226 than the exNK cells without PD1 blocking.	rpmi8226	250-258	programmed cell death 1	Homo sapiens	131-134
27252413-2	2016	Immunotherapy offers a novel approach for the treatment of these patients, with two anti-programmed death 1 (PD-1) checkpoint inhibitors, nivolumab and pembrolizumab, recently approved by the FDA based on large randomized clinical trials showing increased overall survival compared with standard second-line docetaxel.	Docetaxel	308-317	programmed cell death 1	Homo sapiens	109-113
27438833-0	2016	A Mini-Review for Cancer Immunotherapy: Molecular Understanding of PD-1/PD-L1 Pathway &amp;amp; Translational Blockade of Immune Checkpoints.	Adenosine Monophosphate	91-94	programmed cell death 1	Homo sapiens	67-71
27122549-1	2016	Checkpoint inhibitors (CPI), namely anti-CTLA4 and anti-PD1/PD-L1 antibodies, demonstrated efficacy across multiple types of cancer.	methyl 2-isocyano-2-methylpropanoate	23-26	programmed cell death 1	Homo sapiens	56-59
27043246-17	2016	This finding suggests a potential application of TSA for bone regeneration therapy by hPDL cells.	trichostatin A	49-52	programmed cell death 1	Homo sapiens	86-90
27063329-5	2016	The test for blockading the combination of PD-1 with PD-L1 revealed that abilities of 13 AAPDs were higher than that of sulfamethizole, a successful PD-1 inhibitor.	Sulfamethizole	120-134	programmed cell death 1	Homo sapiens	149-153
27063329-6	2016	In particular, large hydrophobic substituents at amine moiety or a nitro at resorcinol skeleton enhanced the inhibitory effect of AAPD even higher than that of sulfamethoxypyridazine, another successful PD-1 inhibitor.	nitro	67-72	programmed cell death 1	Homo sapiens	203-207
27063329-6	2016	In particular, large hydrophobic substituents at amine moiety or a nitro at resorcinol skeleton enhanced the inhibitory effect of AAPD even higher than that of sulfamethoxypyridazine, another successful PD-1 inhibitor.	aapd	130-134	programmed cell death 1	Homo sapiens	203-207
27063329-6	2016	In particular, large hydrophobic substituents at amine moiety or a nitro at resorcinol skeleton enhanced the inhibitory effect of AAPD even higher than that of sulfamethoxypyridazine, another successful PD-1 inhibitor.	Sulfamethoxypyridazine	160-182	programmed cell death 1	Homo sapiens	203-207
26426431-8	2016	Increased infiltration of PD-1(+) cells was associated with prolonged progression-free survival (P = 0.005) and overall survival (P = 0.026) in DLBCL patients treated with rituximab-cyclophosphamide, doxorubicin, vincristine, prednisone (R-CHOP), whereas PD-L1 expression had no prognostic significance.	Cyclophosphamide	182-198	programmed cell death 1	Homo sapiens	26-30
26426431-8	2016	Increased infiltration of PD-1(+) cells was associated with prolonged progression-free survival (P = 0.005) and overall survival (P = 0.026) in DLBCL patients treated with rituximab-cyclophosphamide, doxorubicin, vincristine, prednisone (R-CHOP), whereas PD-L1 expression had no prognostic significance.	Doxorubicin	200-211	programmed cell death 1	Homo sapiens	26-30
26426431-8	2016	Increased infiltration of PD-1(+) cells was associated with prolonged progression-free survival (P = 0.005) and overall survival (P = 0.026) in DLBCL patients treated with rituximab-cyclophosphamide, doxorubicin, vincristine, prednisone (R-CHOP), whereas PD-L1 expression had no prognostic significance.	Vincristine	213-224	programmed cell death 1	Homo sapiens	26-30
26426431-8	2016	Increased infiltration of PD-1(+) cells was associated with prolonged progression-free survival (P = 0.005) and overall survival (P = 0.026) in DLBCL patients treated with rituximab-cyclophosphamide, doxorubicin, vincristine, prednisone (R-CHOP), whereas PD-L1 expression had no prognostic significance.	Prednisone	226-236	programmed cell death 1	Homo sapiens	26-30
27313464-3	2016	Nivolumab is the first PD-1 inhibitor approved for the treatment of advanced-stage squamous cell non-small-cell lung cancer following platinum-based chemotherapy.	Platinum	134-142	programmed cell death 1	Homo sapiens	23-27
27174982-2	2016	We report a photochemical strategy to fabricate a stable atomically dispersed palladium-titanium oxide catalyst (Pd1/TiO2) on ethylene glycolate (EG)-stabilized ultrathin TiO2 nanosheets containing Pd up to 1.5%.	palladium-titanium oxide	78-102	programmed cell death 1	Homo sapiens	113-116
27174982-2	2016	We report a photochemical strategy to fabricate a stable atomically dispersed palladium-titanium oxide catalyst (Pd1/TiO2) on ethylene glycolate (EG)-stabilized ultrathin TiO2 nanosheets containing Pd up to 1.5%.	Ethylene bis(hydroxyacetate)	126-144	programmed cell death 1	Homo sapiens	113-116
27174982-2	2016	We report a photochemical strategy to fabricate a stable atomically dispersed palladium-titanium oxide catalyst (Pd1/TiO2) on ethylene glycolate (EG)-stabilized ultrathin TiO2 nanosheets containing Pd up to 1.5%.	eg	146-148	programmed cell death 1	Homo sapiens	113-116
27174982-2	2016	We report a photochemical strategy to fabricate a stable atomically dispersed palladium-titanium oxide catalyst (Pd1/TiO2) on ethylene glycolate (EG)-stabilized ultrathin TiO2 nanosheets containing Pd up to 1.5%.	ultrathin tio2	161-175	programmed cell death 1	Homo sapiens	113-116
27174982-3	2016	The Pd1/TiO2 catalyst exhibited high catalytic activity in hydrogenation of C=C bonds, exceeding that of surface Pd atoms on commercial Pd catalysts by a factor of 9.	Palladium	113-115	programmed cell death 1	Homo sapiens	4-7
27174982-5	2016	More important, the Pd1/TiO2-EG system could activate H2 in a heterolytic pathway, leading to a catalytic enhancement in hydrogenation of aldehydes by a factor of more than 55.	Hydrogen	54-56	programmed cell death 1	Homo sapiens	20-23
27174982-5	2016	More important, the Pd1/TiO2-EG system could activate H2 in a heterolytic pathway, leading to a catalytic enhancement in hydrogenation of aldehydes by a factor of more than 55.	Aldehydes	138-147	programmed cell death 1	Homo sapiens	20-23
27034168-7	2016	In multivariate analysis, PD1 +8669 G allele-containing genotypes were independently associated with longer OS in each treatment population.	Osmium	108-110	programmed cell death 1	Homo sapiens	26-29
26753722-6	2016	In acute rejection, PD-1 and FOXP3 mRNA were significantly correlated with serum creatinine and Banff histological grade.	Creatinine	81-91	programmed cell death 1	Homo sapiens	20-24
27063329-0	2016	Development of amino- and dimethylcarbamate-substituted resorcinol as programmed cell death-1 (PD-1) inhibitor.	amino- and dimethylcarbamate	15-43	programmed cell death 1	Homo sapiens	95-99
27063329-0	2016	Development of amino- and dimethylcarbamate-substituted resorcinol as programmed cell death-1 (PD-1) inhibitor.	resorcinol	56-66	programmed cell death 1	Homo sapiens	95-99
27063329-5	2016	The test for blockading the combination of PD-1 with PD-L1 revealed that abilities of 13 AAPDs were higher than that of sulfamethizole, a successful PD-1 inhibitor.	aapds	89-94	programmed cell death 1	Homo sapiens	43-47
27063329-5	2016	The test for blockading the combination of PD-1 with PD-L1 revealed that abilities of 13 AAPDs were higher than that of sulfamethizole, a successful PD-1 inhibitor.	Sulfamethizole	120-134	programmed cell death 1	Homo sapiens	43-47
26733476-4	2016	In the course of our studies on the PD1-PDL2 interaction, we discovered that salicylic acids, an extremely common compound subclass in screening libraries, interfere with TR-FRET assays.	Salicylates	77-92	programmed cell death 1	Homo sapiens	36-39
26232179-7	2016	Meta-analysis of PD-1 rs2227982 polymorphism under the T allele versus C allele (OR 1.744, 95 % CI 1.477-2.059, P &lt; 0.0001), TT+TC versus CC (OR 2.292, 95 % CI 1.654-3.175, P &lt; 0.0001), TT versus CC (OR 1.883, 95 % CI 1.299-2.729, P = 0.001) revealed a significant association with AS.	Technetium	131-133	programmed cell death 1	Homo sapiens	17-21
26573233-6	2015	Molecular analysis suggests a reduction in the CD47/SIRPalpha pathway by PD-1 blockade, which regulates MDSCs, TAMs, dendritic cell as well as effector T cells.	tams	111-115	programmed cell death 1	Homo sapiens	73-77
26387142-8	2015	In the combined TH/TP/HP treatment group, in multivariate analysis, higher expression of PD1, MHC2, and STAT1 were linked with pCRB, and higher PDL1, MHC1, or IF-I to lower pCRB.	Thorium	16-18	programmed cell death 1	Homo sapiens	89-92
26351349-0	2015	Safety and Antitumor Activity of Anti-PD-1 Antibody, Nivolumab, in Patients With Platinum-Resistant Ovarian Cancer.	Platinum	81-89	programmed cell death 1	Homo sapiens	38-42
