PMID-sentid	Pub_year	Sent_text	comp_official_name	comp_offset	protein_name	organism	prot_offset
2653437-12	1989	The fluorescence, but not the absorbance, of the enzyme-bound FAD was found to be highly dependent on the redox state of the C-terminal thiols.	Sulfhydryl Compounds	136-142	BRCA2 DNA repair associated	Homo sapiens	62-65
3730361-1	1986	6-Azidoflavins, 6-thiocyanatoflavins, and 6-mercaptoflavins at the lumiflavin, riboflavin, FMN, and FAD level were prepared from the corresponding 6-aminoflavins and some of their properties investigated.	6-azidoflavins	0-14	BRCA2 DNA repair associated	Homo sapiens	100-103
3730361-1	1986	6-Azidoflavins, 6-thiocyanatoflavins, and 6-mercaptoflavins at the lumiflavin, riboflavin, FMN, and FAD level were prepared from the corresponding 6-aminoflavins and some of their properties investigated.	6-thiocyanatoflavins	16-36	BRCA2 DNA repair associated	Homo sapiens	100-103
3730361-1	1986	6-Azidoflavins, 6-thiocyanatoflavins, and 6-mercaptoflavins at the lumiflavin, riboflavin, FMN, and FAD level were prepared from the corresponding 6-aminoflavins and some of their properties investigated.	6-mercaptoflavins	42-59	BRCA2 DNA repair associated	Homo sapiens	100-103
3730361-1	1986	6-Azidoflavins, 6-thiocyanatoflavins, and 6-mercaptoflavins at the lumiflavin, riboflavin, FMN, and FAD level were prepared from the corresponding 6-aminoflavins and some of their properties investigated.	6-aminoflavins	147-161	BRCA2 DNA repair associated	Homo sapiens	100-103
33462368-7	2021	Finally, among eight BRCA2-altered patients who received olaparib, progression-free survival trended longer in those with HRD scores above versus below the median (14.9 vs. 9.9 months).	olaparib	57-65	BRCA2 DNA repair associated	Homo sapiens	21-26
3086319-2	1986	Chromatography on high performance hydroxylapatite resolved the FAD-dependent reductase from holoreductase.	Durapatite	35-50	BRCA2 DNA repair associated	Homo sapiens	64-67
3086319-3	1986	The FAD dependence was matched by a low FAD content, with the ratio of FAD to FMN as low as 0.015.	Flavin Mononucleotide	78-81	BRCA2 DNA repair associated	Homo sapiens	4-7
3086319-3	1986	The FAD dependence was matched by a low FAD content, with the ratio of FAD to FMN as low as 0.015.	Flavin Mononucleotide	78-81	BRCA2 DNA repair associated	Homo sapiens	40-43
3086319-3	1986	The FAD dependence was matched by a low FAD content, with the ratio of FAD to FMN as low as 0.015.	Flavin Mononucleotide	78-81	BRCA2 DNA repair associated	Homo sapiens	40-43
3086319-9	1986	Thus, the FAD site must be the only point of electron uptake from NADPH.	NADP	66-71	BRCA2 DNA repair associated	Homo sapiens	10-13
7171534-7	1982	The conditions required to achieve maximal coupling of FAD to glutathione reductase (NAD(P)H2: glutathione oxidoreductase; EC 1.6.4.2) were therefore examined and found to be 15 min at 35 degrees by comparison with the 5-7 min incubation used by most workers.	nad(p)h2	85-93	BRCA2 DNA repair associated	Homo sapiens	55-58
3925989-1	1985	The mechanism of electron transfer from NADPH to cytochrome P-450 through FAD and FMN of the reductase is largely unknown.	NADP	40-45	BRCA2 DNA repair associated	Homo sapiens	74-77
3925989-3	1985	The resonance Raman spectra of the oxidized forms [FAD; FMN] and [FAD;-] were essentially identical, indicating similar binding interactions of these flavins with the protein.	Flavins	150-157	BRCA2 DNA repair associated	Homo sapiens	66-69
6807985-0	1982	Oxidation-reduction states of FMN and FAD in NADPH-cytochrome P-450 reductase during reduction by NADPH.	NADP	45-50	BRCA2 DNA repair associated	Homo sapiens	38-41
6807985-2	1982	In recent studies in this laboratory, a procedure was devised for selective removal of FMN from the purified enzyme, thus leading to the identification of FMN and FAD as the prosthetic groups of high and low reduction potential, respectively, and to the assignment of known reduction potentials to the individual flavin half-reactions.	4,6-dinitro-o-cresol	313-319	BRCA2 DNA repair associated	Homo sapiens	163-166
7372647-4	1980	Third, the rate of transformation of the C(4a)-peroxyflavin to oxidized FAD is substrate-dependent.	c(4a)-peroxyflavin	41-59	BRCA2 DNA repair associated	Homo sapiens	72-75
7358682-9	1980	These results apparently indicate that FAD in the enzyme functions as a prosthetic group, and that circular dichroic spectroscopy is a good measure of the bound form of flavin in the enzyme.	4,6-dinitro-o-cresol	169-175	BRCA2 DNA repair associated	Homo sapiens	39-42
1210194-0	1975	[The activity of glutathione-reductase and FAD-effect as indicators of the riboflavin level in experiments and in patients with phenylketonuria].	Riboflavin	75-85	BRCA2 DNA repair associated	Homo sapiens	43-46
34021944-4	2021	Patients with BRCA1/BRCA2 PVs display worse clinical outcomes but respond better to platinum-based chemotherapies and PARP inhibitors, a trait termed as "BRCAness".	Platinum	84-92	BRCA2 DNA repair associated	Homo sapiens	20-25
33341987-2	2021	Recently, the Poly(ADP-ribose) polymerase inhibitor (PARPi) olaparib has been approved for maintenance therapy after successful platinum-based chemotherapy in patients with germline mutations in BRCA1 and BRCA2.	olaparib	60-68	BRCA2 DNA repair associated	Homo sapiens	205-210
33524400-13	2021	In four patients, BRCA2 reversion mutations associated with platinum resistance.	Platinum	60-68	BRCA2 DNA repair associated	Homo sapiens	18-23
33990090-14	2021	Patients with a BRCA2 defect showed marked response to both PARP inhibitors and platinum-based chemotherapy.	Platinum	80-88	BRCA2 DNA repair associated	Homo sapiens	16-21
33966140-8	2021	BRCA2 high expression significantly correlated with response to olaparib, a PARP inhibitor, and inversely with cyclophosphamide in ER-positive/HER2-negative tumors, but not in TNBC.	olaparib	64-72	BRCA2 DNA repair associated	Homo sapiens	0-5
33966140-8	2021	BRCA2 high expression significantly correlated with response to olaparib, a PARP inhibitor, and inversely with cyclophosphamide in ER-positive/HER2-negative tumors, but not in TNBC.	Cyclophosphamide	111-127	BRCA2 DNA repair associated	Homo sapiens	0-5
33976553-10	2021	Multivariate analysis showed the TMB level was significantly associated with age (P=0.026), gender (P=0.041) and EGFR mutation status (P=0.015), and in EGFR-mutant patients we found a lower proportion of patients with mutated KRAS and BRCA2.	1,2,4,5-tetramethoxybenzene	33-36	BRCA2 DNA repair associated	Homo sapiens	235-240
33875706-6	2021	A total of 58 and 91 distinct VUS in BRCA1 and BRCA2 were identified in the KOHBRA study (comprising 278 and 453 patients, respectively).	kohbra	76-82	BRCA2 DNA repair associated	Homo sapiens	47-52
33743851-0	2021	Olaparib tablets as maintenance therapy in patients with platinum-sensitive relapsed ovarian cancer and a BRCA1/2 mutation (SOLO2/ENGOT-Ov21): a final analysis of a double-blind, randomised, placebo-controlled, phase 3 trial.	olaparib	0-8	BRCA2 DNA repair associated	Homo sapiens	106-113
33743851-1	2021	BACKGROUND: Olaparib, a poly (ADP-ribose) polymerase (PARP) inhibitor, has previously been shown to extend progression-free survival versus placebo when given to patients with relapsed high-grade serous or endometrioid ovarian cancer who were platinum sensitive and who had a BRCA1 or BRCA2 (BRCA1/2) mutation, as part of the SOLO2/ENGOT-Ov21 trial.	olaparib	12-20	BRCA2 DNA repair associated	Homo sapiens	285-290
33743851-1	2021	BACKGROUND: Olaparib, a poly (ADP-ribose) polymerase (PARP) inhibitor, has previously been shown to extend progression-free survival versus placebo when given to patients with relapsed high-grade serous or endometrioid ovarian cancer who were platinum sensitive and who had a BRCA1 or BRCA2 (BRCA1/2) mutation, as part of the SOLO2/ENGOT-Ov21 trial.	olaparib	12-20	BRCA2 DNA repair associated	Homo sapiens	292-299
33743851-20	2021	INTERPRETATION: Olaparib provided a median overall survival benefit of 12 9 months compared with placebo in patients with platinum-sensitive, relapsed ovarian cancer and a BRCA1/2 mutation.	olaparib	16-24	BRCA2 DNA repair associated	Homo sapiens	172-179
33970096-0	2021	Rapid Response of a BRCA2/TP53/PTEN-Deleted Metastatic Uterine Leiomyosarcoma to Olaparib: A Case Report.	olaparib	81-89	BRCA2 DNA repair associated	Homo sapiens	20-25
33922657-3	2021	In this study, we demonstrated that curcumin, a plant polyphenol, sensitizes BRCA2-deficient cells to CPT-11 by impairing RAD52 recombinase in MCF7 cells.	Curcumin	36-44	BRCA2 DNA repair associated	Homo sapiens	77-82
33922657-3	2021	In this study, we demonstrated that curcumin, a plant polyphenol, sensitizes BRCA2-deficient cells to CPT-11 by impairing RAD52 recombinase in MCF7 cells.	Polyphenols	54-64	BRCA2 DNA repair associated	Homo sapiens	77-82
33922657-3	2021	In this study, we demonstrated that curcumin, a plant polyphenol, sensitizes BRCA2-deficient cells to CPT-11 by impairing RAD52 recombinase in MCF7 cells.	Irinotecan	102-108	BRCA2 DNA repair associated	Homo sapiens	77-82
33922657-6	2021	In vivo, xenograft model studies showed that curcumin combined with CPT-11 reduced the growth of BRCA2-knockout MCF7 tumors but not MCF7 tumors.	Curcumin	45-53	BRCA2 DNA repair associated	Homo sapiens	97-102
33922657-6	2021	In vivo, xenograft model studies showed that curcumin combined with CPT-11 reduced the growth of BRCA2-knockout MCF7 tumors but not MCF7 tumors.	Irinotecan	68-74	BRCA2 DNA repair associated	Homo sapiens	97-102
33922657-7	2021	In conclusion, our data indicate that curcumin, which has RAD52 inhibitor activity, is a promising candidate for sensitizing BRCA2-deficient cells to DNA damage-based cancer therapies.	Curcumin	38-46	BRCA2 DNA repair associated	Homo sapiens	125-130
33968986-0	2021	Long Non-coding RNA DLEU2L Targets miR-210-3p to Suppress Gemcitabine Resistance in Pancreatic Cancer Cells via BRCA2 Regulation.	gemcitabine	58-69	BRCA2 DNA repair associated	Homo sapiens	112-117
33996534-0	2021	The Efficacy of Combined Cisplatin and Nanoparticle Albumin-Bound Paclitaxel in a Stage IV Pancreatic Squamous Cell Carcinoma Patient With a Somatic BRCA2 Mutation: A Case Report.	Cisplatin	25-34	BRCA2 DNA repair associated	Homo sapiens	149-154
33996534-0	2021	The Efficacy of Combined Cisplatin and Nanoparticle Albumin-Bound Paclitaxel in a Stage IV Pancreatic Squamous Cell Carcinoma Patient With a Somatic BRCA2 Mutation: A Case Report.	Paclitaxel	66-76	BRCA2 DNA repair associated	Homo sapiens	149-154
33904759-11	2021	Patients with mCRPC harboring genomic defects in crucial HR genes either in the germline or somatic, especially BRCA2 and ATM, might experience superior outcomes to platinum-based chemotherapy, compared with those harboring CDK12 defect.	Platinum	165-173	BRCA2 DNA repair associated	Homo sapiens	112-117
33893161-3	2021	The POLO trial demonstrated a benefit of maintenance olaparib compared to placebo in patients with germline pathogenic variants in BRCA1 or BRCA2.	olaparib	53-61	BRCA2 DNA repair associated	Homo sapiens	140-145
33827356-7	2021	We also recommend that olaparib or rucaparib be considered relatively early in the treatment sequence in metastatic castration-resistant prostate cancer patients with BRCA1 or BRCA2 mutations.	olaparib	23-31	BRCA2 DNA repair associated	Homo sapiens	176-181
33084436-7	2021	CONCLUSION: Administration of rAMH in the peri-transplant period caused downregulation of BRCA1, but not of BRCA2 expression, in human ovarian cortex.	(R)-alpha-Methylhistamine	30-34	BRCA2 DNA repair associated	Homo sapiens	108-113
33868464-0	2021	Olaparib in hormone receptor-positive, HER2-negative metastatic breast cancer with a somatic BRCA2 mutation.	olaparib	0-8	BRCA2 DNA repair associated	Homo sapiens	93-98
33868464-2	2021	This case report describes a 63-year-old postmenopausal woman with somatic BRCA2-mutated mBC who responded to olaparib treatment following multiple prior lines of therapy.	olaparib	110-118	BRCA2 DNA repair associated	Homo sapiens	75-80
33868464-9	2021	Biopsy of recurrent lesions revealed a novel BRCA2 mutation, E3152del (c.9455_9457delAGG), predicted to restore the open reading frame and presumably the mechanism of resistance to olaparib.	olaparib	181-189	BRCA2 DNA repair associated	Homo sapiens	45-50
33868464-11	2021	This case demonstrated a clinical response with olaparib as a later-line therapy for HR+, HER2- mBC with a somatic BRCA2 mutation.	olaparib	48-56	BRCA2 DNA repair associated	Homo sapiens	115-120
33634895-5	2021	DDX5 associates with DNA-RNA hybrids that form in the vicinity of DSBs, and this association is enhanced by BRCA2.	1,2-di-(4-sulfamidophenyl)-4-butylpyrazolidine-3,5-dione	66-70	BRCA2 DNA repair associated	Homo sapiens	108-113
33443393-0	2021	The Relationship Between GSTT1, GSTM1, GSTO1, GSTP1 and MTHFR Gene Polymorphisms and DNA Damage of BRCA1 and BRCA2 Genes in Arsenic-Exposed Workers.	Arsenic	124-131	BRCA2 DNA repair associated	Homo sapiens	109-114
33443393-5	2021	CONCLUSIONS: Our findings suggest that the DNA damage levels of BRCA1 and BRCA2 genes may modulate by genetic variations of GSTT1 and GSTO1 when individuals are exposed to carcinogens, such as arsenic.	Arsenic	193-200	BRCA2 DNA repair associated	Homo sapiens	74-79
33674744-7	2021	Polbeta small molecular inhibitors (Pamoic acid and NSC666719) were selectively toxic to BRCA2 deficient cells and associated with double-strand breaks (DSB) accumulation, cell cycle arrest and increased apoptosis.	pamoic acid	36-47	BRCA2 DNA repair associated	Homo sapiens	89-94
33653301-15	2021	CONCLUSIONS: According to the evolution model, DNA damage response (DDR)-related ATM or BRCA2 somatic mutations are promising biomarkers for assessing the response of stage III CRC patients to oxaliplatin-based chemotherapy.	Oxaliplatin	193-204	BRCA2 DNA repair associated	Homo sapiens	88-93
32885350-7	2021	An unresectable PDAC patient with BRCA2-mutant disease was successfully treated by conversion surgery using platinum-based neoadjuvant chemotherapy.	Platinum	108-116	BRCA2 DNA repair associated	Homo sapiens	34-39
33334906-7	2021	BRCA2-null prostate cancer cell lines had increased SRC phosphorylation and higher sensitivity to SRC inhibitors (eg, dasatinib, bosutinib, and saracatinib) relative to wild-type cells.	Dasatinib	118-127	BRCA2 DNA repair associated	Homo sapiens	0-5
33334906-7	2021	BRCA2-null prostate cancer cell lines had increased SRC phosphorylation and higher sensitivity to SRC inhibitors (eg, dasatinib, bosutinib, and saracatinib) relative to wild-type cells.	bosutinib	129-138	BRCA2 DNA repair associated	Homo sapiens	0-5
33334906-7	2021	BRCA2-null prostate cancer cell lines had increased SRC phosphorylation and higher sensitivity to SRC inhibitors (eg, dasatinib, bosutinib, and saracatinib) relative to wild-type cells.	saracatinib	144-155	BRCA2 DNA repair associated	Homo sapiens	0-5
33334906-9	2021	Inhibition of SRC signaling by dasatinib augmented DNA damage in BRCA2-null prostate cancer cells.	Dasatinib	31-40	BRCA2 DNA repair associated	Homo sapiens	65-70
33473169-11	2021	BRCA2 mutations were correlated with neratinib and tucatinib response, and high expression of ATM, BRCA2, and BRCA1 were associated with neratinib resistance.	neratinib	37-46	BRCA2 DNA repair associated	Homo sapiens	0-5
33473169-11	2021	BRCA2 mutations were correlated with neratinib and tucatinib response, and high expression of ATM, BRCA2, and BRCA1 were associated with neratinib resistance.	Irbinitinib	51-60	BRCA2 DNA repair associated	Homo sapiens	0-5
33473169-11	2021	BRCA2 mutations were correlated with neratinib and tucatinib response, and high expression of ATM, BRCA2, and BRCA1 were associated with neratinib resistance.	neratinib	137-146	BRCA2 DNA repair associated	Homo sapiens	99-104
33662256-4	2021	In cells, CAM833 diminishes formation of damage-induced RAD51 nuclear foci; inhibits RAD51 molecular clustering, suppressing extended RAD51 filament assembly; potentiates cytotoxicity by ionizing radiation, augmenting 4N cell-cycle arrest and apoptotic cell death and works with poly-ADP ribose polymerase (PARP)1 inhibitors to suppress growth in BRCA2-wildtype cells.	cam833	10-16	BRCA2 DNA repair associated	Homo sapiens	347-352
33619228-2	2021	Similar to HBOC genes, BRCA1 and BRCA2, FANCJ is critical for processing DNA inter-strand crosslinks (ICL) induced by chemotherapeutics, such as cisplatin.	Cisplatin	145-154	BRCA2 DNA repair associated	Homo sapiens	33-38
33784003-4	2021	Here, we found that GSK2578215A, a high-selective and effective leucine-rich repeat kinase 2 (LRRK2) inhibitor, or LRRK2 depletion suppresses HR preventing the recruitment of RAD51 to DNA damage sites through disruption of the interaction of RAD51 and BRCA2.	GSK2578215A	20-31	BRCA2 DNA repair associated	Homo sapiens	252-257
33662256-1	2021	BRCA2 controls RAD51 recombinase during homologous DNA recombination (HDR) through eight evolutionarily conserved BRC repeats, which individually engage RAD51 via the motif Phe-x-x-Ala.	phe-x-x-ala	173-184	BRCA2 DNA repair associated	Homo sapiens	0-5
33375991-14	2021	After adjusting for BRCA mutations, TP53 mutations are associated with platinum sensitivity, and this effect is not dependent on TP53 mutation type.	Platinum	71-79	BRCA2 DNA repair associated	Homo sapiens	20-24
33619265-5	2021	Two unique BRCA2 somatic alterations (p.N255fs and p.D252fs) were identified upon resistance to PARP inhibitor and platinum treatment, respectively.	Platinum	115-123	BRCA2 DNA repair associated	Homo sapiens	11-16
33608381-0	2021	Treatment-emergent neuroendocrine prostate cancer with a germline BRCA2 mutation: identification of a candidate reversion mutation associated with platinum/PARP-inhibitor resistance.	Platinum	147-155	BRCA2 DNA repair associated	Homo sapiens	66-71
