PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
33076532-0	2020	Nonhistone Proteins HMGB1 and HMGB2 Differentially Modulate the Response of Human Embryonic Stem Cells and the Progenitor Cells to the Anticancer Drug Etoposide.	Etoposide	151-160	high mobility group box 1	Homo sapiens	20-25	
33975537-0	2021	Therapeutic administration of etoposide coincides with reduced systemic HMGB1 levels in macrophage activation syndrome.	Etoposide	30-39	high mobility group box 1	Homo sapiens	72-77	
35255342-6	2022	Additionally, 7 at 0.1 and 1.0 microM synergistically enhanced the cytotoxicity of etoposide against SBC-3 cells; compound 7 induced the release of DAMPs; the release of HMGB1, the secretion of ATP, and the exposure of CALR in the SBC-3 cells.	Etoposide	83-92	high mobility group box 1	Homo sapiens	170-175	
33076532-1	2020	HMGB1 and HMGB2 proteins are abundantly expressed in human embryonic stem cells (hESCs) and hESC-derived progenitor cells (neuroectodermal cells, hNECs), though their functional roles in pluripotency and the mechanisms underlying their differentiation in response to the anticancer drug etoposide remain to be elucidated.	Etoposide	287-296	high mobility group box 1	Homo sapiens	0-5	
33076532-3	2020	The objective of this work was to determine whether HMGB1/2 proteins could modulate the sensitivity of hESCs and hESC-derived progenitor cells (hNECs) to etoposide.	Etoposide	154-163	high mobility group box 1	Homo sapiens	52-59	
33076532-4	2020	We observed that HMGB1 KD knockdown (KD) and, to a lesser extent, HMGB2 KD enhanced the sensitivity of hESCs to etoposide.	Etoposide	112-121	high mobility group box 1	Homo sapiens	17-22	
33076532-5	2020	Enhanced accumulation of 53BP1 on telomeres was detected by confocal microscopy in both untreated and etoposide-treated HMGB1 KD hESCs and hNECs, indicating that the loss of HMGB1 could destabilize telomeres.	Etoposide	102-111	high mobility group box 1	Homo sapiens	120-125	
33076532-5	2020	Enhanced accumulation of 53BP1 on telomeres was detected by confocal microscopy in both untreated and etoposide-treated HMGB1 KD hESCs and hNECs, indicating that the loss of HMGB1 could destabilize telomeres.	Etoposide	102-111	high mobility group box 1	Homo sapiens	174-179	
33076532-10	2020	Collectively, we have demonstrated that HMGB1 or HMGB2 differentially modulate the impact of etoposide treatment on human embryonic stem cells and their progenitor cells, suggesting possible strategies for the enhancement of the efficacy of this anticancer drug.	Etoposide	93-102	high mobility group box 1	Homo sapiens	40-45	
29328447-2	2018	Western blot analysis revealed that vincristine (VCR), etoposide (ETO) and carboplatin (CBP) significantly increased the expression of HMGB1 in Weri-Rb-1 and Y79 cells compared with the untreated control (P<0.01).	Etoposide	55-64	high mobility group box 1	Homo sapiens	135-140	
30970518-4	2019	In two AML cell lines and primary AML cells from two patients, etoposide induced necroptosis via cIAP1/2 degradation when caspase activity was inhibited by Z-VAD-fmk, but treatment with extracellular HMGB1 prevented this necroptosis.	Etoposide	63-72	high mobility group box 1	Homo sapiens	200-205	
29328447-2	2018	Western blot analysis revealed that vincristine (VCR), etoposide (ETO) and carboplatin (CBP) significantly increased the expression of HMGB1 in Weri-Rb-1 and Y79 cells compared with the untreated control (P<0.01).	Etoposide	66-69	high mobility group box 1	Homo sapiens	135-140	
26397184-5	2015	Anticancer agents including doxorubicin, cisplatin and etoposide each induced HMGB1 upregulation, promoted cytosolic HMGB1 translocation and the elevation of autophagic activity in human NB cells.	Etoposide	55-64	high mobility group box 1	Homo sapiens	78-83	
26397184-5	2015	Anticancer agents including doxorubicin, cisplatin and etoposide each induced HMGB1 upregulation, promoted cytosolic HMGB1 translocation and the elevation of autophagic activity in human NB cells.	Etoposide	55-64	high mobility group box 1	Homo sapiens	117-122	
25247290-9	2015	Disease control coincided with supplementary etoposide therapy initiated to boost apoptotic cell death, when systemic HMGB1 levels drastically declined and the molecule emerged mainly in its oxidized, noninflammatory isoform.	Etoposide	45-54	high mobility group box 1	Homo sapiens	118-123