25824804-1	2015	OBJECTIVE: We hypothesized that streptozotocin (STZ) has a direct impact on periodontal ligament cell (PDL) damage as a potential direct inducer of periodontitis.	Streptozocin	32-46	programmed cell death 1	Homo sapiens	103-106
25824804-1	2015	OBJECTIVE: We hypothesized that streptozotocin (STZ) has a direct impact on periodontal ligament cell (PDL) damage as a potential direct inducer of periodontitis.	Streptozocin	48-51	programmed cell death 1	Homo sapiens	103-106
26387142-8	2015	In the combined TH/TP/HP treatment group, in multivariate analysis, higher expression of PD1, MHC2, and STAT1 were linked with pCRB, and higher PDL1, MHC1, or IF-I to lower pCRB.	neotetrazolium	19-21	programmed cell death 1	Homo sapiens	89-92
26387142-8	2015	In the combined TH/TP/HP treatment group, in multivariate analysis, higher expression of PD1, MHC2, and STAT1 were linked with pCRB, and higher PDL1, MHC1, or IF-I to lower pCRB.	histidylproline	22-24	programmed cell death 1	Homo sapiens	89-92
26330898-3	2015	Thus, we assessed the changes in the levels of PD-1/PD-L1 in primary human macrophages, brain endothelial cells (hBECs), astrocytes, microglia, and neurons after exposure to METH.	Methamphetamine	174-178	programmed cell death 1	Homo sapiens	47-51
25979485-10	2015	Finally, lenalidomide with PD-1/PD-L1 blockade inhibits MDSC-mediated immune suppression.	Lenalidomide	9-21	programmed cell death 1	Homo sapiens	27-31
25979485-11	2015	CONCLUSIONS: Our data therefore demonstrate that checkpoint signaling plays an important role in providing the tumor-promoting, immune-suppressive microenvironment in multiple myeloma, and that PD-1/PD-L1 blockade induces anti-multiple myeloma immune response that can be enhanced by lenalidomide, providing the framework for clinical evaluation of combination therapy.	Lenalidomide	284-296	programmed cell death 1	Homo sapiens	194-198
26268551-0	2015	Single-Atom Pd1/Graphene Catalyst Achieved by Atomic Layer Deposition: Remarkable Performance in Selective Hydrogenation of 1,3-Butadiene.	1,3-butadiene	124-137	programmed cell death 1	Homo sapiens	12-15
26268551-3	2015	In selective hydrogenation of 1,3-butadiene, the single-atom Pd1/graphene catalyst showed about 100% butenes selectivity at 95% conversion at a mild reaction condition of about 50  C, which is likely due to the changes of 1,3-butadiene adsorption mode and enhanced steric effect on the isolated Pd atoms.	1,3-butadiene	30-43	programmed cell death 1	Homo sapiens	61-64
26268551-3	2015	In selective hydrogenation of 1,3-butadiene, the single-atom Pd1/graphene catalyst showed about 100% butenes selectivity at 95% conversion at a mild reaction condition of about 50  C, which is likely due to the changes of 1,3-butadiene adsorption mode and enhanced steric effect on the isolated Pd atoms.	Graphite	65-73	programmed cell death 1	Homo sapiens	61-64
26268551-3	2015	In selective hydrogenation of 1,3-butadiene, the single-atom Pd1/graphene catalyst showed about 100% butenes selectivity at 95% conversion at a mild reaction condition of about 50  C, which is likely due to the changes of 1,3-butadiene adsorption mode and enhanced steric effect on the isolated Pd atoms.	1,3-butadiene	222-235	programmed cell death 1	Homo sapiens	61-64
26330898-2	2015	Human neuroimmune cells express very low or undetectable levels of PD-1/PD-L1 in normal physiological condition.We seek to examine if exposure of these cells to drug of abuse such as methamphetamine (METH) alters the profile of PD-1/PD-L1 levels, thereby dampens the innate immune response of the host cells.	Methamphetamine	183-198	programmed cell death 1	Homo sapiens	67-71
26330898-2	2015	Human neuroimmune cells express very low or undetectable levels of PD-1/PD-L1 in normal physiological condition.We seek to examine if exposure of these cells to drug of abuse such as methamphetamine (METH) alters the profile of PD-1/PD-L1 levels, thereby dampens the innate immune response of the host cells.	Methamphetamine	183-198	programmed cell death 1	Homo sapiens	228-232
26330898-2	2015	Human neuroimmune cells express very low or undetectable levels of PD-1/PD-L1 in normal physiological condition.We seek to examine if exposure of these cells to drug of abuse such as methamphetamine (METH) alters the profile of PD-1/PD-L1 levels, thereby dampens the innate immune response of the host cells.	Methamphetamine	200-204	programmed cell death 1	Homo sapiens	67-71
26330898-2	2015	Human neuroimmune cells express very low or undetectable levels of PD-1/PD-L1 in normal physiological condition.We seek to examine if exposure of these cells to drug of abuse such as methamphetamine (METH) alters the profile of PD-1/PD-L1 levels, thereby dampens the innate immune response of the host cells.	Methamphetamine	200-204	programmed cell death 1	Homo sapiens	228-232
26359860-9	2015	PD-1 protein expression on the surface of NK cells, CD8+ and CD4+ T cells was similar in patients with active TB disease compared to controls but declined with successful TB treatment, with the greatest decline occurring on the NK cells followed by CD8+ T cells and then CD4+ T cells.	Terbium	110-112	programmed cell death 1	Homo sapiens	0-4
25972478-4	2015	This PD-1(Hi)ROS(Hi) phenotype was specific to alloreactive T cells and was not observed in syngeneic T cells during homeostatic proliferation.	Reactive Oxygen Species	13-16	programmed cell death 1	Homo sapiens	5-9
25972478-5	2015	Blockade of PD-1 signaling decreased both mitochondrial H2O2 and total cellular ROS levels, and PD-1-driven increases in ROS were dependent upon the oxidation of fatty acids, because treatment with etomoxir nullified changes in ROS levels following PD-1 blockade.	Hydrogen Peroxide	56-60	programmed cell death 1	Homo sapiens	12-16
25972478-5	2015	Blockade of PD-1 signaling decreased both mitochondrial H2O2 and total cellular ROS levels, and PD-1-driven increases in ROS were dependent upon the oxidation of fatty acids, because treatment with etomoxir nullified changes in ROS levels following PD-1 blockade.	Reactive Oxygen Species	80-83	programmed cell death 1	Homo sapiens	12-16
25972478-5	2015	Blockade of PD-1 signaling decreased both mitochondrial H2O2 and total cellular ROS levels, and PD-1-driven increases in ROS were dependent upon the oxidation of fatty acids, because treatment with etomoxir nullified changes in ROS levels following PD-1 blockade.	Reactive Oxygen Species	121-124	programmed cell death 1	Homo sapiens	96-100
25972478-5	2015	Blockade of PD-1 signaling decreased both mitochondrial H2O2 and total cellular ROS levels, and PD-1-driven increases in ROS were dependent upon the oxidation of fatty acids, because treatment with etomoxir nullified changes in ROS levels following PD-1 blockade.	Reactive Oxygen Species	121-124	programmed cell death 1	Homo sapiens	96-100
25972478-5	2015	Blockade of PD-1 signaling decreased both mitochondrial H2O2 and total cellular ROS levels, and PD-1-driven increases in ROS were dependent upon the oxidation of fatty acids, because treatment with etomoxir nullified changes in ROS levels following PD-1 blockade.	Fatty Acids	162-173	programmed cell death 1	Homo sapiens	96-100
25972478-5	2015	Blockade of PD-1 signaling decreased both mitochondrial H2O2 and total cellular ROS levels, and PD-1-driven increases in ROS were dependent upon the oxidation of fatty acids, because treatment with etomoxir nullified changes in ROS levels following PD-1 blockade.	Fatty Acids	162-173	programmed cell death 1	Homo sapiens	96-100
25972478-5	2015	Blockade of PD-1 signaling decreased both mitochondrial H2O2 and total cellular ROS levels, and PD-1-driven increases in ROS were dependent upon the oxidation of fatty acids, because treatment with etomoxir nullified changes in ROS levels following PD-1 blockade.	etomoxir	198-206	programmed cell death 1	Homo sapiens	12-16
25972478-5	2015	Blockade of PD-1 signaling decreased both mitochondrial H2O2 and total cellular ROS levels, and PD-1-driven increases in ROS were dependent upon the oxidation of fatty acids, because treatment with etomoxir nullified changes in ROS levels following PD-1 blockade.	etomoxir	198-206	programmed cell death 1	Homo sapiens	96-100
25972478-5	2015	Blockade of PD-1 signaling decreased both mitochondrial H2O2 and total cellular ROS levels, and PD-1-driven increases in ROS were dependent upon the oxidation of fatty acids, because treatment with etomoxir nullified changes in ROS levels following PD-1 blockade.	etomoxir	198-206	programmed cell death 1	Homo sapiens	96-100
25972478-5	2015	Blockade of PD-1 signaling decreased both mitochondrial H2O2 and total cellular ROS levels, and PD-1-driven increases in ROS were dependent upon the oxidation of fatty acids, because treatment with etomoxir nullified changes in ROS levels following PD-1 blockade.	Reactive Oxygen Species	121-124	programmed cell death 1	Homo sapiens	96-100