33407459-6	2021	Due to the novel nonsynonymous BRCA2 point mutation, we decided to change the strategy by administering olaparib.	olaparib	104-112	BRCA2 DNA repair associated	Homo sapiens	31-36
33536335-3	2021	We found that inactivation of Ataxia Telangiectasia- and Rad3-related (ATR), CHK1, BRCA2, and RPA1 overcome chemoresistance to camptothecin (CPT) in SLFN11-KO cells.	Camptothecin	127-139	BRCA2 DNA repair associated	Homo sapiens	83-88
33091613-4	2021	BRCA2 deficient PDAC cells exhibited increased DSBs and enhanced sensitivity to Cyst(e)inase.	dsbs	47-51	BRCA2 DNA repair associated	Homo sapiens	0-5
32965028-7	2021	DDR deficient patients showed beneficial biochemical response to carboplatin, largely driven by all BRCA2mut patients having >50% prostate specific antigen (PSA) decline and objective radiographic response.	Carboplatin	65-76	BRCA2 DNA repair associated	Homo sapiens	100-105
32965028-13	2021	In this cohort, only BRCA2mut patients treated with platinum first (n = 4), responded to both agents.	Platinum	52-60	BRCA2 DNA repair associated	Homo sapiens	21-26
32965028-14	2021	We confirm that BRCA2 inactivation is associated with meaningful responses to carboplatin, suggesting a role for both PARPi and platinum-based chemotherapy in pre-selected mCRPC patients.	Carboplatin	78-89	BRCA2 DNA repair associated	Homo sapiens	16-21
32965028-14	2021	We confirm that BRCA2 inactivation is associated with meaningful responses to carboplatin, suggesting a role for both PARPi and platinum-based chemotherapy in pre-selected mCRPC patients.	Platinum	128-136	BRCA2 DNA repair associated	Homo sapiens	16-21
33250205-0	2021	Olaparib maintenance therapy in patients with newly diagnosed advanced ovarian cancer and a BRCA1 and/or BRCA2 mutation: SOLO1 China cohort.	olaparib	0-8	BRCA2 DNA repair associated	Homo sapiens	105-110
33091561-2	2021	Tumours from these patients tend to lose both copies of the wild type BRCA gene, which makes them exquisitely sensitive to platinum drugs and PARP inhibitors (PARPi), treatments of choice in these disease settings.	Platinum	123-131	BRCA2 DNA repair associated	Homo sapiens	70-74
33271260-6	2021	Further experiments found that DHC-1 induced DNA double-strand damage in BRCA2-/- Capan-1 cells, which was demonstrated by accumulation of gamma-H2AX foci.	gamma-h2ax	139-149	BRCA2 DNA repair associated	Homo sapiens	73-78
33633982-7	2021	BRCA1 carriers tended to exhibit the triple-negative phenotype with a more benign shape and margin (P=0.006 and 0.019), whereas BRCA2 mutations were associated with the luminal phenotype and more malignant features.	Phenobarbital	169-176	BRCA2 DNA repair associated	Homo sapiens	128-133
32979005-4	2021	Unexpectedly, MM2-48 covalently targets a functional cysteine in BCCIP, a BRCA2 and CDKN1A-interacting protein, and significantly inhibits DNA damage repair.	Cysteine	53-61	BRCA2 DNA repair associated	Homo sapiens	74-79
33376347-0	2020	Niraparib as Maintenance Therapy in Germline ATM-mutated and Somatic BRCA2-mutated Ovarian Cancer with Brain Metastases: A Case Report and Literature Review.	niraparib	0-9	BRCA2 DNA repair associated	Homo sapiens	69-74
33426488-0	2021	Pulmonary metastasis secondary to abiraterone-resistant prostate cancer with homozygous deletions of BRCA2: First Japanese case.	abiraterone	34-45	BRCA2 DNA repair associated	Homo sapiens	101-106
32367009-12	2020	Also rucaparib showed a benefit in terms of PSA response rate and ORR in patients with BRCA2 and BRCA1 mutation in a phase-II study.	rucaparib	5-14	BRCA2 DNA repair associated	Homo sapiens	87-92
33044685-8	2020	The PROFOUND phase III trial, comparing olaparib with enzalutamide/abiraterone therapy, revealed increased radiological progression-free survival (rPFS) and overall survival (OS) among patients with metastatic castration-resistant prostate cancer (mCRPC) with BRCA1, BRCA2 or ATM mutations.	olaparib	40-48	BRCA2 DNA repair associated	Homo sapiens	267-272
33017331-0	2020	BRCA2 Reversion Mutation Identified by Liquid Biopsy After Durable Response to FOLFIRINOX in BRCA2-Associated Pancreatic Cancer.	folfirinox	79-89	BRCA2 DNA repair associated	Homo sapiens	0-5
33017331-0	2020	BRCA2 Reversion Mutation Identified by Liquid Biopsy After Durable Response to FOLFIRINOX in BRCA2-Associated Pancreatic Cancer.	folfirinox	79-89	BRCA2 DNA repair associated	Homo sapiens	93-98
33194641-8	2020	In addition, the metastatic ovarian cancer in the proband"s half-sister harboring the same BRCA2 germline mutation also responded well to platinum chemotherapy.	Platinum	138-146	BRCA2 DNA repair associated	Homo sapiens	91-96
32749942-1	2020	PURPOSE: In SOLO1, maintenance olaparib (300 mg twice daily) significantly improved progression-free survival (PFS) for patients with newly diagnosed BRCA1- and/or BRCA2-mutated advanced ovarian cancer compared with placebo (hazard ratio [HR], 0.30; 95% CI, 0.23 to 0.41; median not reached v 13.8 months).	olaparib	31-39	BRCA2 DNA repair associated	Homo sapiens	164-169
32881420-2	2020	After the FDA approvals of the poly ADP ribose polymerase (PARP) inhibitors, olaparib and talazoparib, for treatment of metastatic breast cancer, carrying germline mutations in BRCA1 and BRCA2 genes, the genetic testing result has become critical in their care.	olaparib	77-85	BRCA2 DNA repair associated	Homo sapiens	187-192
32881420-2	2020	After the FDA approvals of the poly ADP ribose polymerase (PARP) inhibitors, olaparib and talazoparib, for treatment of metastatic breast cancer, carrying germline mutations in BRCA1 and BRCA2 genes, the genetic testing result has become critical in their care.	talazoparib	90-101	BRCA2 DNA repair associated	Homo sapiens	187-192
33240400-0	2020	Olaparib is effective for recurrent urothelial carcinoma with BRCA2 pathogenic germline mutation: first report on olaparib response in recurrent UC.	olaparib	0-8	BRCA2 DNA repair associated	Homo sapiens	62-67
33152708-1	2020	BACKGROUND: Maintenance therapy with the PARP inhibitor olaparib for metastatic pancreatic cancer (MPC) with a germline BRCA1 or BRCA2 mutation has been shown to be effective.	olaparib	56-64	BRCA2 DNA repair associated	Homo sapiens	129-134
32816949-1	2020	PURPOSE: Pancreatic ductal adenocarcinoma (PDAC) arising in patients with a germline BRCA1 or BRCA2 (gBRCA) mutation may be sensitive to platinums and poly(adenosine diphosphate-ribose) polymerase inhibitors (PARPi).	Platinum	137-146	BRCA2 DNA repair associated	Homo sapiens	94-99
32816949-1	2020	PURPOSE: Pancreatic ductal adenocarcinoma (PDAC) arising in patients with a germline BRCA1 or BRCA2 (gBRCA) mutation may be sensitive to platinums and poly(adenosine diphosphate-ribose) polymerase inhibitors (PARPi).	Adenosine	156-165	BRCA2 DNA repair associated	Homo sapiens	94-99
32816949-5	2020	RESULTS: We found that biallelic inactivation of BRCA1/BRCA2 is associated with genomic hallmarks of HRD and required for cisplatin and talazoparib (PARPi) sensitivity.	Cisplatin	122-131	BRCA2 DNA repair associated	Homo sapiens	55-60
32816949-5	2020	RESULTS: We found that biallelic inactivation of BRCA1/BRCA2 is associated with genomic hallmarks of HRD and required for cisplatin and talazoparib (PARPi) sensitivity.	talazoparib	136-147	BRCA2 DNA repair associated	Homo sapiens	55-60
33426488-8	2021	We note in this case a heterogeneous response to abiraterone acetate may be related to the somatic BRCA2 deletions.	Abiraterone Acetate	49-68	BRCA2 DNA repair associated	Homo sapiens	99-104
33426488-9	2021	Conclusions: We present the first Japanese case of a metastatic abiraterone acetate-resistant castration-resistant prostate cancer accompanied by BRCA2 mutation.	Abiraterone Acetate	64-83	BRCA2 DNA repair associated	Homo sapiens	146-151
32844710-2	2020	This trial also demostrates that olaparib improves progression free survival (PFS), objective response rate (ORR), and time to pain progression in patients who harbor alterations in BRCA1, BRCA2, and ATM.	olaparib	33-41	BRCA2 DNA repair associated	Homo sapiens	189-194
32314163-3	2020	This study aimed to describe the pathologic complete response rate and long-term survival for patients with germline BRCA1 or BRCA2 mutation (gBRCAm) and borderline resectable pancreatic cancer (BRPC) treated with neoadjuvant FOLFIRINOX.	folfirinox	226-236	BRCA2 DNA repair associated	Homo sapiens	126-131
32699032-1	2020	Reversion mutations in BRCA1 or BRCA2 are associated with resistance to PARP inhibitors and platinum.	Platinum	92-100	BRCA2 DNA repair associated	Homo sapiens	32-37
32532747-0	2020	Phase I trial of the poly(ADP-ribose) polymerase (PARP) inhibitor olaparib and AKT inhibitor capivasertib in patients with BRCA1/2 and non-BRCA1/2 mutant cancers.	olaparib	66-74	BRCA2 DNA repair associated	Homo sapiens	123-130
32532747-0	2020	Phase I trial of the poly(ADP-ribose) polymerase (PARP) inhibitor olaparib and AKT inhibitor capivasertib in patients with BRCA1/2 and non-BRCA1/2 mutant cancers.	capivasertib	93-105	BRCA2 DNA repair associated	Homo sapiens	123-130
32532747-0	2020	Phase I trial of the poly(ADP-ribose) polymerase (PARP) inhibitor olaparib and AKT inhibitor capivasertib in patients with BRCA1/2 and non-BRCA1/2 mutant cancers.	capivasertib	93-105	BRCA2 DNA repair associated	Homo sapiens	139-146
32859641-8	2020	In contrast, UEAs harbored mutations in HRAS, PIK3CA, and BRCA2.	ueas	13-17	BRCA2 DNA repair associated	Homo sapiens	58-63
32675286-9	2020	Cells lacking the BRCA2 were sensitive to 5-FU in the presence of ATRi.	Fluorouracil	42-46	BRCA2 DNA repair associated	Homo sapiens	18-23
32861273-1	2020	BACKGROUND: BRCA1 or BRCA2-mutated breast cancers are sensitive to poly(ADP-ribose) polymerase (PARP) inhibitors and platinum agents owing to deficiency in homologous recombination repair of DNA damage.	Platinum	117-125	BRCA2 DNA repair associated	Homo sapiens	21-26
32957395-0	2020	Olaparib combined with immunotherapy for treating a patient with liver cancer carrying BRCA2 germline mutation: A case report.	olaparib	0-8	BRCA2 DNA repair associated	Homo sapiens	87-92
32771088-2	2020	We aimed to assess the safety and activity of olaparib in combination with the PD-L1-inhibitor, durvalumab, in patients with germline BRCA1-mutated or BRCA2-mutated metastatic breast cancer.	olaparib	46-54	BRCA2 DNA repair associated	Homo sapiens	151-156
32789480-1	2020	Importance: The value of platinum-based adjuvant chemotherapy in patients with triple-negative breast cancer (TNBC) remains controversial, as does whether BRCA1 and BRCA2 (BRCA1/2) germline variants are associated with platinum treatment sensitivity.	Platinum	219-227	BRCA2 DNA repair associated	Homo sapiens	165-170
32789480-1	2020	Importance: The value of platinum-based adjuvant chemotherapy in patients with triple-negative breast cancer (TNBC) remains controversial, as does whether BRCA1 and BRCA2 (BRCA1/2) germline variants are associated with platinum treatment sensitivity.	Platinum	219-227	BRCA2 DNA repair associated	Homo sapiens	172-179
32729618-6	2020	After calculated the TMB in PEG3 mutant and PEG3 wild-type groups, we found the TMB value was significantly higher in PEG3 mutant samples than that in PEG3 wild-type samples (p = 5.6e-07), which was independent of the confounding factors including age, stage, mutations of BRCA1, BRCA2 and POLE (odd ratio, 0.45; 95% CI, 0.20-0.98; p = 0.044).	1,2,4,5-tetramethoxybenzene	80-83	BRCA2 DNA repair associated	Homo sapiens	280-285
32789480-14	2020	In the exploratory and hypothesis-generating subgroup analyses of PCb vs CEF-T, the HR for DFS was 0.44 (95% CI, 0.15-1.31; P = .14) in patients with the BRCA1/2 variant and 0.39 (95% CI, 0.15-0.99; P = .04) in those with the HRR variant.	pcb	66-69	BRCA2 DNA repair associated	Homo sapiens	154-161
32789480-14	2020	In the exploratory and hypothesis-generating subgroup analyses of PCb vs CEF-T, the HR for DFS was 0.44 (95% CI, 0.15-1.31; P = .14) in patients with the BRCA1/2 variant and 0.39 (95% CI, 0.15-0.99; P = .04) in those with the HRR variant.	cef-t	73-78	BRCA2 DNA repair associated	Homo sapiens	154-161
32825620-10	2020	Interestingly, deltaNp73 induction also resulted in inhibition of BRCA1 and BRCA2 expression following DNA damage.	deltanp73	15-24	BRCA2 DNA repair associated	Homo sapiens	76-81
32884538-4	2020	Germline mutations in the BRCA1 and BRCA2 genes promote the incapacity of tumor cells to recover from DNA-accumulated damage caused by cytotoxic drugs, like platinum agents, and, most recently, through a diverse process by poly(adenosine diphosphate-ribose) polymerase inhibitor (PARPi).	Platinum	157-165	BRCA2 DNA repair associated	Homo sapiens	36-41
32497289-0	2020	Clinical outcome and toxicity from taxanes in breast cancer patients with BRCA1 and BRCA2 pathogenic germline mutations.	Taxoids	35-42	BRCA2 DNA repair associated	Homo sapiens	84-89
32497289-2	2020	Because BRCA1 and BRCA2 proteins play a role in DNA damage repair, we postulated that taxane-related toxicity is potentially higher and clinical outcome in different in patients with BRCA pathogenic variants (PV).	taxane	86-92	BRCA2 DNA repair associated	Homo sapiens	18-23
32817374-6	2020	Increasing 5hmC abundance induced the degradation of stalled RFs in KB2P1.21 and human cancer cells by recruiting the base excision repair-associated apurinic/apyrimidinic endonuclease APE1, independent of the BRCA2 status.	5hmc	11-15	BRCA2 DNA repair associated	Homo sapiens	210-215
32884538-4	2020	Germline mutations in the BRCA1 and BRCA2 genes promote the incapacity of tumor cells to recover from DNA-accumulated damage caused by cytotoxic drugs, like platinum agents, and, most recently, through a diverse process by poly(adenosine diphosphate-ribose) polymerase inhibitor (PARPi).	Adenosine	228-237	BRCA2 DNA repair associated	Homo sapiens	36-41
32044806-5	2020	In the setting of advanced disease, predictive biomarkers, such as the presence of DNA repair deficiency mediated by BRCA2 loss or mismatch repair gene defects, may suggest the utility of poly-ADP ribosylase inhibition or immune checkpoint blockade.	Adenosine Diphosphate	188-196	BRCA2 DNA repair associated	Homo sapiens	117-122
32711554-10	2020	CONCLUSIONS: The digitalMLPA is a reliable method to detect a BRCA1- and BRCA2-like pattern on clinical samples and predicts platinum-based chemotherapy benefit in both triple-negative and luminal-type BC.	digitalmlpa	17-28	BRCA2 DNA repair associated	Homo sapiens	73-78
32711554-10	2020	CONCLUSIONS: The digitalMLPA is a reliable method to detect a BRCA1- and BRCA2-like pattern on clinical samples and predicts platinum-based chemotherapy benefit in both triple-negative and luminal-type BC.	Platinum	125-133	BRCA2 DNA repair associated	Homo sapiens	73-78
32454976-0	2020	Long-term response to Olaparib in carcinomatous meningitis of a BRCA2 mutated ovarian cancer: A case report.	olaparib	22-30	BRCA2 DNA repair associated	Homo sapiens	64-69
32468256-2	2020	We reported recently a BRCA2 mutant high grade serous ovarian cancer (HGSOC) patient with acquired resistance to the PARP-1 olaparib due to a STV detected by next generation tumor sequencing (NGTS).	olaparib	124-132	BRCA2 DNA repair associated	Homo sapiens	23-28
32638521-6	2020	OxLDL was found to induce significant reactive oxygen species (ROS) production in BRCA2-silenced ECs.	Reactive Oxygen Species	38-61	BRCA2 DNA repair associated	Homo sapiens	82-87
32638521-6	2020	OxLDL was found to induce significant reactive oxygen species (ROS) production in BRCA2-silenced ECs.	Reactive Oxygen Species	63-66	BRCA2 DNA repair associated	Homo sapiens	82-87
32638521-8	2020	Increased DSBs were associated with enhanced expression and activation of pro-apoptotic p53 and significant apoptosis in oxLDL-treated BRCA2-silenced ECs.	1,2-di-(4-sulfamidophenyl)-4-butylpyrazolidine-3,5-dione	10-14	BRCA2 DNA repair associated	Homo sapiens	135-140
32354836-4	2020	BRCA2 and RAD51 functions are also required to protect stalled replication forks from nucleolytic degradation during response to hydroxyurea (HU).	Hydroxyurea	129-140	BRCA2 DNA repair associated	Homo sapiens	0-5
32354836-4	2020	BRCA2 and RAD51 functions are also required to protect stalled replication forks from nucleolytic degradation during response to hydroxyurea (HU).	Hydroxyurea	142-144	BRCA2 DNA repair associated	Homo sapiens	0-5
32354836-7	2020	Cells carrying BRCA2 DBD mutations are sensitive to ICL-inducing agents but resistant to HU treatment consistent with relatively high HR repair in these cells.	Hydroxyurea	89-91	BRCA2 DNA repair associated	Homo sapiens	15-20
32071115-1	2020	PURPOSE: Prostate cancers with mutations in genes involved in homologous recombination (HR), most commonly BRCA2, respond favorably to PARP inhibition and platinum-based chemotherapy.	Platinum	155-163	BRCA2 DNA repair associated	Homo sapiens	107-112
32468256-3	2020	The aim of this study was to evaluate the versatility of the high-resolution melting analysis (HRMA) obtained by magnetic induction cycler (MIC) to monitor the BRCA2 status in formalin-fixed paraffin-embedded (FFPE) tissue samples of this patient and to compare the results obtained by NGTS.	Formaldehyde	176-184	BRCA2 DNA repair associated	Homo sapiens	160-165
32468256-3	2020	The aim of this study was to evaluate the versatility of the high-resolution melting analysis (HRMA) obtained by magnetic induction cycler (MIC) to monitor the BRCA2 status in formalin-fixed paraffin-embedded (FFPE) tissue samples of this patient and to compare the results obtained by NGTS.	Paraffin	191-199	BRCA2 DNA repair associated	Homo sapiens	160-165