25972478-5	2015	Blockade of PD-1 signaling decreased both mitochondrial H2O2 and total cellular ROS levels, and PD-1-driven increases in ROS were dependent upon the oxidation of fatty acids, because treatment with etomoxir nullified changes in ROS levels following PD-1 blockade.	Reactive Oxygen Species	121-124	programmed cell death 1	Homo sapiens	96-100
25972478-7	2015	Furthermore, PD-1-driven changes in ROS were fundamental to establishing a cell"s susceptibility to subsequent metabolic inhibition, because blockade of PD-1 decreased the efficacy of later F1F0-ATP synthase modulation.	Reactive Oxygen Species	36-39	programmed cell death 1	Homo sapiens	13-17
25972478-7	2015	Furthermore, PD-1-driven changes in ROS were fundamental to establishing a cell"s susceptibility to subsequent metabolic inhibition, because blockade of PD-1 decreased the efficacy of later F1F0-ATP synthase modulation.	Reactive Oxygen Species	36-39	programmed cell death 1	Homo sapiens	153-157
25972478-8	2015	These data indicate that PD-1 facilitates apoptosis in alloreactive T cells by increasing ROS in a process dependent upon the oxidation of fat.	Reactive Oxygen Species	90-93	programmed cell death 1	Homo sapiens	25-29
25827621-4	2015	The PDAC tissues were infiltrated by macrophages, especially CD33+CD163+ M2 macrophages and CD4+ T cells that concomitantly express programmed cell death-1 (PD-1).	pdac	4-8	programmed cell death 1	Homo sapiens	157-161
25747035-9	2015	Moreover, a significant genotype-genotype interaction between IL-28B rs12979860 CC and PD-1 rs10204525 TC+CC was found to be associated with higher rates of spontaneous clearance (adjusted OR=0.689, P=0.032).	Technetium	103-105	programmed cell death 1	Homo sapiens	87-91
25823822-3	2015	In 12 of 27 patients (44%) PD-1 promoter demethylation was observed in sorted peripheral blood T cells isolated over consecutive cycles of treatment with 5-azacytidine (5-aza).	Azacitidine	154-167	programmed cell death 1	Homo sapiens	27-31
25823822-3	2015	In 12 of 27 patients (44%) PD-1 promoter demethylation was observed in sorted peripheral blood T cells isolated over consecutive cycles of treatment with 5-azacytidine (5-aza).	Azacitidine	154-159	programmed cell death 1	Homo sapiens	27-31
25349974-7	2015	In patients treated with EGFR tyrosine kinase inhibitors (N=95), sensitivity to gefitinib or erlotinib was higher in PD-L1+ vs PD-L1 negative in terms of the response rate (RR: P=0.01) time to progression (TTP: P&lt;0.0001) and survival (OS: P=0.09), with no difference in PD1+ vs PD-1 negative.	Gefitinib	80-89	programmed cell death 1	Homo sapiens	281-285
25655521-3	2015	On the Pd1 -terminated PdGa(111) surface, room-temperature adsorption of a small prochiral molecule (9-ethynylphenanthrene) leads to exceptionally high enantiomeric excess ratios of up to 98 %.	9-ethynylphenanthrene	101-122	programmed cell death 1	Homo sapiens	7-10
25916783-6	2015	And the phosphorylation level of programmed death 1 (PD-1) signaling motif tyrosine was measured by Western blot.	Tyrosine	75-83	programmed cell death 1	Homo sapiens	33-51
25916783-6	2015	And the phosphorylation level of programmed death 1 (PD-1) signaling motif tyrosine was measured by Western blot.	Tyrosine	75-83	programmed cell death 1	Homo sapiens	53-57
25349974-7	2015	In patients treated with EGFR tyrosine kinase inhibitors (N=95), sensitivity to gefitinib or erlotinib was higher in PD-L1+ vs PD-L1 negative in terms of the response rate (RR: P=0.01) time to progression (TTP: P&lt;0.0001) and survival (OS: P=0.09), with no difference in PD1+ vs PD-1 negative.	Erlotinib Hydrochloride	93-102	programmed cell death 1	Homo sapiens	281-285
25713477-2	2015	MATERIALS AND METHODS: About 0.5-4.5% OES, 2% CHX and 5.25% NaOCl solutions cytotoxicity was evaluated with cell culture test using PDL fibroblasts.	N-OCTYL-2-HYDROXYETHYL SULFOXIDE	38-41	programmed cell death 1	Homo sapiens	132-135
25415283-9	2015	Immunosuppressive pathways, including regulatory T cells and CTLA-4 expression on T cells were overcome by the addition of vaccine and low-dose cyclophosphamide to PD-1 blockade.	Cyclophosphamide	144-160	programmed cell death 1	Homo sapiens	164-168
25349132-7	2015	In paraffin embedded tissues, we found that tumor infiltrating lymphocytes expressed PD-1 in 3/6 cases.	Paraffin	3-11	programmed cell death 1	Homo sapiens	85-89
25546306-3	2014	We found high levels of 5-hydroxymethylcytosine (5hmC) at the PD-1 (Pdcd1) promoter of non-tolerant T cells.	5-hydroxymethylcytosine	24-47	programmed cell death 1	Homo sapiens	68-73
25546306-3	2014	We found high levels of 5-hydroxymethylcytosine (5hmC) at the PD-1 (Pdcd1) promoter of non-tolerant T cells.	5-hydroxymethylcytosine	49-53	programmed cell death 1	Homo sapiens	62-66
25546306-3	2014	We found high levels of 5-hydroxymethylcytosine (5hmC) at the PD-1 (Pdcd1) promoter of non-tolerant T cells.	5-hydroxymethylcytosine	24-47	programmed cell death 1	Homo sapiens	62-66
25150534-4	2014	RESULTS: High concentrations of glucose increased the production of pro-inflammatory cytokines interleukin-1 beta (IL-1beta), tumour necrosis factor alpha (TNF-alpha), Interleukin-6 (IL-6) at both mRNA and protein levels, and receptor activator of NF-kB ligand (RANKL) at mRNA levels in hPDL cells.	Glucose	32-39	programmed cell death 1	Homo sapiens	287-291
25150534-5	2014	Insulin treatment alleviated the stimulatory effects of high glucose on pro-inflammatory cytokines and RANKL expression by hPDL cells.	Glucose	61-68	programmed cell death 1	Homo sapiens	123-127
25546306-3	2014	We found high levels of 5-hydroxymethylcytosine (5hmC) at the PD-1 (Pdcd1) promoter of non-tolerant T cells.	5-hydroxymethylcytosine	49-53	programmed cell death 1	Homo sapiens	68-73
25546306-6	2014	We describe a model whereby promoter demethylation requires the co-incident expression of permissive histone modifications at the Pdcd1 promoter together with TET availability.	tet	159-162	programmed cell death 1	Homo sapiens	130-135
25464856-3	2014	Blockade of inhibitory receptor programmed cell death protein 1 (PD-1) in vivo increased mTOR activity in virus-specific CTLs, and its therapeutic effects were abrogated by the mTOR inhibitor rapamycin.	Sirolimus	192-201	programmed cell death 1	Homo sapiens	32-63
25464856-3	2014	Blockade of inhibitory receptor programmed cell death protein 1 (PD-1) in vivo increased mTOR activity in virus-specific CTLs, and its therapeutic effects were abrogated by the mTOR inhibitor rapamycin.	Sirolimus	192-201	programmed cell death 1	Homo sapiens	65-69
25574964-3	2014	Atorvastatin was associated with a significant reduction in CD8 T-cell activation (HLA-DR, CD38/HLA-DR) and exhaustion (TIM-3, TIM-3/PD-1) whereas pravastatin had no effect.	Atorvastatin	0-12	programmed cell death 1	Homo sapiens	133-137
25247845-1	2014	Protectin D1 (PD1 (3)), a C22-dihydroxylated polyunsaturated fatty acid biosynthesized from all-Z-docosahexaenoic acid, belongs to the new family of endogenous mediators referred to as specialized pro-resolving lipid mediators.	Fatty Acids, Unsaturated	45-71	programmed cell death 1	Homo sapiens	14-17
25247845-1	2014	Protectin D1 (PD1 (3)), a C22-dihydroxylated polyunsaturated fatty acid biosynthesized from all-Z-docosahexaenoic acid, belongs to the new family of endogenous mediators referred to as specialized pro-resolving lipid mediators.	Docosahexaenoic Acids	92-118	programmed cell death 1	Homo sapiens	14-17
25247845-5	2014	The synthesis and biological evaluations of the omega-22 monohydroxylated metabolite of PD1 (3), named herein 22-OH-PD1 (6), are presented.	omega-22	48-56	programmed cell death 1	Homo sapiens	88-91
25247845-5	2014	The synthesis and biological evaluations of the omega-22 monohydroxylated metabolite of PD1 (3), named herein 22-OH-PD1 (6), are presented.	omega-22	48-56	programmed cell death 1	Homo sapiens	116-119
24863372-5	2014	Based on these data a stability-indicating LC-UV method for simultaneous estimation of PAN, and its most relevant degradation product (PD1) was developed and validated; moreover the method allowed also the separation and the quantification of the preservative system, constituted by a paraben mixture.	Parabens	285-292	programmed cell death 1	Homo sapiens	135-138
24609838-4	2014	In this article, we characterized hypoxia or P. gingivalis lipopolysaccharide (Pg LPS) induced tumor necrosis factor alpha (TNF-alpha), interleukin (IL)-1beta, and IL-6 expression by human periodontal ligament (hPDL) cells.	pg	79-81	programmed cell death 1	Homo sapiens	211-215
24609838-6	2014	We also demonstrated that nuclear factor kappa B pathway was involved in hypoxia augmenting Pg LPS induced cytokine expression in hPDL cells.	pg lps	92-98	programmed cell death 1	Homo sapiens	130-134
25178664-4	2014	Results showed that the expression of PD-1 and its ligands mRNA were significantly increased (p &lt; 0.01) in PBMC from 3 to 7 days post infection (dpi).	3-aminodiphenyleneiodium	148-151	programmed cell death 1	Homo sapiens	38-42
25105535-0	2014	Immune regulatory effects of panobinostat in patients with Hodgkin lymphoma through modulation of serum cytokine levels and T-cell PD1 expression.	Panobinostat	29-41	programmed cell death 1	Homo sapiens	131-134
24812273-0	2014	Preclinical evidence that PD1 blockade cooperates with cancer vaccine TEGVAX to elicit regression of established tumors.	tegvax	70-76	programmed cell death 1	Homo sapiens	26-29
24812273-6	2014	In support of this likelihood, PDL1 upregulation in this setting relied upon IFNgamma-expressing tumor-infiltrating CD4(+) and CD8(+) T cells and administration of a PD1-blocking antibody with TEGVAX elicited complete regression of established tumors.	tegvax	193-199	programmed cell death 1	Homo sapiens	166-169
24906866-8	2014	Finally, we demonstrate that ansamitocin P3, due to its immunomodulatory properties, acts in synergy with antibody-mediated blockade of the T cell inhibitory receptors PD-1 and CTLA-4.	ansamitocins	29-43	programmed cell death 1	Homo sapiens	168-172
24830357-11	2014	CONCLUSION: This analysis supports the observation that bevacizumab exposure after PD1 is associated with longer PPS in mCRC.	pps	113-116	programmed cell death 1	Homo sapiens	83-86
24681107-7	2014	Finally, we showed that PD-1/B7-H1 interactions and IL-10 might be responsible for the enhanced suppressive capability of MSC-exposed Tregs.	tregs	134-139	programmed cell death 1	Homo sapiens	24-28
25276770-1	2014	The aim of this study was to investigate the efficacy of the sequential combined 585 nm PDL and the 1064 nm neodymium:yttrium-aluminium-garnet laser (PDL/Nd:YAG) in the treatment of surgical scars and to evaluate the short-term effects by in vivo confocal microscopy (RCM) and the long-term effects by clinical assessment of the scars.	Aluminum	126-135	programmed cell death 1	Homo sapiens	150-153
24328503-6	2014	Ex vivo analysis of activated CD4(+) T cells showed Fus1-dependent changes in calcium-regulated processes, such as surface expression of CD4 and PD1/PD-L1, proliferation, and Th polarization.	Calcium	78-85	programmed cell death 1	Homo sapiens	145-148
24512518-5	2014	Programmed death-1 (PD-1) and PD-1 ligand inhibitors such as nivolumab, MK3475 and MPDL3280 have demonstrated clinical efficacy in patients with advanced/metastatic NSCLC in early clinical trials.	mpdl3280	83-91	programmed cell death 1	Homo sapiens	0-18
24512518-5	2014	Programmed death-1 (PD-1) and PD-1 ligand inhibitors such as nivolumab, MK3475 and MPDL3280 have demonstrated clinical efficacy in patients with advanced/metastatic NSCLC in early clinical trials.	mpdl3280	83-91	programmed cell death 1	Homo sapiens	30-34
24365761-6	2014	The ethanol exposure during half of the 1st and the whole 2nd human trimester equivalent resulted in an overall trend toward lower values of synaptic indices at PD1 with a fast recovery from these deficits observed already at PD10.	Ethanol	4-11	programmed cell death 1	Homo sapiens	161-164
24969595-4	2014	Blood samples from 16 chronic periodontitis patients were collected at week 0 and 6 after initial therapy for 6 weeks and PD-1 and PD-L1 expression in the surface of CD(+)4 and CD(+)8 T lymphocytes was also determined by flow cytometry.	Cadmium	166-168	programmed cell death 1	Homo sapiens	122-126
25517314-0	2014	Failure to upregulate cell surface PD-1 is associated with dysregulated stimulation of T cells by TGN1412-like CD28 superagonist.	TGN-1412	98-105	programmed cell death 1	Homo sapiens	35-39
23764564-4	2013	In the trinuclear adduct of [2.2]paracyclophane or CHT, a Pd2 unit and a Pd1 unit synfacially coordinate through a (mu-eta(3)-allyl):(eta(3)-allyl) manner.	(2.2)paracyclophane	28-47	programmed cell death 1	Homo sapiens	73-76
24040569-1	2013	PURPOSE: The purpose of the current study was to examine the effect of dexamethasone (Dex) at various concentrations on the apoptosis and mineralization of human periodontal ligament (hPDL) cells.	Dexamethasone	71-84	programmed cell death 1	Homo sapiens	184-188
24040569-1	2013	PURPOSE: The purpose of the current study was to examine the effect of dexamethasone (Dex) at various concentrations on the apoptosis and mineralization of human periodontal ligament (hPDL) cells.	Dexamethasone	86-89	programmed cell death 1	Homo sapiens	184-188
24040569-7	2013	Within the range of Dex concentrations tested in this study, 100 nM of Dex was found to promote the most vigorous differentiation and mineralization of hPDL cells.	Dexamethasone	20-23	programmed cell death 1	Homo sapiens	152-156
24040569-7	2013	Within the range of Dex concentrations tested in this study, 100 nM of Dex was found to promote the most vigorous differentiation and mineralization of hPDL cells.	Dexamethasone	71-74	programmed cell death 1	Homo sapiens	152-156
23788285-8	2013	We also showed that cyclic adenosine monophosphate (cAMP) is a critical regulator of the LPLI-mediated effects on hPDL cells.	Cyclic AMP	20-50	programmed cell death 1	Homo sapiens	114-118
23788285-8	2013	We also showed that cyclic adenosine monophosphate (cAMP) is a critical regulator of the LPLI-mediated effects on hPDL cells.	Cyclic AMP	52-56	programmed cell death 1	Homo sapiens	114-118
23730407-11	2013	Therefore, evaluation of the infiltration of PD-positive cells or Tregs in CRCC may be useful diagnostic tools for the selection of patients who could benefit from PD1- or Treg-based immunotherapy.	Palladium	45-47	programmed cell death 1	Homo sapiens	164-167
23041554-5	2012	METHODS: The genotype frequency of PD-1.3 polymorphism was determined by using a polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method in 236 subjects with HCC and 236 cancer-free control subjects matched on age, gender, smoking and alcohol status.	Alcohols	264-271	programmed cell death 1	Homo sapiens	35-39
24021786-13	2013	CONCLUSION: The standard Peg-IFNa-2a + RBV combination antiviral therapy reduces PD-1 expression on CD4+ and CD8+ T lymphocytes and increases PD-L1 expression on CD8+ T lymphocytes in peripheral blood.	Ribavirin	39-42	programmed cell death 1	Homo sapiens	81-85
23043788-6	2013	In vivo, hPDL-derived cells survive, migrate, and give rise to DCX(+), NF-M(+), GABA(+), GFAP(+), and NG2(+) cells after grafting the adult mouse brain.	gamma-Aminobutyric Acid	80-84	programmed cell death 1	Homo sapiens	9-13
22903385-4	2013	We demonstrated that PD-L1 and PD-L2 siRNA delivery using DLin-KC2-DMA-containing lipid nanoparticles (LNP) mediated efficient and specific knockdown of PD-L expression on human monocyte-derived DC.	N-myristoyl-alaninol	67-70	programmed cell death 1	Homo sapiens	21-25
23215674-6	2013	EXPERT OPINION: Elucidation of the crucial role of MAPK pathway and BRAF kinase mutations in particular has led to development of specific small molecule kinase inhibitors (vemurafenib, dabrafenib, trametinib), and new insight into molecular mechanisms responsible for immune response and tolerance resulted in development of immunomodulatory agents (ipilimumab, anti-PD1, anti-PD-L1).	Vemurafenib	173-184	programmed cell death 1	Homo sapiens	368-371
23215674-6	2013	EXPERT OPINION: Elucidation of the crucial role of MAPK pathway and BRAF kinase mutations in particular has led to development of specific small molecule kinase inhibitors (vemurafenib, dabrafenib, trametinib), and new insight into molecular mechanisms responsible for immune response and tolerance resulted in development of immunomodulatory agents (ipilimumab, anti-PD1, anti-PD-L1).	dabrafenib	186-196	programmed cell death 1	Homo sapiens	368-371
23017670-4	2013	Sixteen hours PMA/Ionomycin stimulation induced iTreg subsets with the phenotype CD4(+)CD25(+)Foxp3(+), CD4(+)IFNgamma(+)Foxp3(+) and CD4(+)CD25(+)IFNgamma(+) co-expressing CD95, CD152, CD178, CD279, Granzyme A, Granzyme B, Perforin, IL-10, and TGFbeta(1).	Ionomycin	18-27	programmed cell death 1	Homo sapiens	193-198
23660203-10	2013	The results of bisulfite genomic sequencing showed that demethylation probability of some CG points in PD-1 promoter region (-601, -553, -538, -483, -463, -317 bp) were significantly correlated with PD-1 expression level (P &lt; 0.05).	hydrogen sulfite	15-24	programmed cell death 1	Homo sapiens	103-107