32408326-0	2020	[Case of Recurrent Breast Cancer with BRCA2 Mutation Successfully Treated with Olaparib Therapy].	olaparib	79-87	BRCA2 DNA repair associated	Homo sapiens	38-43
32293692-5	2020	Olaparib is an additional option for second- and third-line treatment in those with alterations in BRCA1, BRCA2, and ATM.	olaparib	0-8	BRCA2 DNA repair associated	Homo sapiens	106-111
32300630-0	2020	Recurrent uterine serous carcinoma with a germline pathogenic BRCA2 variant treated using olaparib: A case report.	olaparib	90-98	BRCA2 DNA repair associated	Homo sapiens	62-67
32300630-2	2020	Clinical response to olaparib was observed in recurrent uterine serous carcinoma with a germline BRCA2 mutation.	olaparib	21-29	BRCA2 DNA repair associated	Homo sapiens	97-102
32300630-3	2020	Here, we report, for the first time, a long-term clinical response to olaparib in a patient with uterine serous carcinoma and a germline pathogenic BRCA2 variant.	olaparib	70-78	BRCA2 DNA repair associated	Homo sapiens	148-153
31900740-0	2020	1H, 13C and 15N backbone resonance assignment of the human BRCA2 N-terminal region.	Hydrogen	0-2	BRCA2 DNA repair associated	Homo sapiens	59-64
31900740-0	2020	1H, 13C and 15N backbone resonance assignment of the human BRCA2 N-terminal region.	Carbon-13	4-7	BRCA2 DNA repair associated	Homo sapiens	59-64
31900740-0	2020	1H, 13C and 15N backbone resonance assignment of the human BRCA2 N-terminal region.	15n	12-15	BRCA2 DNA repair associated	Homo sapiens	59-64
32062581-4	2020	An unexpected observation was the caffeine-induced depletion of Rad51 (and Brca2) proteins.	Caffeine	34-42	BRCA2 DNA repair associated	Homo sapiens	75-80
32268276-9	2020	Mutations in multiple DNA repair genes (ATM, BRCA1, BRCA2, CHEK2) were associated with time to ADT treatment failure and survival in mHSPC.	adt	95-98	BRCA2 DNA repair associated	Homo sapiens	52-57
32028591-10	2020	The patient-derived xenograft model established from the patient who acquired resistance to olaparib with BRCA2 mutation showed increased sensitivity in irinotecan.	irinotecan	153-163	BRCA2 DNA repair associated	Homo sapiens	106-111
32297440-0	2020	Metastatic Thymoma Harboring a Deleterious BRCA2 Mutation Derives Durable Clinical Benefit from Olaparib.	olaparib	96-104	BRCA2 DNA repair associated	Homo sapiens	43-48
32037829-5	2020	We discovered a dihydroquinolone pyrazoline-based molecule (35d), which disrupts the RAD51-BRCA2 protein-protein interaction, thus mimicking the effect of BRCA2 mutation.	3-carboxy-4-oxo-6-fluoro-7-(1-piperazinyl)-1,4-dihydroquinolone	16-43	BRCA2 DNA repair associated	Homo sapiens	91-96
32037829-5	2020	We discovered a dihydroquinolone pyrazoline-based molecule (35d), which disrupts the RAD51-BRCA2 protein-protein interaction, thus mimicking the effect of BRCA2 mutation.	3-carboxy-4-oxo-6-fluoro-7-(1-piperazinyl)-1,4-dihydroquinolone	16-43	BRCA2 DNA repair associated	Homo sapiens	155-160
31829822-0	2020	Re: Prostate Cancer Risks for Male BRCA1 and BRCA2 Mutation Carriers: A Prospective Cohort Study.	Rhenium	0-2	BRCA2 DNA repair associated	Homo sapiens	45-50
32101536-6	2020	We experimentally validated that afatinib has the strongest cytotoxic activity on BT474 (IC50 = 55.5 nM, BRCA2 and TP53 co-mutant) compared to MCF7 (IC50 = 7.7 muM, both BRCA2 and TP53 wild type) and MDA-MB-231 (IC50 = 7.9 muM, BRCA2 wild type but TP53 mutant).	Afatinib	33-41	BRCA2 DNA repair associated	Homo sapiens	105-110
32101536-6	2020	We experimentally validated that afatinib has the strongest cytotoxic activity on BT474 (IC50 = 55.5 nM, BRCA2 and TP53 co-mutant) compared to MCF7 (IC50 = 7.7 muM, both BRCA2 and TP53 wild type) and MDA-MB-231 (IC50 = 7.9 muM, BRCA2 wild type but TP53 mutant).	Afatinib	33-41	BRCA2 DNA repair associated	Homo sapiens	170-175
32101536-6	2020	We experimentally validated that afatinib has the strongest cytotoxic activity on BT474 (IC50 = 55.5 nM, BRCA2 and TP53 co-mutant) compared to MCF7 (IC50 = 7.7 muM, both BRCA2 and TP53 wild type) and MDA-MB-231 (IC50 = 7.9 muM, BRCA2 wild type but TP53 mutant).	Afatinib	33-41	BRCA2 DNA repair associated	Homo sapiens	170-175
32110220-3	2020	As per the genomic findings of the Foundation One report, FDA-approved therapies were available for other tumor types, such as olaparib for the loss of BRCA2 and everolimus for the loss of PTEN exons 2-9.	olaparib	127-135	BRCA2 DNA repair associated	Homo sapiens	152-157
31705765-5	2020	Concordant PTEN loss and discordant BRCA2 gain were associated with significantly worse outcomes in Epic AR-V7 negative men with mCRPC treated with abiraterone/enzalutamide.	abiraterone	148-159	BRCA2 DNA repair associated	Homo sapiens	36-41
31705765-5	2020	Concordant PTEN loss and discordant BRCA2 gain were associated with significantly worse outcomes in Epic AR-V7 negative men with mCRPC treated with abiraterone/enzalutamide.	enzalutamide	160-172	BRCA2 DNA repair associated	Homo sapiens	36-41
32218813-9	2020	Pharmacological ascorbate enhanced the effects olaparib or veliparib by downregulating the expression of BRCA1, BRCA2 and RAD51.	Ascorbic Acid	16-25	BRCA2 DNA repair associated	Homo sapiens	112-117
32218813-9	2020	Pharmacological ascorbate enhanced the effects olaparib or veliparib by downregulating the expression of BRCA1, BRCA2 and RAD51.	olaparib	47-55	BRCA2 DNA repair associated	Homo sapiens	112-117
32218813-9	2020	Pharmacological ascorbate enhanced the effects olaparib or veliparib by downregulating the expression of BRCA1, BRCA2 and RAD51.	veliparib	59-68	BRCA2 DNA repair associated	Homo sapiens	112-117
32171277-0	2020	Polyclonal BRCA2 mutations following carboplatin treatment confer resistance to the PARP inhibitor rucaparib in a patient with mCRPC: a case report.	Carboplatin	37-48	BRCA2 DNA repair associated	Homo sapiens	11-16
32171277-0	2020	Polyclonal BRCA2 mutations following carboplatin treatment confer resistance to the PARP inhibitor rucaparib in a patient with mCRPC: a case report.	rucaparib	99-108	BRCA2 DNA repair associated	Homo sapiens	11-16
32171277-3	2020	CASE PRESENTATION: A patient with mCRPC associated with a germline BRCA2 mutation was sequentially treated with carboplatin and the PARP inhibitor rucaparib.	Carboplatin	112-123	BRCA2 DNA repair associated	Homo sapiens	67-72
32171277-3	2020	CASE PRESENTATION: A patient with mCRPC associated with a germline BRCA2 mutation was sequentially treated with carboplatin and the PARP inhibitor rucaparib.	rucaparib	147-156	BRCA2 DNA repair associated	Homo sapiens	67-72
32171277-4	2020	Genomic profiling of the available baseline tumor and progression blood samples using next-generation sequencing panel tests identified polyclonal BRCA2 reversion mutations post carboplatin treatment but prior to rucaparib treatment.	Carboplatin	178-189	BRCA2 DNA repair associated	Homo sapiens	147-152
32171277-8	2020	CONCLUSIONS: Here we report a case of a patient with prostate cancer who received a platinum agent and PARP inhibitor sequentially and in whom polyclonal BRCA2 reversion mutations were identified as the likely mechanism of acquired resistance to carboplatin and primary resistance to PARP inhibition.	Platinum	84-92	BRCA2 DNA repair associated	Homo sapiens	154-159
32171277-8	2020	CONCLUSIONS: Here we report a case of a patient with prostate cancer who received a platinum agent and PARP inhibitor sequentially and in whom polyclonal BRCA2 reversion mutations were identified as the likely mechanism of acquired resistance to carboplatin and primary resistance to PARP inhibition.	Carboplatin	246-257	BRCA2 DNA repair associated	Homo sapiens	154-159
32194423-9	2020	AZD compounds did not change the mRNA expression of BRCA1/BRCA in ovarian cancer cells, but AZD8835 inhibited BRCA1/BRCA2 mRNA expression and p-ERK protein expression in OVCAR-8 cells with the KRAS mutation.	AZD8835	92-99	BRCA2 DNA repair associated	Homo sapiens	116-121
31650727-8	2020	Recently, various clinical trials have investigated poly (adenosine diphosphate [ADP]-ribose) polymerase (PARP) inhibitor treatment for advanced-stage BRCA1/BRCA2 pathogenic variant breast cancer.	Poly Adenosine Diphosphate Ribose	52-93	BRCA2 DNA repair associated	Homo sapiens	157-162
31685642-5	2020	Furthermore, we show USP22 is necessary for BRCA2, PALB2, and Rad51 recruitment to DSBs and this is, in part, through USP22 stabilizing BRCA2 and PALB2 levels.	1,2-di-(4-sulfamidophenyl)-4-butylpyrazolidine-3,5-dione	83-87	BRCA2 DNA repair associated	Homo sapiens	44-49
31685642-5	2020	Furthermore, we show USP22 is necessary for BRCA2, PALB2, and Rad51 recruitment to DSBs and this is, in part, through USP22 stabilizing BRCA2 and PALB2 levels.	1,2-di-(4-sulfamidophenyl)-4-butylpyrazolidine-3,5-dione	83-87	BRCA2 DNA repair associated	Homo sapiens	136-141
31792088-0	2020	Alcohol Consumption, Cigarette Smoking, and Risk of Breast Cancer for BRCA1 and BRCA2 Mutation Carriers: Results from The BRCA1 and BRCA2 Cohort Consortium.	Alcohols	0-7	BRCA2 DNA repair associated	Homo sapiens	80-85
31787751-0	2020	Platinum response characteristics of patients with pancreatic ductal adenocarcinoma and a germline BRCA1, BRCA2 or PALB2 mutation.	Platinum	0-8	BRCA2 DNA repair associated	Homo sapiens	106-111
31787751-1	2020	BACKGROUND: Retrospective studies suggest a survival benefit when platinum-based chemotherapy is administered to patients with pancreatic cancer harbouring a germline mutation in BRCA1, BRCA2 or PALB2 (mut-positive PDAC).	Platinum	66-74	BRCA2 DNA repair associated	Homo sapiens	186-191
31199508-9	2020	Expression of the hub genes showed significant clusters between LAM patients and controls and that RAD50 and BRCA2 had the strongest associations with subject phenotypes.	lipoarabinomannan	64-67	BRCA2 DNA repair associated	Homo sapiens	109-114
31576005-1	2020	BRCA1/BRCA2-containing complex 3 (BRCC3) is a Lysine 63-specific deubiquitinating enzyme (DUB) involved in inflammasome activity, interferon signaling, and DNA damage repair.	Lysine	46-52	BRCA2 DNA repair associated	Homo sapiens	6-11
32010625-5	2019	We found that both endogenous, glucose-derived lactate and exogenous, lactate supplementation significantly affected the transcription of key oncogenes (MYC, RAS, and PI3KCA), transcription factors (HIF1A and E2F1), tumor suppressors (BRCA1, BRCA2) as well as cell cycle and proliferation genes involved in breast cancer (AKT1, ATM, CCND1, CDK4, CDKN1A, CDK2B) (0.001 < p < 0.05 for all genes).	Glucose	31-38	BRCA2 DNA repair associated	Homo sapiens	242-247
32010625-5	2019	We found that both endogenous, glucose-derived lactate and exogenous, lactate supplementation significantly affected the transcription of key oncogenes (MYC, RAS, and PI3KCA), transcription factors (HIF1A and E2F1), tumor suppressors (BRCA1, BRCA2) as well as cell cycle and proliferation genes involved in breast cancer (AKT1, ATM, CCND1, CDK4, CDKN1A, CDK2B) (0.001 < p < 0.05 for all genes).	Lactic Acid	47-54	BRCA2 DNA repair associated	Homo sapiens	242-247
32010625-5	2019	We found that both endogenous, glucose-derived lactate and exogenous, lactate supplementation significantly affected the transcription of key oncogenes (MYC, RAS, and PI3KCA), transcription factors (HIF1A and E2F1), tumor suppressors (BRCA1, BRCA2) as well as cell cycle and proliferation genes involved in breast cancer (AKT1, ATM, CCND1, CDK4, CDKN1A, CDK2B) (0.001 < p < 0.05 for all genes).	Lactic Acid	70-77	BRCA2 DNA repair associated	Homo sapiens	242-247
32012241-8	2020	Among high-penetrance cancer susceptibility genes, PGAs were most commonly observed in BRCA1 and BRCA2 (33.3%), which made up 5.3% of the entire cohort, and they were followed by PALB2, BAP1, and PMS2.	pgas	51-55	BRCA2 DNA repair associated	Homo sapiens	97-102
31577852-3	2020	A secondary mutation predicted to restore the BRCA2 open reading frame was detected at low frequency (2.3%) in whole exome sequencing of a peritoneal biopsy at disease progression after treatment that included carboplatin and olaparib.	Carboplatin	210-221	BRCA2 DNA repair associated	Homo sapiens	46-51
31612916-0	2019	Dramatic response of FOLFIRINOX regimen in a collision pancreatic adenocarcinoma patient with a germline BRCA2 mutation: a case report.	folfirinox	21-31	BRCA2 DNA repair associated	Homo sapiens	105-110
31534014-5	2020	Moreover, NCT-501, an ALDH1A1 selective inhibitor, can synergize with olaparib in killing EOC cells carrying BRCA2 mutation in both in vitro cell culture and the in vivo xenograft animal model.	olaparib	70-78	BRCA2 DNA repair associated	Homo sapiens	109-114
33357097-0	2020	The BRCA2 p.N372 H i.a.1342A>C Could Regulate the Sensitivity of Ovarian Cancer Cells to Platinum-Based Drugs.	Platinum	89-97	BRCA2 DNA repair associated	Homo sapiens	4-9
33357097-1	2020	BACKGROUND AND OBJECTIVE: We have previously reported that BRCA2 N372 H i.a.1342A>C heterozygous variation presented in platinum-resistant patients.	Platinum	120-128	BRCA2 DNA repair associated	Homo sapiens	59-64
33357097-2	2020	This study aimed to further investigate the mechanism of BRCA2 N372 H mutation in the development of platinum resistance in ovarian cancer.	Platinum	101-109	BRCA2 DNA repair associated	Homo sapiens	57-62
33357097-13	2020	CONCLUSION: Over expression of mRNA and protein of BRCA2 was detected in the cells with BRCA2 N372 H i.a.1342A>C mutation but not in the lentivirus negative control (lenti-EGFP) or the cells without transfection (empty cells), which may lead to resistance to platinum-based drugs in ovarian cancer cells through homologous recombination repair pathway.	Platinum	259-267	BRCA2 DNA repair associated	Homo sapiens	51-56
31890056-10	2019	In contrast, HMTA clearly increased cell toxicity in FANCD2-, BRCA1- and BRCA2- deficient cells under acidic conditions.	Methenamine	13-17	BRCA2 DNA repair associated	Homo sapiens	73-78
31604666-12	2019	CONCLUSIONS: Platinum-free interval >= 12 months, complete response and normalized CA-125 levels after ultimate platinum-based chemotherapy are associated with prolonged PFS and OS in relapsing BRCA1/BRCA2 mutated ovarian cancer patients who received olaparib as maintenance therapy.	Platinum	13-21	BRCA2 DNA repair associated	Homo sapiens	200-205
31562758-2	2019	In the randomized, double-blind, phase III POLO trial progression-free survival was significantly longer with maintenance olaparib, a poly(ADP-ribose) polymerase inhibitor, than placebo in patients with a germline BRCA1 and/or BRCA2 mutation (gBRCAm) and metastatic pancreatic cancer whose disease had not progressed during first-line platinum-based chemotherapy.	olaparib	122-130	BRCA2 DNA repair associated	Homo sapiens	227-232
31930278-1	2019	The poly (adenosine diphosphate (ADP)-ribosyl) polymerase inhibitors (PARPi) selectively kill cancer cells with BRCA1 or BRCA2 (BRCA)-mutations.	poly If	4-8	BRCA2 DNA repair associated	Homo sapiens	121-126
31930278-1	2019	The poly (adenosine diphosphate (ADP)-ribosyl) polymerase inhibitors (PARPi) selectively kill cancer cells with BRCA1 or BRCA2 (BRCA)-mutations.	poly If	4-8	BRCA2 DNA repair associated	Homo sapiens	112-116
31930278-1	2019	The poly (adenosine diphosphate (ADP)-ribosyl) polymerase inhibitors (PARPi) selectively kill cancer cells with BRCA1 or BRCA2 (BRCA)-mutations.	poly(ADP)-ribosylated proteins	10-45	BRCA2 DNA repair associated	Homo sapiens	121-126
31930278-1	2019	The poly (adenosine diphosphate (ADP)-ribosyl) polymerase inhibitors (PARPi) selectively kill cancer cells with BRCA1 or BRCA2 (BRCA)-mutations.	poly(ADP)-ribosylated proteins	10-45	BRCA2 DNA repair associated	Homo sapiens	112-116
32042831-6	2019	Results suggested that deleterious variants were mostly enriched in the N- and C-terminal domain of the BRCA1 and BRCA2 C-terminus.	Nitrogen	72-73	BRCA2 DNA repair associated	Homo sapiens	114-119
32042831-6	2019	Results suggested that deleterious variants were mostly enriched in the N- and C-terminal domain of the BRCA1 and BRCA2 C-terminus.	Carbon	79-80	BRCA2 DNA repair associated	Homo sapiens	114-119
31604666-12	2019	CONCLUSIONS: Platinum-free interval >= 12 months, complete response and normalized CA-125 levels after ultimate platinum-based chemotherapy are associated with prolonged PFS and OS in relapsing BRCA1/BRCA2 mutated ovarian cancer patients who received olaparib as maintenance therapy.	Platinum	112-120	BRCA2 DNA repair associated	Homo sapiens	200-205
31537621-0	2019	Can somatic BRCA2 status solve a case of olaparib monotherapy resistance?	olaparib	41-49	BRCA2 DNA repair associated	Homo sapiens	12-17
31080125-1	2019	Differential Response to Olaparib Treatment Among Men with Metastatic Castration-resistant Prostate Cancer Harboring BRCA1 or BRCA2 Versus ATM Mutations.	olaparib	25-33	BRCA2 DNA repair associated	Homo sapiens	126-131
31591549-2	2019	The detection of DNA repair aberrations, such as mutation of BRCA2, could help select patients for poly(ADP-ribose) polymerase (PARP) inhibitor or platinum chemotherapy, and mismatch repair gene defects and microsatellite instability have been associated with responses to checkpoint inhibitor immunotherapy.	Platinum	147-155	BRCA2 DNA repair associated	Homo sapiens	61-66
31409613-11	2019	In addition, BRCA1-, BRCA2-, and PALB2-deficient cells were hypersensitive to the indenoisoquinolines.	indenoisoquinolines	82-101	BRCA2 DNA repair associated	Homo sapiens	21-26
31499327-1	2019	Homologous recombination deficiency conferred by alterations in BRCA1 or BRCA2 are common in breast tumors and can drive sensitivity to platinum chemotherapy and PARP inhibitors.	Platinum	136-144	BRCA2 DNA repair associated	Homo sapiens	73-78
31529615-4	2019	In this study, we found that forced mitotic entry upon ATR inhibition potentiates cytotoxic effects of PARP inhibition using olaparib in BRCA2-depleted and Brca2 knock-out cancer cell line models.	olaparib	125-133	BRCA2 DNA repair associated	Homo sapiens	137-142
31529615-7	2019	Furthermore, using genome-wide single cell sequencing, we show that ATR inhibition enhances genomic instability of olaparib-treated BRCA2-depleted cells.	olaparib	115-123	BRCA2 DNA repair associated	Homo sapiens	132-137
31529615-9	2019	Additionally, we show that olaparib treatment leads to increased numbers of micronuclei, which is accompanied by a cGAS/STING-associated inflammatory response in BRCA2-deficient cells.	olaparib	27-35	BRCA2 DNA repair associated	Homo sapiens	162-167
31327751-9	2019	One patient with a BRCA2 loss had a complete response on olaparib (>27 months) and 3 patients (ATM substitution, PALB2 frameshift, CDK12 frameshift) had stable disease with olaparib (10.3, 18.7, and 7.8 months, respectively).	olaparib	57-65	BRCA2 DNA repair associated	Homo sapiens	19-24
30797618-0	2019	Differential Response to Olaparib Treatment Among Men with Metastatic Castration-resistant Prostate Cancer Harboring BRCA1 or BRCA2 Versus ATM Mutations.	olaparib	25-33	BRCA2 DNA repair associated	Homo sapiens	126-131
31065835-10	2019	Patients mutated in BRCA2, KMT2B, SMARCA4 or TSC2 have significantly higher TMB compared to patients with wide-type genes.	1,2,4,5-tetramethoxybenzene	76-79	BRCA2 DNA repair associated	Homo sapiens	20-25
31577767-0	2019	A case report of a dramatic response to olaparib in a patient with metastatic pancreatic cancer harboring a germline BRCA2 mutation.	olaparib	40-48	BRCA2 DNA repair associated	Homo sapiens	117-122
31500345-4	2019	Riboflavin plays a crucial role in cells since its biologically active forms, FMN and FAD, are essential for the metabolism of carbohydrates, amino acids, and lipids.	Riboflavin	0-10	BRCA2 DNA repair associated	Homo sapiens	86-89
31500345-4	2019	Riboflavin plays a crucial role in cells since its biologically active forms, FMN and FAD, are essential for the metabolism of carbohydrates, amino acids, and lipids.	Carbohydrates	127-140	BRCA2 DNA repair associated	Homo sapiens	86-89
30720863-5	2019	The BRCA1 gene had the highest mutation frequency in patients with triple-negative breast cancer (TNBC), which was 9.6% (n = 42), while the BRCA2 gene had the highest mutation frequency in patients with Luminal, which was 3.2% (n = 58).	Phenobarbital	203-210	BRCA2 DNA repair associated	Homo sapiens	140-145
31157963-3	2019	METHODS: We conducted a randomized, double-blind, placebo-controlled, phase 3 trial to evaluate the efficacy of olaparib as maintenance therapy in patients who had a germline BRCA1 or BRCA2 mutation and metastatic pancreatic cancer and disease that had not progressed during first-line platinum-based chemotherapy.	olaparib	112-120	BRCA2 DNA repair associated	Homo sapiens	184-189
33457057-0	2019	Incidence of Hypersensitivity Reactions to Carboplatin or Paclitaxel in Patients With Ovarian, Fallopian Tube, or Primary Peritoneal Cancer With or Without BRCA1 or BRCA2 Mutations.	Carboplatin	43-54	BRCA2 DNA repair associated	Homo sapiens	165-170
31565603-4	2019	Molecular features commonly found in prostate adenocarcinomas are now well-recognized, including defects in homologous recombination (HR) genes, like breast cancer type 2 susceptibility protein (BRCA2), leading to increased sensitivity to deoxyribonucleic acid (DNA)-damaging agents (e.g., platinum chemotherapy or poly adenosine diphosphate-ribose polymerase (PARP) inhibitors).	Amino Acids	239-260	BRCA2 DNA repair associated	Homo sapiens	150-193
31565603-4	2019	Molecular features commonly found in prostate adenocarcinomas are now well-recognized, including defects in homologous recombination (HR) genes, like breast cancer type 2 susceptibility protein (BRCA2), leading to increased sensitivity to deoxyribonucleic acid (DNA)-damaging agents (e.g., platinum chemotherapy or poly adenosine diphosphate-ribose polymerase (PARP) inhibitors).	Amino Acids	239-260	BRCA2 DNA repair associated	Homo sapiens	195-200
31565603-4	2019	Molecular features commonly found in prostate adenocarcinomas are now well-recognized, including defects in homologous recombination (HR) genes, like breast cancer type 2 susceptibility protein (BRCA2), leading to increased sensitivity to deoxyribonucleic acid (DNA)-damaging agents (e.g., platinum chemotherapy or poly adenosine diphosphate-ribose polymerase (PARP) inhibitors).	Amino Acids	262-265	BRCA2 DNA repair associated	Homo sapiens	150-193
31565603-4	2019	Molecular features commonly found in prostate adenocarcinomas are now well-recognized, including defects in homologous recombination (HR) genes, like breast cancer type 2 susceptibility protein (BRCA2), leading to increased sensitivity to deoxyribonucleic acid (DNA)-damaging agents (e.g., platinum chemotherapy or poly adenosine diphosphate-ribose polymerase (PARP) inhibitors).	Amino Acids	262-265	BRCA2 DNA repair associated	Homo sapiens	195-200
31565603-4	2019	Molecular features commonly found in prostate adenocarcinomas are now well-recognized, including defects in homologous recombination (HR) genes, like breast cancer type 2 susceptibility protein (BRCA2), leading to increased sensitivity to deoxyribonucleic acid (DNA)-damaging agents (e.g., platinum chemotherapy or poly adenosine diphosphate-ribose polymerase (PARP) inhibitors).	Platinum	290-298	BRCA2 DNA repair associated	Homo sapiens	150-193
31565603-4	2019	Molecular features commonly found in prostate adenocarcinomas are now well-recognized, including defects in homologous recombination (HR) genes, like breast cancer type 2 susceptibility protein (BRCA2), leading to increased sensitivity to deoxyribonucleic acid (DNA)-damaging agents (e.g., platinum chemotherapy or poly adenosine diphosphate-ribose polymerase (PARP) inhibitors).	Platinum	290-298	BRCA2 DNA repair associated	Homo sapiens	195-200
31273933-5	2019	Additionally, chlorambucil eradicates BRCA2-deficient xenografts and inhibits growth of olaparib-resistant patient-derived tumour xenografts (PDTXs).	Chlorambucil	14-26	BRCA2 DNA repair associated	Homo sapiens	38-43
31273933-8	2019	Because chlorambucil and cisplatin are equally effective inhibitors of BRCA2-compromised tumours, our results indicate that chlorambucil has a higher therapeutic index than cisplatin in targeting BRCA-deficient tumours.	Chlorambucil	8-20	BRCA2 DNA repair associated	Homo sapiens	71-76
31273933-8	2019	Because chlorambucil and cisplatin are equally effective inhibitors of BRCA2-compromised tumours, our results indicate that chlorambucil has a higher therapeutic index than cisplatin in targeting BRCA-deficient tumours.	Cisplatin	25-34	BRCA2 DNA repair associated	Homo sapiens	71-76
31273933-8	2019	Because chlorambucil and cisplatin are equally effective inhibitors of BRCA2-compromised tumours, our results indicate that chlorambucil has a higher therapeutic index than cisplatin in targeting BRCA-deficient tumours.	Chlorambucil	124-136	BRCA2 DNA repair associated	Homo sapiens	71-76
30940721-1	2019	In an interim analysis, the targeted PARP inhibitor rucaparib showed encouraging signs of disease control when used as a maintenance therapy for patients with platinum-sensitive advanced pancreatic cancer and a pathogenic mutation in BRCA1, BRCA2, or PALB2.	rucaparib	52-61	BRCA2 DNA repair associated	Homo sapiens	241-246
31320873-0	2019	Somatic BRCA2 Mutation-Positive Concurrent Accessory Male Breast Cancer (BC) and Non-Small Cell Lung Cancer (NSCLC): Excellent Efficacy of Palbociclib, Fulvestrant and Leuprolide in Platinum-Exposed and Endocrine-Refractory BC Associated with Cyclin D1 and FGFR1 Amplification and of Carboplatin, Paclitaxel and Radiation in NSCLC.	palbociclib	139-150	BRCA2 DNA repair associated	Homo sapiens	8-13
31320873-0	2019	Somatic BRCA2 Mutation-Positive Concurrent Accessory Male Breast Cancer (BC) and Non-Small Cell Lung Cancer (NSCLC): Excellent Efficacy of Palbociclib, Fulvestrant and Leuprolide in Platinum-Exposed and Endocrine-Refractory BC Associated with Cyclin D1 and FGFR1 Amplification and of Carboplatin, Paclitaxel and Radiation in NSCLC.	Platinum	182-190	BRCA2 DNA repair associated	Homo sapiens	8-13
31320873-0	2019	Somatic BRCA2 Mutation-Positive Concurrent Accessory Male Breast Cancer (BC) and Non-Small Cell Lung Cancer (NSCLC): Excellent Efficacy of Palbociclib, Fulvestrant and Leuprolide in Platinum-Exposed and Endocrine-Refractory BC Associated with Cyclin D1 and FGFR1 Amplification and of Carboplatin, Paclitaxel and Radiation in NSCLC.	Carboplatin	284-295	BRCA2 DNA repair associated	Homo sapiens	8-13
31320873-0	2019	Somatic BRCA2 Mutation-Positive Concurrent Accessory Male Breast Cancer (BC) and Non-Small Cell Lung Cancer (NSCLC): Excellent Efficacy of Palbociclib, Fulvestrant and Leuprolide in Platinum-Exposed and Endocrine-Refractory BC Associated with Cyclin D1 and FGFR1 Amplification and of Carboplatin, Paclitaxel and Radiation in NSCLC.	Paclitaxel	297-307	BRCA2 DNA repair associated	Homo sapiens	8-13
30417376-8	2019	Furthermore, we found that KIF4A inhibition suppressed the ability of cisplatin to induce BRCA2 and Rad51 focus formation and limits the further increase in poly(ADP-ribose) polymerase 1 activity induced by cisplatin treatment in human NSCLC cells.	Cisplatin	70-79	BRCA2 DNA repair associated	Homo sapiens	90-95
31409078-4	2019	In addition to anthracyclines, taxanes are effective against tumors with a BRCA2 mutation.	Taxoids	31-38	BRCA2 DNA repair associated	Homo sapiens	75-80
31409079-0	2019	Effectiveness of Neoadjuvant Therapy with Platinum-Based Agents for Patients with BRCA1 and BRCA2 Germline Mutations - A Retrospective Analysis of Breast Cancer Patients Treated at MMCI Brno.	Platinum	42-50	BRCA2 DNA repair associated	Homo sapiens	92-97
31060517-0	2019	Novel BRCA2 pathogenic variant c.5219 T > G; p.(Leu1740Ter) in a consanguineous Senegalese family with hereditary breast cancer.	leu1740ter	51-61	BRCA2 DNA repair associated	Homo sapiens	6-11
30900310-12	2019	OS (HR = 2.21, 95% CI = 1.64-2.30) and CSS (HR = 2.63, 95% CI = 2.00-3.45) were significantly worse among BRCA2 carriers compared to noncarriers, whereas OS (HR = 0.47, 95% CI = 0.11-1.99) and CSS (HR = 1.07, 95% CI = 0.38-2.96) were statistically not significant when comparing BRCA1 carriers and noncarriers.	thiocysteine	39-42	BRCA2 DNA repair associated	Homo sapiens	106-111
30900310-12	2019	OS (HR = 2.21, 95% CI = 1.64-2.30) and CSS (HR = 2.63, 95% CI = 2.00-3.45) were significantly worse among BRCA2 carriers compared to noncarriers, whereas OS (HR = 0.47, 95% CI = 0.11-1.99) and CSS (HR = 1.07, 95% CI = 0.38-2.96) were statistically not significant when comparing BRCA1 carriers and noncarriers.	thiocysteine	193-196	BRCA2 DNA repair associated	Homo sapiens	106-111
31113933-9	2019	Mechanistically, perifosine induced RAD51 ubiquitination and blocked the RAD51-BRCA2 interaction, which in turn decreased ionizing radiation-induced foci (IRIF) of Rad51 and, thereby, homologous recombination (HR)-mediated DNA double strand break repair.	perifosine	17-27	BRCA2 DNA repair associated	Homo sapiens	79-84
30430339-5	2019	Additionally, bioinformatics analysis showed that BRCA2-tryptophan > arginine substitutions result in altered interaction of BRCA1/PALB2/BRCA2/protein complex and impaired HDDR pathway.	Tryptophan	56-66	BRCA2 DNA repair associated	Homo sapiens	50-55
30430339-5	2019	Additionally, bioinformatics analysis showed that BRCA2-tryptophan > arginine substitutions result in altered interaction of BRCA1/PALB2/BRCA2/protein complex and impaired HDDR pathway.	Tryptophan	56-66	BRCA2 DNA repair associated	Homo sapiens	140-145
30725383-10	2019	CDRs ranged from 43.5% (95% CI 29.8-62.9) for the first screening round in BRCA2 carriers to 2.9% (95% CI 1.3-6.3) for subsequent screening rounds in high-risk non-carriers in the age group 30 to 39 years.	cdrs	0-4	BRCA2 DNA repair associated	Homo sapiens	75-80
30430339-5	2019	Additionally, bioinformatics analysis showed that BRCA2-tryptophan > arginine substitutions result in altered interaction of BRCA1/PALB2/BRCA2/protein complex and impaired HDDR pathway.	Arginine	72-80	BRCA2 DNA repair associated	Homo sapiens	50-55
30430339-5	2019	Additionally, bioinformatics analysis showed that BRCA2-tryptophan > arginine substitutions result in altered interaction of BRCA1/PALB2/BRCA2/protein complex and impaired HDDR pathway.	Arginine	72-80	BRCA2 DNA repair associated	Homo sapiens	140-145
30789866-3	2019	RECENT FINDINGS: A recent phase II trial of neoadjuvant talazoparib monotherapy in patients with BRCA1 or BRCA2 germline pathogenic variants and early stage breast cancer demonstrated a pathological complete response in 10/19 (53%) patients.	talazoparib	56-67	BRCA2 DNA repair associated	Homo sapiens	106-111
30620386-2	2019	Pathogenic germline alterations (PGAs) in BRCA2 and potentially targetable somatic alterations (SAs) in ERBB2 and ELF3 have been previously described in AC.	pgas	33-37	BRCA2 DNA repair associated	Homo sapiens	42-47
30636051-11	2019	CONCLUSIONS: In this series, 4% and 17% of BRCA2 patients developed PDAC and IPMN, respectively.	pdac	68-72	BRCA2 DNA repair associated	Homo sapiens	43-48
30689707-1	2019	BACKGROUND: In the OlympiAD study, olaparib was shown to improve progression-free survival compared with chemotherapy treatment of physician"s choice (TPC) in patients with a germline BRCA1 and/or BRCA2 mutation (BRCAm) and human epidermal growth factor receptor 2 (HER2)-negative metastatic breast cancer (mBC).	olaparib	35-43	BRCA2 DNA repair associated	Homo sapiens	197-202
30747491-2	2019	We previously found that SNP rs34259 in the uracil-DNA glycosylase gene (UNG) might decrease ovarian cancer risk in BRCA2 mutation carriers.	Uracil	44-50	BRCA2 DNA repair associated	Homo sapiens	116-121
30747491-5	2019	In addition, we found that this SNP is associated with significantly lower oxidative stress susceptibility and lower uracil accumulation at telomeres in BRCA2 mutation carriers.	Uracil	117-123	BRCA2 DNA repair associated	Homo sapiens	153-158
31080552-4	2019	Here, we report that in a Brca2 model treated with olaparib, P-gp upregulation is observed but is not sufficient to confer resistance.	olaparib	51-59	BRCA2 DNA repair associated	Homo sapiens	26-31
30824427-1	2019	Niraparib showed promising signs of efficacy in the phase II GALAHAD trial of men with advanced prostate cancer whose tumors harbor mutations in the DNA damage-response pathway, especially among patients with gene defects in BRCA1 or BRCA2.	niraparib	0-9	BRCA2 DNA repair associated	Homo sapiens	234-239
30603998-0	2019	Folic acid supplement use and breast cancer risk in BRCA1 and BRCA2 mutation carriers: a case-control study.	Folic Acid	0-10	BRCA2 DNA repair associated	Homo sapiens	62-67
30871108-6	2019	Poly ADP-ribose polymerase (PARP) inhibitors and platinum-based chemotherapy have proven to be effective in the treatment of other tumor types linked to BRCA1 and BRCA2 alterations and several trials are currently evaluating their efficacy in prostate cancer.	Platinum	49-57	BRCA2 DNA repair associated	Homo sapiens	163-168
30625039-11	2019	CSS (24.0 v 17.0 months) and PFS2 (18.9 v 8.6 months) were greater in g BRCA2 carriers treated in first line with abiraterone or enzalutamide compared with taxanes.	abiraterone	114-125	BRCA2 DNA repair associated	Homo sapiens	72-77
30660828-0	2019	Rad51/BRCA2 disruptors inhibit homologous recombination and synergize with olaparib in pancreatic cancer cells.	olaparib	75-83	BRCA2 DNA repair associated	Homo sapiens	6-11
30660828-4	2019	Recently, we identified a series of triazole derivatives that mimic BRCA2 mutations by disrupting the Rad51-BRCA2 interaction and thus double-strand break repair.	Triazoles	36-44	BRCA2 DNA repair associated	Homo sapiens	68-73
30660828-4	2019	Recently, we identified a series of triazole derivatives that mimic BRCA2 mutations by disrupting the Rad51-BRCA2 interaction and thus double-strand break repair.	Triazoles	36-44	BRCA2 DNA repair associated	Homo sapiens	108-113
30660828-7	2019	These compounds synergized with olaparib to target pancreatic cancer cells with functional BRCA2.	olaparib	32-40	BRCA2 DNA repair associated	Homo sapiens	91-96
30496017-9	2019	Expressions of Brca2, Xpc, Mlh3, Rad51, Xrcc2, Hus1, Rad9a, Cdkn1a, Gadd45a which are the DNA-repair genes were found to be significantly higher in NAC + ALC + IR group than those in individual treatment of ALC or NAC.	Acetylcysteine	148-151	BRCA2 DNA repair associated	Homo sapiens	15-20
30496017-9	2019	Expressions of Brca2, Xpc, Mlh3, Rad51, Xrcc2, Hus1, Rad9a, Cdkn1a, Gadd45a which are the DNA-repair genes were found to be significantly higher in NAC + ALC + IR group than those in individual treatment of ALC or NAC.	Acetylcarnitine	154-157	BRCA2 DNA repair associated	Homo sapiens	15-20
30496017-9	2019	Expressions of Brca2, Xpc, Mlh3, Rad51, Xrcc2, Hus1, Rad9a, Cdkn1a, Gadd45a which are the DNA-repair genes were found to be significantly higher in NAC + ALC + IR group than those in individual treatment of ALC or NAC.	Acetylcysteine	214-217	BRCA2 DNA repair associated	Homo sapiens	15-20
30625039-10	2019	Significant interactions between g BRCA2 status and treatment type (androgen signaling inhibitor v taxane therapy) were observed (CSS adjusted P = .014; PFS2 adjusted P = .005).	taxane	99-105	BRCA2 DNA repair associated	Homo sapiens	35-40
30520109-11	2019	Olaparib treatment significantly increased cell death in BRCA2 mutated tumors slices as compared to slices from BRCA2 wild type tumors.	olaparib	0-8	BRCA2 DNA repair associated	Homo sapiens	57-62