23660203-10	2013	The results of bisulfite genomic sequencing showed that demethylation probability of some CG points in PD-1 promoter region (-601, -553, -538, -483, -463, -317 bp) were significantly correlated with PD-1 expression level (P &lt; 0.05).	hydrogen sulfite	15-24	programmed cell death 1	Homo sapiens	199-203
23212936-2	2013	In this work, we report the preparation of the new nanocapsule 3 (CF(3)SO(3))(8) with a A(4 B(2) tetragonal prismatic geometry, where A corresponds to the dipalladium hexaazamacrocyclic complex Pd-1, and B corresponds to the tetraanionic form of palladium 5,10,15,20-tetrakis(4-carboxyphenyl)porphyrin (2).	dipalladium hexaazamacrocyclic	155-185	programmed cell death 1	Homo sapiens	194-205
23212637-2	2012	The present study investigated the activity of five derivatives (PD2-6) of 4-(4"-bromophenyl)-4-piperidinol (PD1), against pain and platelet aggregation mediated by the release of prostaglandins and thromboxane A2, respectively.	4-(4"-bromophenyl)-4-piperidinol	75-107	programmed cell death 1	Homo sapiens	109-112
23212637-2	2012	The present study investigated the activity of five derivatives (PD2-6) of 4-(4"-bromophenyl)-4-piperidinol (PD1), against pain and platelet aggregation mediated by the release of prostaglandins and thromboxane A2, respectively.	Prostaglandins	180-194	programmed cell death 1	Homo sapiens	109-112
23212637-2	2012	The present study investigated the activity of five derivatives (PD2-6) of 4-(4"-bromophenyl)-4-piperidinol (PD1), against pain and platelet aggregation mediated by the release of prostaglandins and thromboxane A2, respectively.	Thromboxane A2	199-213	programmed cell death 1	Homo sapiens	109-112
22964327-2	2012	This study investigated the direct effect of high glucose on the expression of receptor activator of nuclear factor-kappa B ligand (RANKL) in human PDL (hPDL) cells.	Glucose	50-57	programmed cell death 1	Homo sapiens	148-151
22964327-2	2012	This study investigated the direct effect of high glucose on the expression of receptor activator of nuclear factor-kappa B ligand (RANKL) in human PDL (hPDL) cells.	Glucose	50-57	programmed cell death 1	Homo sapiens	153-157
22964327-7	2012	RESULTS: High glucose levels caused an increase in RANKL mRNA and protein expression in hPDL cells.	Glucose	14-21	programmed cell death 1	Homo sapiens	88-92
22964327-8	2012	Moreover, the amount of p-AMPK and AMPK activity was lower in hPDL cells exposed to high glucose levels than in cells exposed to normal glucose levels.	Glucose	89-96	programmed cell death 1	Homo sapiens	62-66
22964327-8	2012	Moreover, the amount of p-AMPK and AMPK activity was lower in hPDL cells exposed to high glucose levels than in cells exposed to normal glucose levels.	Glucose	136-143	programmed cell death 1	Homo sapiens	62-66
22964327-9	2012	Suppression of AMPK by Compound C augmented RANKL expression, and AMPK activation by metformin significantly decreased RANKL expression in hPDL cells.	Metformin	85-94	programmed cell death 1	Homo sapiens	139-143
22964327-10	2012	Additionally, metformin down-regulated RANKL expression in hPDL cells exposed to high glucose via AMPK activation.	Metformin	14-23	programmed cell death 1	Homo sapiens	59-63
22964327-10	2012	Additionally, metformin down-regulated RANKL expression in hPDL cells exposed to high glucose via AMPK activation.	Glucose	86-93	programmed cell death 1	Homo sapiens	59-63
22964327-11	2012	CONCLUSION: High glucose-induced up-regulation of RANKL could be due to decreased AMPK activity, and AMPK activation may be involved in regulating of RANKL expression in hPDL cells.	Glucose	17-24	programmed cell death 1	Homo sapiens	170-174
22173154-9	2012	The decrease in PD-1 expression on CD4(+) and CD8(+) T cells during the first 12 weeks on telbivudine treatment was not correlated with changes in IL-21 concentrations.	Telbivudine	90-101	programmed cell death 1	Homo sapiens	16-20
22400279-3	2011	The structure of the Pd1-xFe(x) thin film with x = 0.14, 0.24, and 0.52 was determined by X-ray diffraction (XRD) and transmission electron microscopy (TEM) as a solid solution of iron in palladium face-centered cubic lattice with the (111) orientation of nanograins relatively to the substrate surface.	Iron	180-184	programmed cell death 1	Homo sapiens	21-24
22568077-5	2012	The aim of this study was to investigate the AEA level in periodontal regions and the osteogenic effect of AEA on hPDL cells.	anandamide	107-110	programmed cell death 1	Homo sapiens	114-118
22568077-10	2012	IL-11 production from hPDL cells was significantly enhanced by AEA stimulation and this IL-11 production was suppressed by capsazepine.	anandamide	63-66	programmed cell death 1	Homo sapiens	22-26
22568077-10	2012	IL-11 production from hPDL cells was significantly enhanced by AEA stimulation and this IL-11 production was suppressed by capsazepine.	capsazepine	123-134	programmed cell death 1	Homo sapiens	22-26
22246361-1	2011	OBJECTIVE: To observe the demethylation effect of demethylation inhibitor 5-azacytidine (5-Zac) on programmed death receptor 1 (PD-1) in Molt-4 cells (T lymphocyte cell line) and to investigate the relationship between DNA demethylation and expression of PD-1.	Azacitidine	74-87	programmed cell death 1	Homo sapiens	128-132
22246361-1	2011	OBJECTIVE: To observe the demethylation effect of demethylation inhibitor 5-azacytidine (5-Zac) on programmed death receptor 1 (PD-1) in Molt-4 cells (T lymphocyte cell line) and to investigate the relationship between DNA demethylation and expression of PD-1.	Azacitidine	74-87	programmed cell death 1	Homo sapiens	255-259
22400279-3	2011	The structure of the Pd1-xFe(x) thin film with x = 0.14, 0.24, and 0.52 was determined by X-ray diffraction (XRD) and transmission electron microscopy (TEM) as a solid solution of iron in palladium face-centered cubic lattice with the (111) orientation of nanograins relatively to the substrate surface.	Palladium	188-197	programmed cell death 1	Homo sapiens	21-24
21492509-0	2011	[Relationship between PD-1 expression on peripheral T lymphcytes and HBeAg seroconversion after entecavir treatment in chronic hepatitis B patients].	entecavir	96-105	programmed cell death 1	Homo sapiens	22-26
21130420-9	2011	At 72h, there was a significant increase in non-transfected hPDL cell proliferation after estradiol stimulation.	Estradiol	90-99	programmed cell death 1	Homo sapiens	60-64
21130420-11	2011	A clear increase in periostin mRNA expression levels was observed after incubating hPDL cells with estradiol.	Estradiol	99-108	programmed cell death 1	Homo sapiens	83-87
21394295-6	2011	RESULTS: The up-regulated genes on day 7 by hPDL cells cultured in osteogenic medium were thought to be associated with calcium/iron/metal ion binding or homeostasis (PDE1A, HFE and PCDH9) and cell viability (PCDH9), and the down-regulated genes were thought to be associated with proliferation (PHGDH and PSAT1).	Calcium	120-127	programmed cell death 1	Homo sapiens	44-48
21394295-6	2011	RESULTS: The up-regulated genes on day 7 by hPDL cells cultured in osteogenic medium were thought to be associated with calcium/iron/metal ion binding or homeostasis (PDE1A, HFE and PCDH9) and cell viability (PCDH9), and the down-regulated genes were thought to be associated with proliferation (PHGDH and PSAT1).	Iron	128-132	programmed cell death 1	Homo sapiens	44-48
21394295-6	2011	RESULTS: The up-regulated genes on day 7 by hPDL cells cultured in osteogenic medium were thought to be associated with calcium/iron/metal ion binding or homeostasis (PDE1A, HFE and PCDH9) and cell viability (PCDH9), and the down-regulated genes were thought to be associated with proliferation (PHGDH and PSAT1).	Metals	133-138	programmed cell death 1	Homo sapiens	44-48
21394295-8	2011	CONCLUSIONS: This study suggests that when appropriately triggered, the stem cells in the hPDL differentiate into osteoblasts/cementoblasts, and the genes related to calcium binding (PDE1A and PCDH9), which were strongly expressed at the stage of matrix maturation, may be associated with differentiation of the hPDL cells into osteoblasts/cementoblasts.	Calcium	166-173	programmed cell death 1	Homo sapiens	90-94
21394295-8	2011	CONCLUSIONS: This study suggests that when appropriately triggered, the stem cells in the hPDL differentiate into osteoblasts/cementoblasts, and the genes related to calcium binding (PDE1A and PCDH9), which were strongly expressed at the stage of matrix maturation, may be associated with differentiation of the hPDL cells into osteoblasts/cementoblasts.	Calcium	166-173	programmed cell death 1	Homo sapiens	312-316
21867913-2	2011	We report an aspirin-triggered DHA metabolome that biosynthesizes a potent product in inflammatory exudates and human leukocytes, namely aspirin-triggered Neuroprotectin D1/Protectin D1 [AT-(NPD1/PD1)].	Aspirin	13-20	programmed cell death 1	Homo sapiens	192-195