30625039-11	2019	CSS (24.0 v 17.0 months) and PFS2 (18.9 v 8.6 months) were greater in g BRCA2 carriers treated in first line with abiraterone or enzalutamide compared with taxanes.	enzalutamide	129-141	BRCA2 DNA repair associated	Homo sapiens	72-77
30717758-8	2019	Mechanistic studies reveal that NFBD1 loss blocks olaparib-induced homologous recombination repair by decreasing the formation of BRCA1, BRCA2 and RAD51 foci.	olaparib	50-58	BRCA2 DNA repair associated	Homo sapiens	137-142
30270052-0	2019	Tumor Lysis Syndrome After Platinum-based Chemotherapy in Castration-resistant Prostate Cancer With a BRCA2 Mutation: A Case Report.	Platinum	27-35	BRCA2 DNA repair associated	Homo sapiens	102-107
30177840-10	2019	In line with these findings, BRCA2-depleted and BRCA2-mutant human cell lines, or tumor cell lines derived from Brca2-/-;p53-/- mice showed increased sensitivity to the Aurora-A kinase inhibitor alisertib, with delayed mitotic progression and frequent mitotic failure.	MLN 8237	195-204	BRCA2 DNA repair associated	Homo sapiens	29-34
30954761-1	2019	The poly-(ADP-ribose) polymerase (PARP) inhibitor (PARPi) olaparib was the first licenced cancer drug that targeted an inherited form of cancer, namely ovarian cancers caused by germline BRCA1 or BRCA2 gene mutations.	olaparib	58-66	BRCA2 DNA repair associated	Homo sapiens	196-201
30177840-10	2019	In line with these findings, BRCA2-depleted and BRCA2-mutant human cell lines, or tumor cell lines derived from Brca2-/-;p53-/- mice showed increased sensitivity to the Aurora-A kinase inhibitor alisertib, with delayed mitotic progression and frequent mitotic failure.	MLN 8237	195-204	BRCA2 DNA repair associated	Homo sapiens	48-53
30177840-10	2019	In line with these findings, BRCA2-depleted and BRCA2-mutant human cell lines, or tumor cell lines derived from Brca2-/-;p53-/- mice showed increased sensitivity to the Aurora-A kinase inhibitor alisertib, with delayed mitotic progression and frequent mitotic failure.	MLN 8237	195-204	BRCA2 DNA repair associated	Homo sapiens	112-117
31099631-5	2019	Maintenance olaparib was FDA-approved on December 19, 2018, for frontline maintenance among those with advanced EOC who respond to frontline chemotherapy and harbor a germline or somatic BRCA1 or BRCA2 mutation.	olaparib	12-20	BRCA2 DNA repair associated	Homo sapiens	196-201
30352801-3	2019	We hypothesized that PBD-based antibody-drug conjugates (ADC) will have enhanced killing of cells in which homologous recombination processes are defective by inactivation of BRCA1 or BRCA2 genes.	1,1'-((propane-1,3-diyl)dioxy)bis(7-methoxy-2-methylidene-1,2,3,10,11,11a-hexahydro-5H-pyrrolo(2,1-c)(1,4)benzodiazepin-5,11-dione)	21-24	BRCA2 DNA repair associated	Homo sapiens	184-189
31045513-7	2019	Meanwhile, the following gene sets were highly enriched in BRCA2: cell cycle, DNA replication, homologous recombination, oocyte meiosis, ubiquitin-mediated proteolysis, base excision repair, progestin mediated oocyte maturation, basal transcription factor, biosynthesis of N polysaccharide, mismatch repair, sliceosome, purine metabolism as well as P53 and neurotrophic factor signaling pathway, etc.CONCLUSION: These findings suggested that the BRCA2 gene mutation is a good prognostic factor and can be used as a gene to predict the prognosis in the bladder cancer patients.	n polysaccharide	273-289	BRCA2 DNA repair associated	Homo sapiens	59-64
31045513-7	2019	Meanwhile, the following gene sets were highly enriched in BRCA2: cell cycle, DNA replication, homologous recombination, oocyte meiosis, ubiquitin-mediated proteolysis, base excision repair, progestin mediated oocyte maturation, basal transcription factor, biosynthesis of N polysaccharide, mismatch repair, sliceosome, purine metabolism as well as P53 and neurotrophic factor signaling pathway, etc.CONCLUSION: These findings suggested that the BRCA2 gene mutation is a good prognostic factor and can be used as a gene to predict the prognosis in the bladder cancer patients.	purine	320-326	BRCA2 DNA repair associated	Homo sapiens	59-64
30345884-3	2018	METHODS: We conducted an international, randomized, double-blind, phase 3 trial to evaluate the efficacy of olaparib as maintenance therapy in patients with newly diagnosed advanced (International Federation of Gynecology and Obstetrics stage III or IV) high-grade serous or endometrioid ovarian cancer, primary peritoneal cancer, or fallopian-tube cancer (or a combination thereof) with a mutation in BRCA1, BRCA2, or both ( BRCA1/2) who had a complete or partial clinical response after platinum-based chemotherapy.	olaparib	108-116	BRCA2 DNA repair associated	Homo sapiens	409-414
30547773-0	2018	Complete pathological response following neoadjuvant FOLFOX chemotherapy in BRCA2-mutant locally advanced rectal cancer: a case report.	Folfox protocol	53-59	BRCA2 DNA repair associated	Homo sapiens	76-81
30547773-5	2018	CONCLUSIONS: This case indicated an association of BRCA2 mutation with high mutation loads and an excellent response of oxaliplatin-based chemotherapy regimen for LARC.	Oxaliplatin	120-131	BRCA2 DNA repair associated	Homo sapiens	51-56
30245363-0	2018	Food and Alcohol Disturbance (FAD) in the U.S. and France: Nationality and gender effects and relations to drive for thinness and alcohol use.	Alcohols	9-16	BRCA2 DNA repair associated	Homo sapiens	30-33
30245363-1	2018	OBJECTIVE: Food and Alcohol Disturbance (FAD), colloquially coined "drunkorexia," is a set of behaviors that encompasses restriction of calories, over-exercise, and other compensatory behaviors before, during, or after alcohol use to offset caloric intake or maximize intoxication.	Alcohols	20-27	BRCA2 DNA repair associated	Homo sapiens	41-44
30245363-1	2018	OBJECTIVE: Food and Alcohol Disturbance (FAD), colloquially coined "drunkorexia," is a set of behaviors that encompasses restriction of calories, over-exercise, and other compensatory behaviors before, during, or after alcohol use to offset caloric intake or maximize intoxication.	Alcohols	219-226	BRCA2 DNA repair associated	Homo sapiens	41-44
30245363-5	2018	Nationality was found to be a significant moderator of the relationship between alcohol use and FAD for both compensatory (p = .013) and intoxication (p = .01) purposes, such that Americans who drank more engaged in more FAD.	Alcohols	80-87	BRCA2 DNA repair associated	Homo sapiens	96-99
30245363-5	2018	Nationality was found to be a significant moderator of the relationship between alcohol use and FAD for both compensatory (p = .013) and intoxication (p = .01) purposes, such that Americans who drank more engaged in more FAD.	Alcohols	80-87	BRCA2 DNA repair associated	Homo sapiens	221-224
28374118-1	2018	In the proposed work, we have explicated the mechanism of dibenzo[a,l]pyrene (DBP) and benzo[a]pyrene (BP) modulated cell proliferation by assessing the plausible binding with CASPASES, BAX, Bcl-2, MDM2, p53, p21, p16, CylinD1-CDK4 complex, CylinE1-CDK2 complex, H-Ras, K-Ras, BRCA1, and BRCA2 through exploiting the inherent potential of AutoDock Tools 4.0.	Benzo(a)pyrene	87-101	BRCA2 DNA repair associated	Homo sapiens	288-293
30155608-4	2018	In the present study, barbatolic acid was isolated from the acetone extract of Bryoria capillaris, and its anti-breast cancer and anti-angiogenic potential was investigated using human umbilical vein endothelial cells (HUVECs), human breast ductal carcinoma (T-47D) and cisplatin-resistant BRCA2-mutated human breast TNM stage IV adenocarcinoma (HCC1428) cells.	Barbatolic acid	22-37	BRCA2 DNA repair associated	Homo sapiens	290-295
28374118-1	2018	In the proposed work, we have explicated the mechanism of dibenzo[a,l]pyrene (DBP) and benzo[a]pyrene (BP) modulated cell proliferation by assessing the plausible binding with CASPASES, BAX, Bcl-2, MDM2, p53, p21, p16, CylinD1-CDK4 complex, CylinE1-CDK2 complex, H-Ras, K-Ras, BRCA1, and BRCA2 through exploiting the inherent potential of AutoDock Tools 4.0.	dibenzo(a,l)pyrene	58-76	BRCA2 DNA repair associated	Homo sapiens	288-293
28374118-1	2018	In the proposed work, we have explicated the mechanism of dibenzo[a,l]pyrene (DBP) and benzo[a]pyrene (BP) modulated cell proliferation by assessing the plausible binding with CASPASES, BAX, Bcl-2, MDM2, p53, p21, p16, CylinD1-CDK4 complex, CylinE1-CDK2 complex, H-Ras, K-Ras, BRCA1, and BRCA2 through exploiting the inherent potential of AutoDock Tools 4.0.	Benzo(a)pyrene	79-81	BRCA2 DNA repair associated	Homo sapiens	288-293
30407325-0	2018	Response of germline BRCA2-mutated advanced pancreatic acinar cell carcinoma to olaparib: A case report.	olaparib	80-88	BRCA2 DNA repair associated	Homo sapiens	21-26
30407790-0	2018	Epidermal Growth Factor Receptor-Targeting Peptide Nanoparticles Simultaneously Deliver Gemcitabine and Olaparib To Treat Pancreatic Cancer with Breast Cancer 2 ( BRCA2) Mutation.	olaparib	104-112	BRCA2 DNA repair associated	Homo sapiens	145-160
30407790-0	2018	Epidermal Growth Factor Receptor-Targeting Peptide Nanoparticles Simultaneously Deliver Gemcitabine and Olaparib To Treat Pancreatic Cancer with Breast Cancer 2 ( BRCA2) Mutation.	olaparib	104-112	BRCA2 DNA repair associated	Homo sapiens	163-168
30386134-8	2018	The lowest Bland-Altman limit of agreement was observed with GLM-3 (mean difference, -0.0 +- 5.1 Hounsfield units/grams of iodine [HU/gI]; 95% confidence interval [CI], -10.1, 10.1), followed by DeltaHUCCTA (-0.0 +- 5.9 HU/gI; 95% CI, -11.9, 11.9) and TBW (1.1 +- 6.2 HU/gI; 95% CI, -11.2, 13.4).	Iodine	123-129	BRCA2 DNA repair associated	Homo sapiens	61-66
30386134-8	2018	The lowest Bland-Altman limit of agreement was observed with GLM-3 (mean difference, -0.0 +- 5.1 Hounsfield units/grams of iodine [HU/gI]; 95% confidence interval [CI], -10.1, 10.1), followed by DeltaHUCCTA (-0.0 +- 5.9 HU/gI; 95% CI, -11.9, 11.9) and TBW (1.1 +- 6.2 HU/gI; 95% CI, -11.2, 13.4).	deltahuccta	195-206	BRCA2 DNA repair associated	Homo sapiens	61-66
30415210-2	2018	To minimise the proportion of VUS in BRCA1/2, we performed the multifactorial likelihood analysis and validated this method using an independent cohort of patients with breast cancer.	3-[(3~{a}~{S},4~{S},6~{a}~{R})-4-carboxy-2,3,4,5,6,6~{a}-hexahydro-1~{H}-pyrrolo[2,3-c]pyrrol-3~{a}-yl]propyl-$l^{3}-oxidanyl-bis(oxidanyl)boranuide	30-33	BRCA2 DNA repair associated	Homo sapiens	37-44
30386134-8	2018	The lowest Bland-Altman limit of agreement was observed with GLM-3 (mean difference, -0.0 +- 5.1 Hounsfield units/grams of iodine [HU/gI]; 95% confidence interval [CI], -10.1, 10.1), followed by DeltaHUCCTA (-0.0 +- 5.9 HU/gI; 95% CI, -11.9, 11.9) and TBW (1.1 +- 6.2 HU/gI; 95% CI, -11.2, 13.4).	tbw	252-255	BRCA2 DNA repair associated	Homo sapiens	61-66
30407325-4	2018	Herein, we report the first case of a germline BRCA2-mutated unresectable advanced PACC patient who responded well to olaparib treatment.	olaparib	118-126	BRCA2 DNA repair associated	Homo sapiens	47-52
30092674-5	2018	Areas covered: This review focuses on the rationale for olaparib therapy in the context of relapsed epithelial ovarian cancer associated with a BRCA1 or BRCA2 mutation and summarizes the existing efficacy and safety data in this context.	olaparib	56-64	BRCA2 DNA repair associated	Homo sapiens	153-158
30333000-0	2018	Response to olaparib in metastatic castration-resistant prostate cancer with germline BRCA2 mutation: a case report.	olaparib	12-20	BRCA2 DNA repair associated	Homo sapiens	86-91
30333000-4	2018	CASE PRESENTATION: In this study, we describe a patient with metastatic castration-resistant prostate cancer (mCRPC) containing a BRCA2 germline mutation who underwent olaparib treatment.	olaparib	168-176	BRCA2 DNA repair associated	Homo sapiens	130-135
30041945-7	2018	This case illustrates that sarcoma patients may present unexpected but targetable genetic abnormalities and that BRCA2 loss-of-function may be targetable in sarcoma as it is associated with enhanced sensitivity to cisplatin.	Cisplatin	214-223	BRCA2 DNA repair associated	Homo sapiens	113-118
29313279-15	2018	Patients with BRCA1 or BRCA2 mutation, HRD positivity, and platinum sensitivity were more sensitive to ABT-767.	2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid	103-106	BRCA2 DNA repair associated	Homo sapiens	23-28
30271179-0	2018	Treatment with olaparib monotherapy for BRCA2-mutated refractory intrahepatic cholangiocarcinoma: a case report.	olaparib	15-23	BRCA2 DNA repair associated	Homo sapiens	40-45
30032296-7	2018	We found that BRCA2-deficient cells are less sensitive to PARP inhibitor and cisplatin treatment after E2F7 depletion.	Cisplatin	77-86	BRCA2 DNA repair associated	Homo sapiens	14-19
30271179-1	2018	Olaparib is an oral poly ADP-ribose polymerase inhibitor with activity in germline BRCA1 and BRCA2 (BRCA1/2)-associated breast and ovarian cancers.	olaparib	0-8	BRCA2 DNA repair associated	Homo sapiens	93-98
30271179-1	2018	Olaparib is an oral poly ADP-ribose polymerase inhibitor with activity in germline BRCA1 and BRCA2 (BRCA1/2)-associated breast and ovarian cancers.	olaparib	0-8	BRCA2 DNA repair associated	Homo sapiens	100-107
30271179-3	2018	This study is to observe the efficacy and safety of olaparib monotherapy in the refractory BRCA1/2-mutant intrahepatic cholangiocarcinoma (ICC) patient.	olaparib	52-60	BRCA2 DNA repair associated	Homo sapiens	91-98
30271179-4	2018	The clinical record of a patient with BRCA2-mutated refractory advanced ICC treated with olaparib was analyzed.	olaparib	89-97	BRCA2 DNA repair associated	Homo sapiens	38-43
30271179-11	2018	Olaparib in the treatment of BRCA2-mutation-associated refractory advanced ICC patent is effective, and the adverse effects are tolerated.	olaparib	0-8	BRCA2 DNA repair associated	Homo sapiens	29-34
30234108-3	2018	New intriguing scenarios are opening nowadays for the management of prostate cancer in patients with germline or somatic mutations in components of DNA repair pathways (e.g., BRCA1 and BRCA2 genes), such as specific screening policies and new therapeutic strategies involving PARP inhibitors or platinum-based chemotherapy.	Platinum	295-303	BRCA2 DNA repair associated	Homo sapiens	185-190
29748182-11	2018	Finally, we observed maximum cytotoxicity to the PARP inhibitor olaparib in BRCA2-/- organoids, similar to responses observed in patients.Conclusions: The LuCaP PDX/organoid models provide an expansive, genetically characterized platform to investigate the mechanisms of pathogenesis as well as therapeutic responses and their molecular correlates in mCRPC.	olaparib	64-72	BRCA2 DNA repair associated	Homo sapiens	76-81
30111871-1	2018	BACKGROUND: Mutations in BRCA1 and BRCA2 are associated with better survival in ovarian cancer (OC) patients due to a better response to platinum-based chemotherapy.	Platinum	137-145	BRCA2 DNA repair associated	Homo sapiens	35-40
29580149-2	2018	By using target capture-based deep sequencing to identify potential pathogenic germline mutations, followed by Sanger sequencing to determine the loci of the mutations, we identified a novel pathogenic BRCA2 mutation caused by a cytosine-to-guanine base substitution at position 4211, resulting in protein truncation (p.Ser1404Ter), which was confirmed by immunohistochemistry.	Cytosine	229-237	BRCA2 DNA repair associated	Homo sapiens	202-207
30110579-1	2018	BACKGROUND: The poly(adenosine diphosphate-ribose) inhibitor talazoparib has shown antitumor activity in patients with advanced breast cancer and germline mutations in BRCA1 and BRCA2 ( BRCA1/2).	talazoparib	61-72	BRCA2 DNA repair associated	Homo sapiens	178-183
30110579-1	2018	BACKGROUND: The poly(adenosine diphosphate-ribose) inhibitor talazoparib has shown antitumor activity in patients with advanced breast cancer and germline mutations in BRCA1 and BRCA2 ( BRCA1/2).	talazoparib	61-72	BRCA2 DNA repair associated	Homo sapiens	186-193
30110579-10	2018	CONCLUSIONS: Among patients with advanced breast cancer and a germline BRCA1/2 mutation, single-agent talazoparib provided a significant benefit over standard chemotherapy with respect to progression-free survival.	talazoparib	102-113	BRCA2 DNA repair associated	Homo sapiens	71-78
30258276-10	2018	Germline mutations in CDKN2A, BRCA2, STK11, PALB2, PRSS1, etc., as well as certain syndromes have been well associated with predisposition to PDAC.	pdac	142-146	BRCA2 DNA repair associated	Homo sapiens	30-35
30028120-2	2018	Owing to the ability of let-7a to repress DNA repair mechanisms (e.g., BRCA1 and BRCA2) and downregulate drug efflux pumps (e.g., ABCG2), delivery of let-7a could sensitize chemoresistant breast cancer cells (MDA-MB-231) to subsequent doxorubicin chemotherapy both in vitro and in vivo.	AN 7 peptide complex	28-30	BRCA2 DNA repair associated	Homo sapiens	81-86
30028120-2	2018	Owing to the ability of let-7a to repress DNA repair mechanisms (e.g., BRCA1 and BRCA2) and downregulate drug efflux pumps (e.g., ABCG2), delivery of let-7a could sensitize chemoresistant breast cancer cells (MDA-MB-231) to subsequent doxorubicin chemotherapy both in vitro and in vivo.	let-7a	24-30	BRCA2 DNA repair associated	Homo sapiens	81-86
30028120-2	2018	Owing to the ability of let-7a to repress DNA repair mechanisms (e.g., BRCA1 and BRCA2) and downregulate drug efflux pumps (e.g., ABCG2), delivery of let-7a could sensitize chemoresistant breast cancer cells (MDA-MB-231) to subsequent doxorubicin chemotherapy both in vitro and in vivo.	Doxorubicin	235-246	BRCA2 DNA repair associated	Homo sapiens	81-86