21867913-2	2011	We report an aspirin-triggered DHA metabolome that biosynthesizes a potent product in inflammatory exudates and human leukocytes, namely aspirin-triggered Neuroprotectin D1/Protectin D1 [AT-(NPD1/PD1)].	dehydroacetic acid	31-34	programmed cell death 1	Homo sapiens	192-195
21867913-2	2011	We report an aspirin-triggered DHA metabolome that biosynthesizes a potent product in inflammatory exudates and human leukocytes, namely aspirin-triggered Neuroprotectin D1/Protectin D1 [AT-(NPD1/PD1)].	Aspirin	137-144	programmed cell death 1	Homo sapiens	192-195
21867913-3	2011	The complete stereochemistry of AT-(NPD1/PD1) proved to be 10R,17R-dihydroxydocosa-4Z,7Z,11E,13E,15Z,19Z-hexaenoic acid.	17r-dihydroxydocosa-4z	63-85	programmed cell death 1	Homo sapiens	37-40
21867913-3	2011	The complete stereochemistry of AT-(NPD1/PD1) proved to be 10R,17R-dihydroxydocosa-4Z,7Z,11E,13E,15Z,19Z-hexaenoic acid.	7z	86-88	programmed cell death 1	Homo sapiens	37-40
21867913-3	2011	The complete stereochemistry of AT-(NPD1/PD1) proved to be 10R,17R-dihydroxydocosa-4Z,7Z,11E,13E,15Z,19Z-hexaenoic acid.	hex-2-enoic acid	105-119	programmed cell death 1	Homo sapiens	37-40
21408177-6	2011	Indeed, the TCR-induced calcium and ERK responses were reduced in peripheral blood T cells transfected with PD-1.	Calcium	24-31	programmed cell death 1	Homo sapiens	108-112
21408177-7	2011	Inhibition by sodium stibogluconate of the SHP-1 and SHP-2 phosphatases that associate with several inhibitory receptors including PD-1, relieves part of the anergy apparent in TIL or in PD-1-transfected T cells.	Antimony Sodium Gluconate	14-35	programmed cell death 1	Homo sapiens	131-135
21091911-8	2011	Successful HCV treatment with pegylated interferon/ribavirin or blocking PD-1/PDL-1 engagement ex vivo led to reduced PD-1 expression and improved IL-12 production as well as STAT-1 activation in M/Mphi from HCV-infected individuals.	Ribavirin	51-60	programmed cell death 1	Homo sapiens	118-122
21117699-8	2011	The related mixed-metal phase, Pd(1/2)Pt(1/2)(CN)(2) qH(2)O (q ~ 0.50), is also nanocrystalline (sheet size ~15 A x 15 A).	Metals	18-23	programmed cell death 1	Homo sapiens	31-37
21117699-10	2011	Removal of the final traces of water or ammonia by heating results in decomposition of the compounds to Pd and Pt metal, or in the case of the mixed-metal cyanide, the alloy, Pd(1/2)Pt(1/2), making it impossible to prepare the simple cyanides, Pd(CN)(2), Pt(CN)(2), or Pd(1/2)Pt(1/2)(CN)(2), by this method.	Water	31-36	programmed cell death 1	Homo sapiens	175-181
21117699-10	2011	Removal of the final traces of water or ammonia by heating results in decomposition of the compounds to Pd and Pt metal, or in the case of the mixed-metal cyanide, the alloy, Pd(1/2)Pt(1/2), making it impossible to prepare the simple cyanides, Pd(CN)(2), Pt(CN)(2), or Pd(1/2)Pt(1/2)(CN)(2), by this method.	Water	31-36	programmed cell death 1	Homo sapiens	269-275
21117699-10	2011	Removal of the final traces of water or ammonia by heating results in decomposition of the compounds to Pd and Pt metal, or in the case of the mixed-metal cyanide, the alloy, Pd(1/2)Pt(1/2), making it impossible to prepare the simple cyanides, Pd(CN)(2), Pt(CN)(2), or Pd(1/2)Pt(1/2)(CN)(2), by this method.	Ammonia	40-47	programmed cell death 1	Homo sapiens	175-181
21117699-10	2011	Removal of the final traces of water or ammonia by heating results in decomposition of the compounds to Pd and Pt metal, or in the case of the mixed-metal cyanide, the alloy, Pd(1/2)Pt(1/2), making it impossible to prepare the simple cyanides, Pd(CN)(2), Pt(CN)(2), or Pd(1/2)Pt(1/2)(CN)(2), by this method.	Ammonia	40-47	programmed cell death 1	Homo sapiens	269-275
21467633-4	2011	The cellular response to TGF-beta1 by hPDL cells was measured using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and Western blot analysis.	thiazolyl blue	72-132	programmed cell death 1	Homo sapiens	38-42
21467633-4	2011	The cellular response to TGF-beta1 by hPDL cells was measured using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and Western blot analysis.	monooxyethylene trimethylolpropane tristearate	134-137	programmed cell death 1	Homo sapiens	38-42
21907333-0	2011	DNA demethylation in PD-1 gene promoter induced by 5-azacytidine activates PD-1 expression on Molt-4 cells.	Azacitidine	51-64	programmed cell death 1	Homo sapiens	21-25
21907333-0	2011	DNA demethylation in PD-1 gene promoter induced by 5-azacytidine activates PD-1 expression on Molt-4 cells.	Azacitidine	51-64	programmed cell death 1	Homo sapiens	75-79
21907333-3	2011	This study shows the changes of PD-1 expression levels and the demethylation status of the PD-1 promoter region in Molt-4 cells under different concentrations of 5-azacytidine (5-Zac).	Azacitidine	162-175	programmed cell death 1	Homo sapiens	32-36
21907333-3	2011	This study shows the changes of PD-1 expression levels and the demethylation status of the PD-1 promoter region in Molt-4 cells under different concentrations of 5-azacytidine (5-Zac).	Azacitidine	162-175	programmed cell death 1	Homo sapiens	91-95
20833872-1	2011	Docosahexaenoic acid (DHA), an important component of marine lipids, exhibits anti-inflammatory activity related to some of its oxygenated metabolites, such as neuroprotectin/protectin D1 [NPD1/PD1; 10(R),17(S)-dihydroxy-docosa-4Z,7Z, 11E,13E,15Z,19Z-hexaenoic acid] produced through the 15-lipoxygenase pathway.	Docosahexaenoic Acids	0-20	programmed cell death 1	Homo sapiens	190-193
20833872-1	2011	Docosahexaenoic acid (DHA), an important component of marine lipids, exhibits anti-inflammatory activity related to some of its oxygenated metabolites, such as neuroprotectin/protectin D1 [NPD1/PD1; 10(R),17(S)-dihydroxy-docosa-4Z,7Z, 11E,13E,15Z,19Z-hexaenoic acid] produced through the 15-lipoxygenase pathway.	Docosahexaenoic Acids	22-25	programmed cell death 1	Homo sapiens	190-193
20833872-1	2011	Docosahexaenoic acid (DHA), an important component of marine lipids, exhibits anti-inflammatory activity related to some of its oxygenated metabolites, such as neuroprotectin/protectin D1 [NPD1/PD1; 10(R),17(S)-dihydroxy-docosa-4Z,7Z, 11E,13E,15Z,19Z-hexaenoic acid] produced through the 15-lipoxygenase pathway.	neuroprotectin	160-174	programmed cell death 1	Homo sapiens	190-193
20833872-7	2011	Interestingly, all the metabolites tested exhibiting the E,Z,E-conjugated triene were active, whereas E,E,Z trienes (as in PD1) or all-trans (E,E,E) trienes were inactive.	e,e,z trienes	102-115	programmed cell death 1	Homo sapiens	123-126
20924071-7	2010	These results suggest that FAK regulates the production of prostaglandin E(2) via the transcriptional regulation of COX-2 mRNA in compressive stimulated PDL cells.	Dinoprostone	59-77	programmed cell death 1	Homo sapiens	153-156
20943073-12	2010	CONCLUSIONS: Direct suppression of HBV replication by telbivudine in CHB patients can decrease PD-1 and PD-L1 expressions and restore HBV-specific CD8+T cells.	Telbivudine	54-65	programmed cell death 1	Homo sapiens	95-99
20541802-9	2010	Chemically and biochemically the cir-PDL adjacent to bone and cementum was identified by relatively higher carbon and lower calcium including the localization of small leucine rich proteins responsible for maintaining soft-hard tissue cohesion, stiffness and hygroscopic nature of PDL-bone and PDL-cementum attachment sites.	Carbon	107-113	programmed cell death 1	Homo sapiens	37-40
20541802-9	2010	Chemically and biochemically the cir-PDL adjacent to bone and cementum was identified by relatively higher carbon and lower calcium including the localization of small leucine rich proteins responsible for maintaining soft-hard tissue cohesion, stiffness and hygroscopic nature of PDL-bone and PDL-cementum attachment sites.	Calcium	124-131	programmed cell death 1	Homo sapiens	37-40
19818771-1	2009	Our study aimed to establish the complete structure of the main dihydroxy conjugated triene issued from the lipoxygenation (soybean enzyme) of docosahexaenoic acid, named PDX, an isomer of protectin/neuroprotectin D1 (PD1/NPD1) described by Bazan and Serhan.	TRIETHYLENETETRAMINE	85-91	programmed cell death 1	Homo sapiens	218-221
20066438-6	2010	The frequency of GCG(C) haplotype of PD1 containing -606G allele was significantly higher in SSPE patients than in controls both in Japanese and in Filipinos.	gallocatechin gallate	17-20	programmed cell death 1	Homo sapiens	37-40
19919182-6	2010	In addition, we also attempted crystallization with another peptide ligand (PD1) where the residue at anchor position P(-3) is a tyrosine.	Tyrosine	129-137	programmed cell death 1	Homo sapiens	76-79
20826917-12	2010	CONCLUSIONS: Increased number of PD-1+ tumor-infiltrating lymphocytes is associated with significantly improved DSS in FL and may be useful to predict its heterogeneous clinical behavior.	dss	112-115	programmed cell death 1	Homo sapiens	33-37
20718345-2	2009	METHODS: Stick the PD-1 protein on the surface of CM5 sensor chip by the method of Ammine coupling after being preconsentrated.	ammine	83-89	programmed cell death 1	Homo sapiens	19-23
19818771-1	2009	Our study aimed to establish the complete structure of the main dihydroxy conjugated triene issued from the lipoxygenation (soybean enzyme) of docosahexaenoic acid, named PDX, an isomer of protectin/neuroprotectin D1 (PD1/NPD1) described by Bazan and Serhan.	Docosahexaenoic Acids	143-163	programmed cell death 1	Homo sapiens	218-221
19818771-1	2009	Our study aimed to establish the complete structure of the main dihydroxy conjugated triene issued from the lipoxygenation (soybean enzyme) of docosahexaenoic acid, named PDX, an isomer of protectin/neuroprotectin D1 (PD1/NPD1) described by Bazan and Serhan.	10-propargyl-10-deazaaminopterin	171-174	programmed cell death 1	Homo sapiens	218-221
19729077-3	2009	MATERIALS AND METHODS: Western blotting was used to examine the effect of apigenin (10-40 microM) on the LPS- and nicotine-induced expression of cyclooxygenase-2 (COX-2), inducible nitric oxide synthase (iNOS), and heme oxygenase-1 (HO-1), as well as the phosphorylation of mitogen-activated protein kinases (MAPKs), in hPDL cells.	Nicotine	114-122	programmed cell death 1	Homo sapiens	320-324
19729077-5	2009	RESULTS: Incubation of hPDL cells with apigenin decreased LPS- and nicotine-induced HO-1 protein expression and activity.	Nicotine	67-75	programmed cell death 1	Homo sapiens	23-27
19729077-6	2009	Apigenin significantly inhibited the nicotine- and LPS-induced production of NO, PGE2, IL-1beta, TNF-alpha, IL-6, and IL-12, and the upregulation of iNOS and COX-2 in hPDL cells.	Nicotine	37-45	programmed cell death 1	Homo sapiens	167-171
19564339-2	2009	In this study, we show that high expression of PD-1 correlates with increased ex vivo spontaneous and CD95/Fas-induced apoptosis, particularly in the "effector-memory" CD8(+) T cell population from HIV(+) donors.	ammonium ferrous sulfate	107-110	programmed cell death 1	Homo sapiens	47-51
19651643-7	2009	The mechanisms by which PD-1 blockade mediated immune enhancement included direct augmentation of melanoma antigen-specific CTL proliferation, heightening their resistance to inhibition by Treg and direct limitation of the inhibitory ability of Treg.	treg	189-193	programmed cell death 1	Homo sapiens	24-28
19651643-7	2009	The mechanisms by which PD-1 blockade mediated immune enhancement included direct augmentation of melanoma antigen-specific CTL proliferation, heightening their resistance to inhibition by Treg and direct limitation of the inhibitory ability of Treg.	treg	245-249	programmed cell death 1	Homo sapiens	24-28
19606370-2	2009	hPDL cells were cultured and treated with: (1) 500 ng/ml of rhBMP-7, (2) 10 mg of DFDBA or PepGen P-15 and (3) their combination.	rhbmp-7	60-67	programmed cell death 1	Homo sapiens	0-4
19606370-2	2009	hPDL cells were cultured and treated with: (1) 500 ng/ml of rhBMP-7, (2) 10 mg of DFDBA or PepGen P-15 and (3) their combination.	dfdba	82-87	programmed cell death 1	Homo sapiens	0-4
19564339-8	2009	Contrary to CD57, high expression of PD-1 was characterized by translocation of PD-1 into the area of CD95/Fas-capping, an early necessary step of CD95/Fas-induced apoptosis.	ammonium ferrous sulfate	107-110	programmed cell death 1	Homo sapiens	37-41
19564339-8	2009	Contrary to CD57, high expression of PD-1 was characterized by translocation of PD-1 into the area of CD95/Fas-capping, an early necessary step of CD95/Fas-induced apoptosis.	ammonium ferrous sulfate	107-110	programmed cell death 1	Homo sapiens	80-84
19539220-4	2009	The CMV disease group had a significantly higher mean fluorescein intensity of PD-1 in CD4+ (P &lt; .05) and CD8+ (P &lt; .05) lymphocytes at all time points studied.	Fluorescein	54-65	programmed cell death 1	Homo sapiens	79-83
18587005-3	2008	Results showed that 1) CSF PD1- T(reg) cells were significantly augmented in MS patients; 2) PD1- T(reg) cells were significantly increased in the peripheral blood of patients with stable disease (SMS) compared to those with acute (AMS) disease, and in patients responding to glatiramer acetate (COPA) compared to AMS- and COPA-unresponsive patients; and 3) PD1+ T(reg) cells were similar in CSF and peripheral blood of all groups analyzed.	Glatiramer Acetate	276-294	programmed cell death 1	Homo sapiens	93-96
18799583-7	2008	Nef-induced PD-1 upregulation requires its proline-rich motif and the activation of the downstream kinase p38.	Proline	43-50	programmed cell death 1	Homo sapiens	12-16
18587005-3	2008	Results showed that 1) CSF PD1- T(reg) cells were significantly augmented in MS patients; 2) PD1- T(reg) cells were significantly increased in the peripheral blood of patients with stable disease (SMS) compared to those with acute (AMS) disease, and in patients responding to glatiramer acetate (COPA) compared to AMS- and COPA-unresponsive patients; and 3) PD1+ T(reg) cells were similar in CSF and peripheral blood of all groups analyzed.	Glatiramer Acetate	276-294	programmed cell death 1	Homo sapiens	93-96
18771377-4	2008	METHODS: We used a short interfering RNA technique to inhibit estrogen receptor beta (ERbeta) expression in hPDL cells; the cells were cultured with a saturating concentration of 17beta-estradiol (10(7) M) for 48 hours.	Estradiol	179-195	programmed cell death 1	Homo sapiens	108-112
18771377-6	2008	RESULTS: Estradiol caused an increase in OPG expression and decreased RANKL expression in hPDL cells.	Estradiol	9-18	programmed cell death 1	Homo sapiens	90-94
18401354-5	2008	EMSA results confirmed that oligonucleotides with the PD1.3 G allele bind RUNX1 but not those with the A allele.	Oligonucleotides	28-44	programmed cell death 1	Homo sapiens	54-57
18500822-4	2008	The calculated potential decrease of approximately 140 mV can explain the inhibition of Y Z oxidation in the former complexes and in turn implies that the charge localization on P D1 upon formation of the core complex increases the P680 potential to the level necessary for water oxidation.	Water	274-279	programmed cell death 1	Homo sapiens	178-182
18261710-2	2008	DESIGN: We employed a short interfering RNA (siRNA) technique to inhibit ERbeta expression in hPDL cells; the cells were cultured with a saturating concentration of 17beta-estradiol (10(-7)M).	Estradiol	165-181	programmed cell death 1	Homo sapiens	94-98
18261710-4	2008	RESULTS: It was shown that estradiol significantly enhanced the ALP activity and the production of OCN in hPDL cells.	Estradiol	27-36	programmed cell death 1	Homo sapiens	106-110
18455515-1	2008	BACKGROUND &amp; AIMS: Recent studies have shown that programmed death 1 (PD-1) expression can impair virus-specific CD8 T-cell responses during chronic viral infection, including hepatitis B virus (HBV).	Adenosine Monophosphate	12-15	programmed cell death 1	Homo sapiens	74-78
18549878-1	2008	BACKGROUND &amp; AIMS: The immunoinhibitory receptor programmed death-1 (PD-1) is up-regulated on dysfunctional virus-specific CD8 T cells during chronic viral infections, and blockade of PD-1/PD-ligand (PD-L) interactions can restore their function.	Adenosine Monophosphate	12-15	programmed cell death 1	Homo sapiens	53-71
18549878-1	2008	BACKGROUND &amp; AIMS: The immunoinhibitory receptor programmed death-1 (PD-1) is up-regulated on dysfunctional virus-specific CD8 T cells during chronic viral infections, and blockade of PD-1/PD-ligand (PD-L) interactions can restore their function.	Adenosine Monophosphate	12-15	programmed cell death 1	Homo sapiens	73-77
18401354-6	2008	However, binding to PD1.3 G oligonucleotides was much lower than binding to positive control oligonucleotides.	Oligonucleotides	28-44	programmed cell death 1	Homo sapiens	20-23
17055291-1	2007	Resolvin D1 (RvD1) and protectin D1 (Neuroprotectin D1, PD1/NPD1) are newly identified anti-inflammatory lipid mediators biosynthesized from docosahexaenoic acid (DHA).	Docosahexaenoic Acids	141-161	programmed cell death 1	Homo sapiens	56-59
18253710-11	2008	Poly(I:C)-conditioned DCs promoted accumulation of phosphorylated SHP-2, the intracellular phosphatase mediating PD-1 inhibitory effects.	Poly I-C	0-9	programmed cell death 1	Homo sapiens	113-117