29580149-2	2018	By using target capture-based deep sequencing to identify potential pathogenic germline mutations, followed by Sanger sequencing to determine the loci of the mutations, we identified a novel pathogenic BRCA2 mutation caused by a cytosine-to-guanine base substitution at position 4211, resulting in protein truncation (p.Ser1404Ter), which was confirmed by immunohistochemistry.	Guanine	241-248	BRCA2 DNA repair associated	Homo sapiens	202-207
30026002-0	2018	Health-related quality of life and patient-centred outcomes with olaparib maintenance after chemotherapy in patients with platinum-sensitive, relapsed ovarian cancer and a BRCA1/2 mutation (SOLO2/ENGOT Ov-21): a placebo-controlled, phase 3 randomised trial.	olaparib	65-73	BRCA2 DNA repair associated	Homo sapiens	172-179
29937315-1	2018	A 42-year-old woman with a germline BRCA2 mutation and recurrent low-grade endometrioid endometrial adenocarcinoma experienced clinical and radiographic response to the poly (ADP ribose) polymerase (PARP) inhibitor, olaparib.	olaparib	216-224	BRCA2 DNA repair associated	Homo sapiens	36-41
30051491-4	2018	We suggest a broader and more accurate phrase to guide future work with this phenomenon: Food and alcohol disturbance (FAD).	Alcohols	98-105	BRCA2 DNA repair associated	Homo sapiens	119-122
29719197-0	2018	Metabolic cofactors NAD(P)H and FAD as potential indicators of cancer cell response to chemotherapy with paclitaxel.	Paclitaxel	105-115	BRCA2 DNA repair associated	Homo sapiens	32-35
29719197-3	2018	In this study we considered the auto-fluorescent metabolic cofactors NAD(P)H and FAD as possible indicators of cancer cell response to therapy with paclitaxel.	Paclitaxel	148-158	BRCA2 DNA repair associated	Homo sapiens	81-84
29719197-4	2018	It was found that, among the tested parameters (the fluorescence intensity-based redox ratio FAD/NAD(P)H, and the fluorescence lifetimes of NAD(P)H and FAD), the fluorescence lifetime of NAD(P)H is the most sensitive in tracking the drug response, and is capable of indicating heterogeneous cellular responses both in cell monolayers and in multicellular tumor spheroids.	nad(p)h	97-104	BRCA2 DNA repair associated	Homo sapiens	93-96
30026002-1	2018	BACKGROUND: In the phase 3 SOLO2 trial (ENGOT Ov-21), maintenance therapy with olaparib tablets significantly prolonged progression-free survival (primary endpoint) compared with placebo in patients with a germline BRCA1 or BRCA2 (BRCA1/2) mutation and platinum-sensitive, relapsed ovarian cancer who had received two or more lines of previous chemotherapy.	olaparib	79-87	BRCA2 DNA repair associated	Homo sapiens	224-229
30026002-1	2018	BACKGROUND: In the phase 3 SOLO2 trial (ENGOT Ov-21), maintenance therapy with olaparib tablets significantly prolonged progression-free survival (primary endpoint) compared with placebo in patients with a germline BRCA1 or BRCA2 (BRCA1/2) mutation and platinum-sensitive, relapsed ovarian cancer who had received two or more lines of previous chemotherapy.	olaparib	79-87	BRCA2 DNA repair associated	Homo sapiens	231-238
29802286-1	2018	Mutations in genes of the breast cancer susceptibility gene (BRCA) pathway, namely, BRCA1, BRCA2, and PALB2, can provide useful information for the efficacy of platinum-based or poly ADP-ribose polymerase inhibitors chemotherapeutic regimens.	Platinum	160-168	BRCA2 DNA repair associated	Homo sapiens	91-96
30050710-4	2018	This case represents a patient with metastatic breast cancer and germline BRCA2 mutation who developed erythema nodosum after initiation of therapy with olaparib capsules.	olaparib	153-161	BRCA2 DNA repair associated	Homo sapiens	74-79
29997359-2	2018	Olaparib is a targeted therapy used in patients presenting mutations in BRCA1 and BRCA2 genes.	olaparib	0-8	BRCA2 DNA repair associated	Homo sapiens	82-87
30038706-3	2018	The combination of everolimus and olaparib was tested in BRCA2-mutated patient-derived xenografts (PDX) carrying alterations in the PI3K/AKT/mTOR pathway.	olaparib	34-42	BRCA2 DNA repair associated	Homo sapiens	57-62
29729664-5	2018	While a previous case report demonstrated a surprising cure of platinum-resistant ovarian cancer with BRCA2 mutation by orally administered melphalan.	Platinum	63-71	BRCA2 DNA repair associated	Homo sapiens	102-107
29729664-5	2018	While a previous case report demonstrated a surprising cure of platinum-resistant ovarian cancer with BRCA2 mutation by orally administered melphalan.	Melphalan	140-149	BRCA2 DNA repair associated	Homo sapiens	102-107
29617652-0	2018	Multifaceted Impact of MicroRNA 493-5p on Genome-Stabilizing Pathways Induces Platinum and PARP Inhibitor Resistance in BRCA2-Mutated Carcinomas.	Platinum	78-86	BRCA2 DNA repair associated	Homo sapiens	120-125
28929593-0	2018	Efficacy of anthracycline/taxane-based neo-adjuvant chemotherapy on triple-negative breast cancer in BRCA1/BRCA2 mutation carriers.	Anthracyclines	12-25	BRCA2 DNA repair associated	Homo sapiens	107-112
28929593-0	2018	Efficacy of anthracycline/taxane-based neo-adjuvant chemotherapy on triple-negative breast cancer in BRCA1/BRCA2 mutation carriers.	taxane	26-32	BRCA2 DNA repair associated	Homo sapiens	107-112
29617652-3	2018	Utilizing primary and recurrent BRCA1/2-mutated carcinomas from OC patients, patient-derived lines, and an in vivo BRCA2-mutated mouse model, we identified a microRNA, miR-493-5p, that induced platinum/PARPi resistance exclusively in BRCA2-mutated carcinomas.	Platinum	193-201	BRCA2 DNA repair associated	Homo sapiens	115-120
29617652-7	2018	We conclude that impact of miR-493-5p on multiple pathways pertinent to genome stability cumulatively causes PARPi/platinum resistance in BRCA2 mutant carcinomas.	Platinum	115-123	BRCA2 DNA repair associated	Homo sapiens	138-143
29325860-0	2018	BRCA2 Reversion Mutation Associated With Acquired Resistance to Olaparib in Estrogen Receptor-positive Breast Cancer Detected by Genomic Profiling of Tissue and Liquid Biopsy.	olaparib	64-72	BRCA2 DNA repair associated	Homo sapiens	0-5
30345412-4	2018	Here we review recent advances in our understanding of BRCA1 and BRCA2, including how they genetically interact with other repair factors, how they protect stalled replication forks, how they affect the response to aldehydes, and how loss of their functions links to mutation signatures.	Aldehydes	215-224	BRCA2 DNA repair associated	Homo sapiens	65-70
29309945-9	2018	Within the BRCA1/BRCA2 mutated group, having had platinum-based adjuvant chemotherapy (n = 10) was associated with better survival than alternative chemotherapy (n = 8) or no adjuvant therapy (n = 4) (31.0 vs 17.8 vs 9.3 months, respectively, p < 0.001).	Platinum	49-57	BRCA2 DNA repair associated	Homo sapiens	17-22
29309945-11	2018	However, platinum-based chemotherapy regimens were associated with markedly improved survival in patients with BRCA1/BRCA2 mutations, with survival differences no longer appreciated with wild-type patients.	Platinum	9-17	BRCA2 DNA repair associated	Homo sapiens	117-122
29541174-2	2018	BRCA2-associated ovarian carcinomas predominantly possess a high-grade serous phenotype, which respond to platinum and targeted therapy with PARP inhibitors.	Platinum	106-114	BRCA2 DNA repair associated	Homo sapiens	0-5
29389832-0	2018	Treatment With Azacitidine in the Context of Palliative Care for a Patient With Acute Myeloid Leukemia Complicating Fanconi Anemia With Biallelic FANCD1/BRCA 2 Mutations.	Azacitidine	15-26	BRCA2 DNA repair associated	Homo sapiens	146-152
29389832-0	2018	Treatment With Azacitidine in the Context of Palliative Care for a Patient With Acute Myeloid Leukemia Complicating Fanconi Anemia With Biallelic FANCD1/BRCA 2 Mutations.	Azacitidine	15-26	BRCA2 DNA repair associated	Homo sapiens	153-159
28751443-2	2017	The FDA also approved the FoundationFocus CDx BRCA test (Foundation Medicine, Inc.), the first next-generation sequencing-based companion diagnostic, for identifying patients with advanced ovarian cancer eligible for treatment with rucaparib based on detection of deleterious BRCA1 and/or BRCA2 mutations in tumor tissue.	rucaparib	232-241	BRCA2 DNA repair associated	Homo sapiens	289-294
29382645-1	2018	The FDA has approved olaparib, a PARP inhibitor, for use in patients with metastatic breast cancer who also carry a germline BRCA1 or BRCA2 mutation.	olaparib	21-29	BRCA2 DNA repair associated	Homo sapiens	134-139
32913984-0	2018	Polyclonal BRCA2 Reversion Mutations Detected in Circulating Tumor DNA After Platinum Chemotherapy in a Patient With Metastatic Prostate Cancer.	Platinum	77-85	BRCA2 DNA repair associated	Homo sapiens	11-16
29331492-10	2018	Furthermore, BRCA2 was an independent unfavorable prognostic factor for disease-free survival and overall survival (P < 0.001) in GC patients who underwent platinum-based adjuvant chemotherapy.	Platinum	159-167	BRCA2 DNA repair associated	Homo sapiens	13-18
29298688-0	2018	Enhanced response rate to pegylated liposomal doxorubicin in high grade serous ovarian carcinomas harbouring BRCA1 and BRCA2 aberrations.	Doxorubicin	46-57	BRCA2 DNA repair associated	Homo sapiens	119-124
29298688-3	2018	Here, we seek to investigate whether BRCA1/2 status influences the response rate to single-agent pegylated liposomal doxorubicin (PLD) in high grade serous (HGS) OC.	Doxorubicin	117-128	BRCA2 DNA repair associated	Homo sapiens	37-44
29066501-0	2018	Knockdown of BRCA2 enhances cisplatin and cisplatin-induced autophagy in ovarian cancer cells.	Cisplatin	28-37	BRCA2 DNA repair associated	Homo sapiens	13-18
29066501-0	2018	Knockdown of BRCA2 enhances cisplatin and cisplatin-induced autophagy in ovarian cancer cells.	Cisplatin	42-51	BRCA2 DNA repair associated	Homo sapiens	13-18
29066501-2	2018	Here, we demonstrated that platinum-resistant cancer had a higher percentage of high BRCA2 level (87.5% vs 43.6%, P = 0.001), and that patients with a low BRCA2 level in cancer tissues had longer progression-free survival (with a median time of 28.0 vs 12.0 months, P < 0.001) and platinum-free duration (with a median time of 19.0 vs 5.0 months, P < 0.001) compared with those with a high BRCA2 level.	Platinum	27-35	BRCA2 DNA repair associated	Homo sapiens	85-90
29066501-2	2018	Here, we demonstrated that platinum-resistant cancer had a higher percentage of high BRCA2 level (87.5% vs 43.6%, P = 0.001), and that patients with a low BRCA2 level in cancer tissues had longer progression-free survival (with a median time of 28.0 vs 12.0 months, P < 0.001) and platinum-free duration (with a median time of 19.0 vs 5.0 months, P < 0.001) compared with those with a high BRCA2 level.	Platinum	27-35	BRCA2 DNA repair associated	Homo sapiens	155-160
29066501-2	2018	Here, we demonstrated that platinum-resistant cancer had a higher percentage of high BRCA2 level (87.5% vs 43.6%, P = 0.001), and that patients with a low BRCA2 level in cancer tissues had longer progression-free survival (with a median time of 28.0 vs 12.0 months, P < 0.001) and platinum-free duration (with a median time of 19.0 vs 5.0 months, P < 0.001) compared with those with a high BRCA2 level.	Platinum	27-35	BRCA2 DNA repair associated	Homo sapiens	155-160
29066501-2	2018	Here, we demonstrated that platinum-resistant cancer had a higher percentage of high BRCA2 level (87.5% vs 43.6%, P = 0.001), and that patients with a low BRCA2 level in cancer tissues had longer progression-free survival (with a median time of 28.0 vs 12.0 months, P < 0.001) and platinum-free duration (with a median time of 19.0 vs 5.0 months, P < 0.001) compared with those with a high BRCA2 level.	Platinum	284-292	BRCA2 DNA repair associated	Homo sapiens	155-160
29066501-2	2018	Here, we demonstrated that platinum-resistant cancer had a higher percentage of high BRCA2 level (87.5% vs 43.6%, P = 0.001), and that patients with a low BRCA2 level in cancer tissues had longer progression-free survival (with a median time of 28.0 vs 12.0 months, P < 0.001) and platinum-free duration (with a median time of 19.0 vs 5.0 months, P < 0.001) compared with those with a high BRCA2 level.	Platinum	284-292	BRCA2 DNA repair associated	Homo sapiens	155-160
29066501-3	2018	In human ovarian cancer cell lines CAOV-3 and ES-2, cisplatin induced an upregulation of the RAD51 protein, which was inhibited after silencing BRCA2; silencing BRCA2 enhanced the action of cisplatin in vitro and in vivo Knockdown of BRCA2 promoted cisplatin-induced autophagy.	Cisplatin	52-61	BRCA2 DNA repair associated	Homo sapiens	144-149
29066501-3	2018	In human ovarian cancer cell lines CAOV-3 and ES-2, cisplatin induced an upregulation of the RAD51 protein, which was inhibited after silencing BRCA2; silencing BRCA2 enhanced the action of cisplatin in vitro and in vivo Knockdown of BRCA2 promoted cisplatin-induced autophagy.	Cisplatin	52-61	BRCA2 DNA repair associated	Homo sapiens	161-166
29066501-3	2018	In human ovarian cancer cell lines CAOV-3 and ES-2, cisplatin induced an upregulation of the RAD51 protein, which was inhibited after silencing BRCA2; silencing BRCA2 enhanced the action of cisplatin in vitro and in vivo Knockdown of BRCA2 promoted cisplatin-induced autophagy.	Cisplatin	52-61	BRCA2 DNA repair associated	Homo sapiens	161-166
29066501-3	2018	In human ovarian cancer cell lines CAOV-3 and ES-2, cisplatin induced an upregulation of the RAD51 protein, which was inhibited after silencing BRCA2; silencing BRCA2 enhanced the action of cisplatin in vitro and in vivo Knockdown of BRCA2 promoted cisplatin-induced autophagy.	Cisplatin	190-199	BRCA2 DNA repair associated	Homo sapiens	144-149
29066501-3	2018	In human ovarian cancer cell lines CAOV-3 and ES-2, cisplatin induced an upregulation of the RAD51 protein, which was inhibited after silencing BRCA2; silencing BRCA2 enhanced the action of cisplatin in vitro and in vivo Knockdown of BRCA2 promoted cisplatin-induced autophagy.	Cisplatin	190-199	BRCA2 DNA repair associated	Homo sapiens	161-166
29066501-3	2018	In human ovarian cancer cell lines CAOV-3 and ES-2, cisplatin induced an upregulation of the RAD51 protein, which was inhibited after silencing BRCA2; silencing BRCA2 enhanced the action of cisplatin in vitro and in vivo Knockdown of BRCA2 promoted cisplatin-induced autophagy.	Cisplatin	190-199	BRCA2 DNA repair associated	Homo sapiens	161-166
29066501-3	2018	In human ovarian cancer cell lines CAOV-3 and ES-2, cisplatin induced an upregulation of the RAD51 protein, which was inhibited after silencing BRCA2; silencing BRCA2 enhanced the action of cisplatin in vitro and in vivo Knockdown of BRCA2 promoted cisplatin-induced autophagy.	Cisplatin	190-199	BRCA2 DNA repair associated	Homo sapiens	144-149
29066501-3	2018	In human ovarian cancer cell lines CAOV-3 and ES-2, cisplatin induced an upregulation of the RAD51 protein, which was inhibited after silencing BRCA2; silencing BRCA2 enhanced the action of cisplatin in vitro and in vivo Knockdown of BRCA2 promoted cisplatin-induced autophagy.	Cisplatin	190-199	BRCA2 DNA repair associated	Homo sapiens	161-166
29066501-3	2018	In human ovarian cancer cell lines CAOV-3 and ES-2, cisplatin induced an upregulation of the RAD51 protein, which was inhibited after silencing BRCA2; silencing BRCA2 enhanced the action of cisplatin in vitro and in vivo Knockdown of BRCA2 promoted cisplatin-induced autophagy.	Cisplatin	190-199	BRCA2 DNA repair associated	Homo sapiens	161-166
29066501-4	2018	Interestingly, the autophagy blocker chloroquine enhanced cisplatin in BRCA2-silenced cells accompanied by an increase in apoptotic cells, which did not occur in BRCA2-intact cells; chloroquine enhanced the efficacy of cisplatin against BRCA2-silenced CAOV-3 tumors in vivo, with an increase in LC3-II level in tumor tissues.	Chloroquine	37-48	BRCA2 DNA repair associated	Homo sapiens	71-76
29066501-4	2018	Interestingly, the autophagy blocker chloroquine enhanced cisplatin in BRCA2-silenced cells accompanied by an increase in apoptotic cells, which did not occur in BRCA2-intact cells; chloroquine enhanced the efficacy of cisplatin against BRCA2-silenced CAOV-3 tumors in vivo, with an increase in LC3-II level in tumor tissues.	Cisplatin	58-67	BRCA2 DNA repair associated	Homo sapiens	71-76
29066501-5	2018	Sensitization of cisplatin was also observed in BRCA2-silenced CAOV-3 cells after inhibiting ATG7, confirming that chloroquine modulated the sensitivity via the autophagy pathway.	Cisplatin	17-26	BRCA2 DNA repair associated	Homo sapiens	48-53
29066501-5	2018	Sensitization of cisplatin was also observed in BRCA2-silenced CAOV-3 cells after inhibiting ATG7, confirming that chloroquine modulated the sensitivity via the autophagy pathway.	Chloroquine	115-126	BRCA2 DNA repair associated	Homo sapiens	48-53
29066501-6	2018	These data suggest that a low BRCA2 level can predict better platinum sensitivity and prognosis, and that the modulation of autophagy can be a chemosensitizer for certain cancers.	Platinum	61-69	BRCA2 DNA repair associated	Homo sapiens	30-35
30051098-17	2018	Conclusion: Rucaparib provided clinical benefit to patients with advanced pancreatic cancer and a BRCA1/2 mutation, and demonstrated an acceptable safety profile.	rucaparib	12-21	BRCA2 DNA repair associated	Homo sapiens	98-105
31501807-0	2018	Acquired Resistance to Poly (ADP-ribose) Polymerase Inhibitor Olaparib in BRCA2-Associated Prostate Cancer Resulting From Biallelic BRCA2 Reversion Mutations Restores Both Germline and Somatic Loss-of-Function Mutations.	olaparib	62-70	BRCA2 DNA repair associated	Homo sapiens	74-79
31501807-4	2018	We describe a case of metastatic CRPC with germline BRCA2 mutation with acquired resistance to olaparib related to biallelic BRCA2 reversion mutations of both the germline and somatic loss of function alleles detected by circulating tumor DNA testing.	olaparib	95-103	BRCA2 DNA repair associated	Homo sapiens	125-130
31501807-6	2018	Within the germline BRCA2-positive cases exposed to platinum chemotherapy or PARP inhibition, the prevalence of reversion mutations was 40%.	Platinum	52-60	BRCA2 DNA repair associated	Homo sapiens	20-25
29651367-0	2018	"Lazarus Response" to Olaparib in a Virtually Chemonaive Breast Cancer Patient Carrying Gross BRCA2 Gene Deletion.	olaparib	22-30	BRCA2 DNA repair associated	Homo sapiens	94-99
29545922-8	2018	We found that BRCA2 protein expression was downregulated following pimasertib treatment under hypoxic conditions.	N-(2,3-dihydroxypropyl)-1-((2-fluoro-4-iodophenyl)amino)isonicotinamide	67-77	BRCA2 DNA repair associated	Homo sapiens	14-19
29346284-2	2018	The BRCA2 p.Lys3326Ter (K3326X) (rs11571833) mutation identified in our patient is a debated substitution of thymidine for adenine which is currently regarded as benign polymorphism in main gene databases.	Thymidine	109-118	BRCA2 DNA repair associated	Homo sapiens	4-9
29346284-2	2018	The BRCA2 p.Lys3326Ter (K3326X) (rs11571833) mutation identified in our patient is a debated substitution of thymidine for adenine which is currently regarded as benign polymorphism in main gene databases.	Adenine	123-130	BRCA2 DNA repair associated	Homo sapiens	4-9
28765325-1	2017	Purpose: Resistance to platinum-based chemotherapy or PARP inhibition in germline BRCA1 or BRCA2 mutation carriers may occur through somatic reversion mutations or intragenic deletions that restore BRCA1 or BRCA2 function.	Platinum	23-31	BRCA2 DNA repair associated	Homo sapiens	91-96
29121949-6	2017	The BRCA2, CYP1A1, CYP1B1, CDK1, SFN and VEGFA genes were observed to be upregulated specifically from increased CdSe exposure and suggests their possible utility as biomarkers for toxicity.	cdse	113-117	BRCA2 DNA repair associated	Homo sapiens	4-9
28765325-1	2017	Purpose: Resistance to platinum-based chemotherapy or PARP inhibition in germline BRCA1 or BRCA2 mutation carriers may occur through somatic reversion mutations or intragenic deletions that restore BRCA1 or BRCA2 function.	Platinum	23-31	BRCA2 DNA repair associated	Homo sapiens	207-212
28841282-3	2017	When administered with a BRCA2-Rad51 disruptor in nonmutant cells, Olaparib showed anticancer activity comparable to that shown when administered alone in BRCA2-defective cells.	olaparib	67-75	BRCA2 DNA repair associated	Homo sapiens	25-30
28882436-0	2017	Antitumor activity and safety of the PARP inhibitor rucaparib in patients with high-grade ovarian carcinoma and a germline or somatic BRCA1 or BRCA2 mutation: Integrated analysis of data from Study 10 and ARIEL2.	rucaparib	52-61	BRCA2 DNA repair associated	Homo sapiens	143-148
28882436-13	2017	CONCLUSIONS: Rucaparib has antitumor activity in advanced BRCA1/2-mutated HGOC and a manageable safety profile.	rucaparib	13-22	BRCA2 DNA repair associated	Homo sapiens	58-65
28841282-3	2017	When administered with a BRCA2-Rad51 disruptor in nonmutant cells, Olaparib showed anticancer activity comparable to that shown when administered alone in BRCA2-defective cells.	olaparib	67-75	BRCA2 DNA repair associated	Homo sapiens	155-160
29093017-12	2017	Notably, four of five talazoparib-sensitive models did not harbor germline BRCA1/2 mutations, but several had somatic alterations in homologous repair pathways, including ATM deletion and BRCA2 alterations.Conclusions: PDXs capture the molecular and phenotypic heterogeneity of TNBC.	talazoparib	22-33	BRCA2 DNA repair associated	Homo sapiens	188-193
29285471-9	2017	Among 45 samples of Ca-ex-PA, 93.3% of showed positivity for BRCA1 and 80% of samples showed positivity for BRCA2.	ca-ex-pa	20-28	BRCA2 DNA repair associated	Homo sapiens	108-113
28715532-18	2017	Conclusions and Relevance: Under the nonstandard GeparSixto polychemotherapy regimen, patients without BRCA1 and BRCA2 germline mutations benefited from the addition of carboplatin and those with BRCA1 and BRCA2 mutations showed superior response rates without additive effects observed for carboplatin.	Carboplatin	169-180	BRCA2 DNA repair associated	Homo sapiens	206-211
28982360-6	2017	CONCLUSIONS: The present study shows that the G allele carriers of BRCA2 rs9534275 were associated with increased serum TC and ApoB levels in the CAD patients and increased risk of CAD and IS.	Technetium	120-122	BRCA2 DNA repair associated	Homo sapiens	67-72
28604461-1	2017	OBJECTIVE: Serous adenocarcinomas that arise in patients with inherited mutations in the tumor suppressor genes BRCA1 and BRCA2 are initially well treatable with platinum/paclitaxel.	Platinum	162-170	BRCA2 DNA repair associated	Homo sapiens	122-127
28604461-1	2017	OBJECTIVE: Serous adenocarcinomas that arise in patients with inherited mutations in the tumor suppressor genes BRCA1 and BRCA2 are initially well treatable with platinum/paclitaxel.	Paclitaxel	171-181	BRCA2 DNA repair associated	Homo sapiens	122-127
28604461-2	2017	For recurrent disease in patients with BRCA1 or BRCA2 mutations, olaparib treatment is available.	olaparib	65-73	BRCA2 DNA repair associated	Homo sapiens	48-53
28729482-0	2017	BRCA1 and BRCA2 tumor suppressors protect against endogenous acetaldehyde toxicity.	Acetaldehyde	61-73	BRCA2 DNA repair associated	Homo sapiens	10-15
28729482-4	2017	We demonstrate that inactivation of HR factors BRCA1, BRCA2, or RAD51 hypersensitizes cells to acetaldehyde treatment, in spite of the FA pathway being functional.	Acetaldehyde	95-107	BRCA2 DNA repair associated	Homo sapiens	54-59
28729482-8	2017	Hypersensitivity of cells lacking BRCA2 to acetaldehyde stems from accumulation of toxic replication-associated DNA damage, leading to checkpoint activation, G2/M arrest, and cell death.	Acetaldehyde	43-55	BRCA2 DNA repair associated	Homo sapiens	34-39
28729482-9	2017	Acetaldehyde-arrested replication forks require BRCA2 and FANCD2 for protection against MRE11-dependent degradation.	Acetaldehyde	0-12	BRCA2 DNA repair associated	Homo sapiens	48-53
28588062-1	2017	High-grade epithelial ovarian carcinomas containing mutated BRCA1 or BRCA2 (BRCA1/2) homologous recombination (HR) genes are sensitive to platinum-based chemotherapy and PARP inhibitors (PARPi), while restoration of HR function due to secondary mutations in BRCA1/2 has been recognized as an important resistance mechanism.	Platinum	138-146	BRCA2 DNA repair associated	Homo sapiens	69-74
28608931-0	2017	The association between germline BRCA2 variants and sensitivity to platinum-based chemotherapy among men with metastatic prostate cancer.	Platinum	67-75	BRCA2 DNA repair associated	Homo sapiens	33-38
28608931-1	2017	BACKGROUND: Breast cancer 2 (BRCA2)-associated breast and ovarian cancers are sensitive to platinum-based chemotherapy.	Platinum	91-99	BRCA2 DNA repair associated	Homo sapiens	12-27
28608931-1	2017	BACKGROUND: Breast cancer 2 (BRCA2)-associated breast and ovarian cancers are sensitive to platinum-based chemotherapy.	Platinum	91-99	BRCA2 DNA repair associated	Homo sapiens	29-34
28608931-3	2017	METHODS: A retrospective analysis of a single-institution cohort of men with castration-resistant, metastatic prostate cancer was performed to determine the association between carrier status of pathogenic BRCA2 germline variants and prostate-specific antigen response to carboplatin-based chemotherapy.	Carboplatin	272-283	BRCA2 DNA repair associated	Homo sapiens	206-211
28608931-8	2017	Associations between BRCA2 mutation status and response to carboplatin-based chemotherapy were tested using the Fisher exact test, with a 2-sided P value < .05 as the threshold for significance.	Carboplatin	59-70	BRCA2 DNA repair associated	Homo sapiens	21-26
28608931-12	2017	CONCLUSIONS: BRCA2-associated, castration-resistant prostate cancer is associated with a higher likelihood of response to carboplatin-based chemotherapy than non-BRCA2-associated prostate cancer.	Carboplatin	122-133	BRCA2 DNA repair associated	Homo sapiens	13-18
28450425-6	2017	At disease progression, following response to olaparib, multiple subclonal aberrations reverting germline and somatic DNA repair mutations (BRCA2, PALB2) back in frame emerged as mechanisms of resistance.	olaparib	46-54	BRCA2 DNA repair associated	Homo sapiens	140-145
28450426-1	2017	Approximately 20% of metastatic prostate cancers harbor mutations in genes required for DNA repair by homologous recombination repair (HRR) such as BRCA2 HRR defects confer synthetic lethality to PARP inhibitors (PARPi) such as olaparib and talazoparib.	olaparib	228-236	BRCA2 DNA repair associated	Homo sapiens	148-153
28450426-1	2017	Approximately 20% of metastatic prostate cancers harbor mutations in genes required for DNA repair by homologous recombination repair (HRR) such as BRCA2 HRR defects confer synthetic lethality to PARP inhibitors (PARPi) such as olaparib and talazoparib.	talazoparib	241-252	BRCA2 DNA repair associated	Homo sapiens	148-153
28450426-2	2017	In ovarian or breast cancers, olaparib resistance has been associated with HRR restoration, including by BRCA2 mutation reversion.	olaparib	30-38	BRCA2 DNA repair associated	Homo sapiens	105-110
28450426-4	2017	Here, we identify BRCA2 reversion mutations associated with olaparib and talazoparib resistance in patients with prostate cancer.	olaparib	60-68	BRCA2 DNA repair associated	Homo sapiens	18-23
28450426-4	2017	Here, we identify BRCA2 reversion mutations associated with olaparib and talazoparib resistance in patients with prostate cancer.	talazoparib	73-84	BRCA2 DNA repair associated	Homo sapiens	18-23
28450426-6	2017	Here, we show BRCA2 reversion mutations in patients with prostate cancer with metastatic disease who developed resistance to talazoparib and olaparib.	talazoparib	125-136	BRCA2 DNA repair associated	Homo sapiens	14-19
28450426-6	2017	Here, we show BRCA2 reversion mutations in patients with prostate cancer with metastatic disease who developed resistance to talazoparib and olaparib.	olaparib	141-149	BRCA2 DNA repair associated	Homo sapiens	14-19
28588062-1	2017	High-grade epithelial ovarian carcinomas containing mutated BRCA1 or BRCA2 (BRCA1/2) homologous recombination (HR) genes are sensitive to platinum-based chemotherapy and PARP inhibitors (PARPi), while restoration of HR function due to secondary mutations in BRCA1/2 has been recognized as an important resistance mechanism.	Platinum	138-146	BRCA2 DNA repair associated	Homo sapiens	76-83
28588062-1	2017	High-grade epithelial ovarian carcinomas containing mutated BRCA1 or BRCA2 (BRCA1/2) homologous recombination (HR) genes are sensitive to platinum-based chemotherapy and PARP inhibitors (PARPi), while restoration of HR function due to secondary mutations in BRCA1/2 has been recognized as an important resistance mechanism.	Platinum	138-146	BRCA2 DNA repair associated	Homo sapiens	258-265
27357817-7	2017	The development of poly(adenosine diphosphate-ribose) polymerase inhibitors represents a novel therapeutic strategy, in which poly(adenosine diphosphate-ribose) inhibition leads to the formation of double-stranded DNA breaks that cannot be accurately repaired in BRCA1- or BRCA2-mutated tumors, thus leading to tumor cell death.	Poly Adenosine Diphosphate Ribose	19-53	BRCA2 DNA repair associated	Homo sapiens	273-278
28223274-8	2017	In the olaparib LT group, 244 genetic alterations were detected, with TP53, BRCA1, and BRCA2 mutations being most common (90%, 25%, and 35%, respectively).	olaparib	7-15	BRCA2 DNA repair associated	Homo sapiens	87-92
28928839-6	2017	BRCA2 knockdown with small interfering RNA decreased the docetaxel resistance of PC3DR2 cells.	Docetaxel	57-66	BRCA2 DNA repair associated	Homo sapiens	0-5
28928839-7	2017	These results suggest that BRCA2 serves an important role in the docetaxel resistance of prostate cancer cells.	Docetaxel	65-74	BRCA2 DNA repair associated	Homo sapiens	27-32
28928839-8	2017	In addition, BRCA2 modulation may be a strategy to partially reverse docetaxel resistance in prostate cancer.	Docetaxel	69-78	BRCA2 DNA repair associated	Homo sapiens	13-18
28431939-0	2017	Modulation of HAT activity by the BRCA2 N372H variation is a novel mechanism of paclitaxel resistance in breast cancer cell lines.	Paclitaxel	80-90	BRCA2 DNA repair associated	Homo sapiens	34-39
28431939-3	2017	In the present study, we define a new resistance mechanism to paclitaxel based on BRCA2 variation.	Paclitaxel	62-72	BRCA2 DNA repair associated	Homo sapiens	82-87
28431939-14	2017	Forced expression of the BRCA2 heterozygous variant induced paclitaxel resistance due to altered HAT activity (p<0.001).	Paclitaxel	60-70	BRCA2 DNA repair associated	Homo sapiens	25-30
28431939-16	2017	Restoration of wild BRCA2 from variant type improved paclitaxel sensitivity (p<0.001).	Paclitaxel	53-63	BRCA2 DNA repair associated	Homo sapiens	20-25
28431939-17	2017	Modulation of HAT activity by BRCA2 N372H variation is a new mechanism of paclitaxel resistance in breast cancer.	Paclitaxel	74-84	BRCA2 DNA repair associated	Homo sapiens	30-35
28739695-8	2017	Increased radiosensitivity by arsenite was also abolished following knock-down of BRCA2.	arsenite	30-38	BRCA2 DNA repair associated	Homo sapiens	82-87
28739695-9	2017	In addition, the increased radiosensitization by arsenite was correlated with AAC, which was abolished by BRCA2 knock-down.	arsenite	49-57	BRCA2 DNA repair associated	Homo sapiens	106-111
28739695-10	2017	CONCLUSION: We conclude that radiosensitization by arsenite is related to ROS and BRCA2 function.	arsenite	51-59	BRCA2 DNA repair associated	Homo sapiens	82-87
28467918-2	2017	The tetrahydroisoquinolone trabectedin administered at 1.3 mg/m2 as a 3-h intravenous infusion every 3 weeks showed activity in patients with pretreated metastatic breast cancer (MBC) and BRCA germline mutations, but mainly in BRCA2 carriers.	Trabectedin	27-38	BRCA2 DNA repair associated	Homo sapiens	227-232
28467918-9	2017	77% of BRCA1 and 31% of BRCA2 carriers were platinum-pretreated.	Platinum	44-52	BRCA2 DNA repair associated	Homo sapiens	24-29
28356425-1	2017	Purpose: We aimed to establish the MTD of the poly (ADP-ribose) (PAR) polymerase inhibitor, veliparib, in combination with carboplatin in germline BRCA1- and BRCA2- (BRCA)-associated metastatic breast cancer (MBC), to assess the efficacy of single-agent veliparib, and of the combination treatment after progression, and to correlate PAR levels with clinical outcome.Experimental Design: Phase I patients received carboplatin (AUC of 5-6, every 21 days), with escalating doses (50-20 mg) of oral twice-daily (BID) veliparib.	veliparib	92-101	BRCA2 DNA repair associated	Homo sapiens	158-163
28356425-1	2017	Purpose: We aimed to establish the MTD of the poly (ADP-ribose) (PAR) polymerase inhibitor, veliparib, in combination with carboplatin in germline BRCA1- and BRCA2- (BRCA)-associated metastatic breast cancer (MBC), to assess the efficacy of single-agent veliparib, and of the combination treatment after progression, and to correlate PAR levels with clinical outcome.Experimental Design: Phase I patients received carboplatin (AUC of 5-6, every 21 days), with escalating doses (50-20 mg) of oral twice-daily (BID) veliparib.	Carboplatin	123-134	BRCA2 DNA repair associated	Homo sapiens	158-163
28754483-0	2017	Olaparib tablets as maintenance therapy in patients with platinum-sensitive, relapsed ovarian cancer and a BRCA1/2 mutation (SOLO2/ENGOT-Ov21): a double-blind, randomised, placebo-controlled, phase 3 trial.	olaparib	0-8	BRCA2 DNA repair associated	Homo sapiens	107-114
28754483-2	2017	We aimed to confirm these findings in patients with a BRCA1 or BRCA2 (BRCA1/2) mutation using a tablet formulation of olaparib.	olaparib	118-126	BRCA2 DNA repair associated	Homo sapiens	63-68
28754483-2	2017	We aimed to confirm these findings in patients with a BRCA1 or BRCA2 (BRCA1/2) mutation using a tablet formulation of olaparib.	olaparib	118-126	BRCA2 DNA repair associated	Homo sapiens	70-77
28754483-3	2017	METHODS: This international, multicentre, double-blind, randomised, placebo-controlled, phase 3 trial evaluated olaparib tablet maintenance treatment in platinum-sensitive, relapsed ovarian cancer patients with a BRCA1/2 mutation who had received at least two lines of previous chemotherapy.	olaparib	112-120	BRCA2 DNA repair associated	Homo sapiens	213-220
28754483-18	2017	INTERPRETATION: Olaparib tablet maintenance treatment provided a significant progression-free survival improvement with no detrimental effect on quality of life in patients with platinum-sensitive, relapsed ovarian cancer and a BRCA1/2 mutation.	olaparib	16-24	BRCA2 DNA repair associated	Homo sapiens	228-235
28467918-2	2017	The tetrahydroisoquinolone trabectedin administered at 1.3 mg/m2 as a 3-h intravenous infusion every 3 weeks showed activity in patients with pretreated metastatic breast cancer (MBC) and BRCA germline mutations, but mainly in BRCA2 carriers.	tetrahydroisoquinolone	4-26	BRCA2 DNA repair associated	Homo sapiens	227-232
28459440-4	2017	Thiolutin also inhibits the JAMM metalloproteases Csn5, the deneddylase of the COP9 signalosome; AMSH, which regulates ubiquitin-dependent sorting of cell-surface receptors; and BRCC36, a K63-specific deubiquitinase of the BRCC36-containing isopeptidase complex and the BRCA1-BRCA2-containing complex.	acetopyrrothine	0-9	BRCA2 DNA repair associated	Homo sapiens	276-281
28676659-7	2017	Patients with a BRCA2 mutation showed a response rate of 25% to docetaxel in comparison to 71.1% in men with wildtype BRCA2 (p = 0.019).	Docetaxel	64-73	BRCA2 DNA repair associated	Homo sapiens	16-21
28676659-11	2017	Our results suggest that a close oncological monitoring of patients with BRCA2 mutations for taxane resistance is warranted.	taxane	93-99	BRCA2 DNA repair associated	Homo sapiens	73-78