18275840-1	2008	The influence of the histidine axial ligand to the PD1 chlorophyll of photosystem II on the redox potential and spectroscopic properties of the primary electron donor, P680, was investigated in mutant oxygen-evolving photosystem II (PSII) complexes purified from the thermophilic cyanobacterium Thermosynechococcus elongatus.	Histidine	21-30	programmed cell death 1	Homo sapiens	51-54
17965005-3	2008	PCC6803 in which the axial ligand, D1-His198, of special pair chlorophyll PD1 was replaced with Gln and where D1-Thr179, which overlies monomeric chlorophyll ChlD1, was replaced with His.	Histidine	38-41	programmed cell death 1	Homo sapiens	74-77
18218840-2	2008	The objective of this study was to elucidate the potential bone-sparing effect of estrogen (17beta-estradiol, E(2)) via modulation of inflammatory cytokine production in human periodontal ligament (hPDL) cells.	Estradiol	92-108	programmed cell death 1	Homo sapiens	198-202
17376899-2	2007	Following infection, the majority (&gt;95%) of Gag-specific CD8 T cells expressed PD-1, and the level of PD-1 expression per cell increased over time.	Glycosaminoglycans	47-50	programmed cell death 1	Homo sapiens	82-86
17376899-2	2007	Following infection, the majority (&gt;95%) of Gag-specific CD8 T cells expressed PD-1, and the level of PD-1 expression per cell increased over time.	Glycosaminoglycans	47-50	programmed cell death 1	Homo sapiens	105-109
17141806-1	2007	We studied the interaction of hematopoietic cell kinase SH3 domain (HckSH3) with an artificial 12-residue proline-rich peptide PD1 (HSKYPLPPLPSL) identified as high affinity ligand (K(D)=0.2 muM).	Proline	106-113	programmed cell death 1	Homo sapiens	127-130
17141806-2	2007	PD1 shows an unusual ligand sequence for SH3 binding in type I orientation because it lacks the typical basic anchor residue at position P(-3), but instead has a tyrosine residue at this position.	Tyrosine	162-170	programmed cell death 1	Homo sapiens	0-3
17141806-4	2007	The solution structure of the HckSH3:PD1 complex, which is the first HckSH3 complex structure available, clearly reveals that the P(-3) tyrosine residue of PD1 does not take the position of the typical anchor residue but rather forms additional van der Waals interactions with the HckSH3 RT loop.	Tyrosine	136-144	programmed cell death 1	Homo sapiens	37-40
17141806-4	2007	The solution structure of the HckSH3:PD1 complex, which is the first HckSH3 complex structure available, clearly reveals that the P(-3) tyrosine residue of PD1 does not take the position of the typical anchor residue but rather forms additional van der Waals interactions with the HckSH3 RT loop.	Tyrosine	136-144	programmed cell death 1	Homo sapiens	156-159
17141806-5	2007	Instead, lysine at position P(-4) of PD1 substitutes the function of the P(-3) anchor residue.	Lysine	9-15	programmed cell death 1	Homo sapiens	37-40
17055291-1	2007	Resolvin D1 (RvD1) and protectin D1 (Neuroprotectin D1, PD1/NPD1) are newly identified anti-inflammatory lipid mediators biosynthesized from docosahexaenoic acid (DHA).	Docosahexaenoic Acids	163-166	programmed cell death 1	Homo sapiens	56-59
17176370-9	2006	RESULTS: The mean moxifloxacin concentration in the Dianeal PD1 1.36% solution remained &gt; or =90% of the initial concentration for 14 days at 4 degrees C, 7 days at 25 degrees C and 3 days at 37 degrees C. For Dianeal PD1 3.86% moxifloxacin concentrations remained &gt; or =90% for 14 days at 4 degrees C, 3 days at 25 degrees C and 12 h at 37 degrees C. CONCLUSIONS: Moxifloxacin shows sufficient stability in both PD bags for use in PD patients.	Moxifloxacin	18-30	programmed cell death 1	Homo sapiens	60-63
17076781-4	2006	MATERIAL AND METHODS: hPDL cells cultured in Dulbecco"s modified Eagles"s medium (DMEM) containing 10% fetal bovine serum (FBS) and antibiotics.	dulbecco"s modified eagles"s medium	45-80	programmed cell death 1	Homo sapiens	22-26
16018756-6	2005	RESULTS: The TD(50) for TCN after short-term treatment was 4 mg/ml for both hGF and hPDL.	Tetracycline	24-27	programmed cell death 1	Homo sapiens	84-88
16513785-5	2006	When D1-His(190) is protonated, corresponding to a thermally activated state, the calculated E(m)(Y(Z)) was +1216 mV, which is as high as the E(m) for P(D1/D2).	Histidine	8-11	programmed cell death 1	Homo sapiens	151-158
16511840-1	2006	Exposure to atypical antipsychotic drugs such as valproate increases the expression of chaperones that assist in the folding of proteins in the endoplasmic reticulum (ER) including calreticulin, GRP78/BiP, GRP94, and PD1.	Valproic Acid	49-58	programmed cell death 1	Homo sapiens	217-220
16696901-3	2006	In present study, the extracellular domain of human PD-1 with a carboxyl terminal His-tag (designated as sPD-1) was expressed as inclusion bodies in Escherichia coli.	Histidine	82-85	programmed cell death 1	Homo sapiens	52-56
16265694-8	2005	PD-1-positive SS salivary lymphocytes expressed IL-10 intracellularly upon PMA/ionomycin stimulation.	Tetradecanoylphorbol Acetate	75-78	programmed cell death 1	Homo sapiens	0-4
16265694-8	2005	PD-1-positive SS salivary lymphocytes expressed IL-10 intracellularly upon PMA/ionomycin stimulation.	Ionomycin	79-88	programmed cell death 1	Homo sapiens	0-4
10993345-4	2000	In addition, compound 1 also works as an effective ligand for the palladium-catalyzed reaction under conventional homogeneous conditions in an organic medium, in which the catalyst (Pd-1 complex) can be recovered by simple acid/base extraction and reused in the second reaction.	Palladium	66-75	programmed cell death 1	Homo sapiens	182-186
15378682-4	2004	FENOP3 gives rise to a PdL* catalyst of moderate enantioselectivity (42 % ee, R product).	fenop3	0-6	programmed cell death 1	Homo sapiens	23-27
15308630-4	2004	The precursor form of D1 (pD1) contains a C-terminal extension, which is removed by the protease CtpA to yield PSII complexes with oxygen evolution activity.	4-((1,4,8,11-tetraazacyclotetradec-1-yl)methyl)benzoic acid	97-101	programmed cell death 1	Homo sapiens	26-29
15308630-4	2004	The precursor form of D1 (pD1) contains a C-terminal extension, which is removed by the protease CtpA to yield PSII complexes with oxygen evolution activity.	Oxygen	131-137	programmed cell death 1	Homo sapiens	26-29
15240681-0	2004	SHP-1 and SHP-2 associate with immunoreceptor tyrosine-based switch motif of programmed death 1 upon primary human T cell stimulation, but only receptor ligation prevents T cell activation.	Tyrosine	46-54	programmed cell death 1	Homo sapiens	77-95
15240681-3	2004	The cytoplasmic tail of PD-1 contains two structural motifs, an ITIM and an immunoreceptor tyrosine-based switch motif (ITSM).	Tyrosine	91-99	programmed cell death 1	Homo sapiens	24-28
9141617-4	1997	We observed a time-dependent upregulation of hPD-1 mRNA and protein levels in Jurkat cells during phorbol ester (12-O-tetradecanoylphorbol 13-acetate, TPA)-induced differentiation.	Tetradecanoylphorbol Acetate	113-149	programmed cell death 1	Homo sapiens	45-50
10992810-9	2000	Changes of leptin concentration were significantly correlated with the changes of peritoneal glucose absorption at PD1.	Glucose	93-100	programmed cell death 1	Homo sapiens	115-118
9248694-6	1997	Now the tooth is kept bathed in an emesis basin filled with HBSS, which maintains the viability of the PDL for 30 minutes.	hbss	60-64	programmed cell death 1	Homo sapiens	103-106
9141617-4	1997	We observed a time-dependent upregulation of hPD-1 mRNA and protein levels in Jurkat cells during phorbol ester (12-O-tetradecanoylphorbol 13-acetate, TPA)-induced differentiation.	Tetradecanoylphorbol Acetate	151-154	programmed cell death 1	Homo sapiens	45-50
9141617-6	1997	Additionally, TPA stimulation of Jurkat cells induces tyrosine phosphorylation of hPD-1, putatively on its cytoplasmic tail signal transduction motif.	Tetradecanoylphorbol Acetate	14-17	programmed cell death 1	Homo sapiens	82-87
9141617-6	1997	Additionally, TPA stimulation of Jurkat cells induces tyrosine phosphorylation of hPD-1, putatively on its cytoplasmic tail signal transduction motif.	Tyrosine	54-62	programmed cell death 1	Homo sapiens	82-87
8784282-2	1996	OBJECTIVE: Our purpose was to investigate the use of the 585 nm flashlamp-pumped pulsed dye laser (585 nm PDL) for the treatment of pyogenic granulomas in terms of efficacy, advantages in technique, and side effects.	flashlamp	64-73	programmed cell death 1	Homo sapiens	106-109
8058761-2	1994	Posttranslational processing of the pD1 protein is essential to establish water oxidation activity of the PSII complex.	Water	74-79	programmed cell death 1	Homo sapiens	36-39
9141617-4	1997	We observed a time-dependent upregulation of hPD-1 mRNA and protein levels in Jurkat cells during phorbol ester (12-O-tetradecanoylphorbol 13-acetate, TPA)-induced differentiation.	Phorbol Esters	98-111	programmed cell death 1	Homo sapiens	45-50