28087643-1	2017	Purpose: In germline BRCA1 or BRCA2 (BRCA1/2) mutation carriers, restoration of tumor BRCA1/2 function by a secondary mutation is recognized as a mechanism of resistance to platinum and PARP inhibitors, primarily in ovarian cancer.	Platinum	173-181	BRCA2 DNA repair associated	Homo sapiens	30-35
28087643-1	2017	Purpose: In germline BRCA1 or BRCA2 (BRCA1/2) mutation carriers, restoration of tumor BRCA1/2 function by a secondary mutation is recognized as a mechanism of resistance to platinum and PARP inhibitors, primarily in ovarian cancer.	Platinum	173-181	BRCA2 DNA repair associated	Homo sapiens	37-44
28087643-1	2017	Purpose: In germline BRCA1 or BRCA2 (BRCA1/2) mutation carriers, restoration of tumor BRCA1/2 function by a secondary mutation is recognized as a mechanism of resistance to platinum and PARP inhibitors, primarily in ovarian cancer.	Platinum	173-181	BRCA2 DNA repair associated	Homo sapiens	86-93
28623073-0	2017	Commentary on "Biallelic inactivation of BRCA2 in platinum-sensitive metastatic castration-resistant prostate cancer".	Platinum	50-58	BRCA2 DNA repair associated	Homo sapiens	41-46
28623073-8	2017	Biallelic BRCA2 inactivation in mCRPC warrants further exploration as a predictive biomarker for sensitivity to platinum chemotherapy.	Platinum	112-120	BRCA2 DNA repair associated	Homo sapiens	10-15
28525389-0	2017	Biological and clinical evidence for somatic mutations in BRCA1 and BRCA2 as predictive markers for olaparib response in high-grade serous ovarian cancers in the maintenance setting.	olaparib	100-108	BRCA2 DNA repair associated	Homo sapiens	68-73
28410213-4	2017	The results showed that carrying a BRCA2 mutation was correlated with a reduced CSS and OS when compared with that of non-carriers, with pooled Hazard Ratios (HRs) of 2.53 (95% confidence interval (CI): 2.10-3.06, P < 0.001) and 2.21 (95% CI: 1.64-2.99, P < 0.001), respectively.	thiocysteine	80-83	BRCA2 DNA repair associated	Homo sapiens	35-40
28944232-5	2017	RESULTS: In this series, we found four pathogenic mutations, three previously reported (BRCA1: c.302-1G>C and c.815_824dup10; BRCA2: c.5946delT) and a duplication of adenines in exon 15 in BRCA1 gene (c.4647_4648dupAA, ClinVar SCV000256598.1).	Adenine	169-177	BRCA2 DNA repair associated	Homo sapiens	129-134
28445046-4	2017	We demonstrate that a properly decorated thieno[3,2-c]quinolin-4(5H)-one stabilizes the G4 fold in vitro and in cells, induces a DNA damage response localized to telomeres, inhibits PARylation in cells, and has an antiproliferative effect in BRCA2 deficient tumor cells.	Thieno[3,2-c]quinolin-4(5H)-one	41-72	BRCA2 DNA repair associated	Homo sapiens	242-247
28575672-3	2017	Formaldehyde selectively depletes BRCA2 via proteasomal degradation, a mechanism of toxicity that affects very few additional cellular proteins.	Formaldehyde	0-12	BRCA2 DNA repair associated	Homo sapiens	34-39
28575672-4	2017	Heterozygous BRCA2 truncations, by lowering pre-existing BRCA2 expression, sensitize to BRCA2 haploinsufficiency induced by transient exposure to natural concentrations of formaldehyde.	Formaldehyde	172-184	BRCA2 DNA repair associated	Homo sapiens	13-18
28575672-4	2017	Heterozygous BRCA2 truncations, by lowering pre-existing BRCA2 expression, sensitize to BRCA2 haploinsufficiency induced by transient exposure to natural concentrations of formaldehyde.	Formaldehyde	172-184	BRCA2 DNA repair associated	Homo sapiens	57-62
28575672-4	2017	Heterozygous BRCA2 truncations, by lowering pre-existing BRCA2 expression, sensitize to BRCA2 haploinsufficiency induced by transient exposure to natural concentrations of formaldehyde.	Formaldehyde	172-184	BRCA2 DNA repair associated	Homo sapiens	57-62
28575672-6	2017	Ribonuclease H1 ameliorates replication fork instability and chromosomal aberrations provoked by aldehyde-induced BRCA2 haploinsufficiency, suggesting that BRCA2 inactivation triggers spontaneous mutagenesis during DNA replication via aberrant RNA-DNA hybrids (R-loops).	Aldehydes	97-105	BRCA2 DNA repair associated	Homo sapiens	114-119
28575676-0	2017	Aldehydes Pose a Threat to BRCA2 Mutation Carriers.	Aldehydes	0-9	BRCA2 DNA repair associated	Homo sapiens	27-32
28575676-3	2017	find that environmental and metabolic aldehydes pose a threat to these individuals by promoting degradation of wild-type BRCA2 protein, thereby predisposing them to genomic instability and perhaps to cancer.	Aldehydes	38-47	BRCA2 DNA repair associated	Homo sapiens	121-126
28222073-10	2017	The rucaparib/carboplatin combination had radiologic antitumour activity, primarily in BRCA1- or BRCA2-mutated breast and ovarian/peritoneal cancers.	rucaparib	4-13	BRCA2 DNA repair associated	Homo sapiens	97-102
28375947-9	2017	After adjusting for age, alcohol use, and smoking, BRCA2 mutation carriers were almost 25 times more likely to demonstrate chronic pancreatitis-like changes.	Alcohols	25-32	BRCA2 DNA repair associated	Homo sapiens	51-56
28626402-0	2017	Effect of the Combination of Trabectedin and Pegylated Liposomal Doxorubicin in a BRCA2 Mutation Carrier with Recurrent Platinum-Sensitive Ovarian Cancer.	Doxorubicin	65-76	BRCA2 DNA repair associated	Homo sapiens	82-87
28626402-0	2017	Effect of the Combination of Trabectedin and Pegylated Liposomal Doxorubicin in a BRCA2 Mutation Carrier with Recurrent Platinum-Sensitive Ovarian Cancer.	Platinum	120-128	BRCA2 DNA repair associated	Homo sapiens	82-87
28626402-10	2017	As the patient was a BRCA2 mutation carrier, third-line chemotherapy was initiated with carboplatin and gemcitabine every 3 weeks.	Carboplatin	88-99	BRCA2 DNA repair associated	Homo sapiens	21-26
28626402-10	2017	As the patient was a BRCA2 mutation carrier, third-line chemotherapy was initiated with carboplatin and gemcitabine every 3 weeks.	gemcitabine	104-115	BRCA2 DNA repair associated	Homo sapiens	21-26
28626402-14	2017	CONCLUSIONS: Second-line chemotherapy with a nonplatinum combination - trabectedin plus PLD - was effective in a BRCA2 mutation carrier with recurrent partially platinum-sensitive ovarian cancer.	Platinum	48-56	BRCA2 DNA repair associated	Homo sapiens	113-118
28291774-0	2017	BRCA2 secondary mutation-mediated resistance to platinum and PARP inhibitor-based therapy in pancreatic cancer.	Platinum	48-56	BRCA2 DNA repair associated	Homo sapiens	0-5
28291774-6	2017	RESULTS: Initially, the patient had an exceptional response to platinum and PARP inhibitor therapy, most likely due to the BRCA2 mutation.	Platinum	63-71	BRCA2 DNA repair associated	Homo sapiens	123-128
28471200-0	2017	[Fullerene Doxorubicin Nanotransporter for Target Interaction with mutated gene BRCA2].	Fullerenes	1-10	BRCA2 DNA repair associated	Homo sapiens	80-85
28471200-0	2017	[Fullerene Doxorubicin Nanotransporter for Target Interaction with mutated gene BRCA2].	Doxorubicin	11-22	BRCA2 DNA repair associated	Homo sapiens	80-85
28222073-10	2017	The rucaparib/carboplatin combination had radiologic antitumour activity, primarily in BRCA1- or BRCA2-mutated breast and ovarian/peritoneal cancers.	Carboplatin	14-25	BRCA2 DNA repair associated	Homo sapiens	97-102
28066861-0	2017	The incidence of cardiomyopathy in BRCA1 and BRCA2 mutation carriers after anthracycline-based adjuvant chemotherapy.	Anthracyclines	75-88	BRCA2 DNA repair associated	Homo sapiens	45-50
27692705-0	2017	Extreme Response to High-dose Testosterone in BRCA2- and ATM-mutated Prostate Cancer.	Testosterone	30-42	BRCA2 DNA repair associated	Homo sapiens	46-51
28247011-0	2017	Population pharmacokinetics of ABT-767 in BRCA1 or BRCA2 mutation carriers with advanced solid tumors or in subjects with high grade serous ovarian, primary peritoneal or fallopian tube cancer.	2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid	31-34	BRCA2 DNA repair associated	Homo sapiens	51-56
28066861-5	2017	Therefore, we conducted a retrospective matched cohort study to determine the rates of anthracycline-induced cardiomyopathy in breast cancer patients with germline mutation in BRCA1 or BRCA2 genes compared to age-matched patients without a BRCA1 or BRCA2 gene mutation.	Anthracyclines	87-100	BRCA2 DNA repair associated	Homo sapiens	185-190
28066861-5	2017	Therefore, we conducted a retrospective matched cohort study to determine the rates of anthracycline-induced cardiomyopathy in breast cancer patients with germline mutation in BRCA1 or BRCA2 genes compared to age-matched patients without a BRCA1 or BRCA2 gene mutation.	Anthracyclines	87-100	BRCA2 DNA repair associated	Homo sapiens	249-254
27908594-18	2017	Median progression-free survival after rucaparib treatment was 12 8 months (95% CI 9 0-14 7) in the BRCA mutant subgroup, 5 7 months (5 3-7 6) in the LOH high subgroup, and 5 2 months (3 6-5 5) in the LOH low subgroup.	rucaparib	39-48	BRCA2 DNA repair associated	Homo sapiens	100-104
27739325-2	2017	Tumor cells with deleterious BRCA1 or BRCA2 mutations are deficient in homologous recombination DNA repair and are intrinsically sensitive to platinum therapy and poly(ADP-ribose) polymerase inhibitors.	Platinum	142-150	BRCA2 DNA repair associated	Homo sapiens	38-43
27739325-3	2017	We describe herein the design and rationale of a Phase II trial investigating whether the addition of veliparib to temozolomide or carboplatin/paclitaxel provides clinical benefit over carboplatin/paclitaxel with placebo in patients with locally recurrent or metastatic breast cancer harboring a deleterious BRCA1 or BRCA2 germline mutation (Trial registration: EudraCT 2011-002913-12, NCT01506609).	veliparib	102-111	BRCA2 DNA repair associated	Homo sapiens	317-322
28057616-1	2017	The FDA approved the PARP inhibitor rucaparib to treat women with advanced ovarian cancer who have already been treated with at least two chemotherapies and have a BRCA1 or BRCA2 gene mutation identified by an approved companion diagnostic test.	rucaparib	36-45	BRCA2 DNA repair associated	Homo sapiens	173-178
27767231-4	2017	Our smMIP-based NGS approach provides analysis of both strands of the open reading frame of BRCA1 and BRCA2, enabling the discrimination between real variants and formalin-induced artefacts.	Formaldehyde	163-171	BRCA2 DNA repair associated	Homo sapiens	102-107
27796716-2	2017	To investigate whether common variants associated with DAE were involved in breast cancer susceptibility among BRCA1 and BRCA2 mutation carriers, a list of 175 genes was developed based of their involvement in cancer-related pathways.	o,p-dinitrophenyl aminoethyldiphosphate-beryllium trifluoride	55-58	BRCA2 DNA repair associated	Homo sapiens	121-126
27908594-24	2017	INTERPRETATION: In patients with BRCA mutant or BRCA wild-type and LOH high platinum-sensitive ovarian carcinomas treated with rucaparib, progression-free survival was longer than in patients with BRCA wild-type LOH low carcinomas.	rucaparib	127-136	BRCA2 DNA repair associated	Homo sapiens	48-52
27908594-24	2017	INTERPRETATION: In patients with BRCA mutant or BRCA wild-type and LOH high platinum-sensitive ovarian carcinomas treated with rucaparib, progression-free survival was longer than in patients with BRCA wild-type LOH low carcinomas.	rucaparib	127-136	BRCA2 DNA repair associated	Homo sapiens	33-37
27908594-24	2017	INTERPRETATION: In patients with BRCA mutant or BRCA wild-type and LOH high platinum-sensitive ovarian carcinomas treated with rucaparib, progression-free survival was longer than in patients with BRCA wild-type LOH low carcinomas.	rucaparib	127-136	BRCA2 DNA repair associated	Homo sapiens	48-52
27886673-5	2016	A case-control study of VUS confirmed the polymorphisms of the c.67+62A>G, c.7008-62A>G and c.8851G>A BRCA2 variants previously published.	3-[(3~{a}~{S},4~{S},6~{a}~{R})-4-carboxy-2,3,4,5,6,6~{a}-hexahydro-1~{H}-pyrrolo[2,3-c]pyrrol-3~{a}-yl]propyl-$l^{3}-oxidanyl-bis(oxidanyl)boranuide	24-27	BRCA2 DNA repair associated	Homo sapiens	111-116
27908594-25	2017	Our results suggest that assessment of tumour LOH can be used to identify patients with BRCA wild-type platinum-sensitive ovarian cancers who might benefit from rucaparib.	Platinum	103-111	BRCA2 DNA repair associated	Homo sapiens	88-92
27908594-25	2017	Our results suggest that assessment of tumour LOH can be used to identify patients with BRCA wild-type platinum-sensitive ovarian cancers who might benefit from rucaparib.	rucaparib	161-170	BRCA2 DNA repair associated	Homo sapiens	88-92
27473273-8	2016	siRNA-mediated silencing of the FA-associated genes FANCL and RAD18 and the HR-associated genes BRCA1 and BRCA2 significantly potentiated the sensitivity of A549/DR cells to cisplatin compared to A549 and Calu-1 cells, suggesting that the acquired cisplatin resistance in A549/DR cells may be attributed to enhanced FA and HR pathway capacities responsible for ICL repair.	Cisplatin	174-183	BRCA2 DNA repair associated	Homo sapiens	106-111
27614696-8	2016	Tumor regressions were induced by single-agent niraparib in one of two PDX models with deleterious BRCA2 mutations and in a PDX with RAD51C promoter methylation.	niraparib	47-56	BRCA2 DNA repair associated	Homo sapiens	99-104
27614696-10	2016	Niraparib generally failed to enhance responses to carboplatin/paclitaxel chemotherapy, but maintenance niraparib therapy delayed progression in a BRCA2-deficient PDX.	niraparib	104-113	BRCA2 DNA repair associated	Homo sapiens	147-152
27533083-5	2016	Co-depletion of BRCA2 and POLQ by siRNA markedly increased sensitivity of A549/DR cells to cisplatin, which was accompanied with impairment of double strand breaks (DSBs) repair reflected by prominent cell cycle checkpoint response, increased chromosomal aberrations and persistent colocalization of p-ATM and 53BP1 foci induced by cisplatin.	Cisplatin	91-100	BRCA2 DNA repair associated	Homo sapiens	16-21
27533083-5	2016	Co-depletion of BRCA2 and POLQ by siRNA markedly increased sensitivity of A549/DR cells to cisplatin, which was accompanied with impairment of double strand breaks (DSBs) repair reflected by prominent cell cycle checkpoint response, increased chromosomal aberrations and persistent colocalization of p-ATM and 53BP1 foci induced by cisplatin.	Cisplatin	332-341	BRCA2 DNA repair associated	Homo sapiens	16-21
27533083-8	2016	Importantly, the sensitization effects to cisplatin and BMN673 in A549/DR cells by co-depleting BRCA2 and POLQ was stronger than those by co-depleting BRCA2 and other TLS factors including POLH, REV3, or REV1.	Cisplatin	42-51	BRCA2 DNA repair associated	Homo sapiens	96-101
27511924-7	2016	Increasing evidence on the molecular role of the BRCA2 protein in the homologous recombination of DNA damages suggest that BRCA2-related PDAC are sensitive to agents causing DNA cross-linking damage, such as platinum salts, and treatments targeting rescue DNA repair pathways, such as poly(ADP-ribose) polymerase inhibitors that are currently under investigation.	Platinum	208-216	BRCA2 DNA repair associated	Homo sapiens	49-54
27561088-1	2016	We report an interesting clinical case of a patient carrying a specific BRCA2 germline variant affected by bone and hepatic metastases from a high grade uterine stromal sarcoma who obtained a complete metabolic response after only 3 cycles of trabectedin treatment (1.5 mg/m2 given intravenously over 24 hours every 21 days).	Trabectedin	243-254	BRCA2 DNA repair associated	Homo sapiens	72-77
27511924-7	2016	Increasing evidence on the molecular role of the BRCA2 protein in the homologous recombination of DNA damages suggest that BRCA2-related PDAC are sensitive to agents causing DNA cross-linking damage, such as platinum salts, and treatments targeting rescue DNA repair pathways, such as poly(ADP-ribose) polymerase inhibitors that are currently under investigation.	Platinum	208-216	BRCA2 DNA repair associated	Homo sapiens	123-128
26845104-9	2016	Less than 1% of patients carried VUS in BRCA1 or BRCA2.	3-[(3~{a}~{S},4~{S},6~{a}~{R})-4-carboxy-2,3,4,5,6,6~{a}-hexahydro-1~{H}-pyrrolo[2,3-c]pyrrol-3~{a}-yl]propyl-$l^{3}-oxidanyl-bis(oxidanyl)boranuide	33-36	BRCA2 DNA repair associated	Homo sapiens	49-54
27643881-6	2016	The expression of PARP1, gammaH2AX, and BRCA2 were significantly associated with shorter disease-specific survival (DSS) and event-free survival (EFS) by univariate analysis.	dss	116-119	BRCA2 DNA repair associated	Homo sapiens	40-45
26785283-4	2016	Retrospective studies have shown an improved prognosis, higher response rates to platinum-containing regimens, and longer treatment-free intervals between relapses in patients with BRCA 1 and BRCA 2 (BRCA1/2)-mutated ovarian cancer (BMOC) compared with patients who are not carriers of this mutation.	Platinum	81-89	BRCA2 DNA repair associated	Homo sapiens	192-198
27643881-9	2016	BRCA2 expression was an independent indicator of poor prognosis of DSS.	dss	67-70	BRCA2 DNA repair associated	Homo sapiens	0-5
27643881-10	2016	In addition, the combined expressional patterns of PARP1, gammaH2AX, BRCA1, and BRCA2 (CSddrm) were independent prognostic predictors of DSS (P < 0.001) and EFS (P = 0.016).	dss	137-140	BRCA2 DNA repair associated	Homo sapiens	80-85
27296776-1	2016	Mitochondrial Complex II (Succinate: ubiquinone oxidoreductase) has a covalently bound FAD cofactor in its largest subunit (SDHA), which accepts electrons from oxidation of succinate during catalysis.	Succinic Acid	173-182	BRCA2 DNA repair associated	Homo sapiens	87-90
28003870-0	2016	New perspective on maintenance therapies for platinum- sensitive recurrent ovarian cancer in women with germline and somatic mutations in BRCA1 and BRCA2 genes.	Platinum	45-53	BRCA2 DNA repair associated	Homo sapiens	148-153
28003870-5	2016	Loss-of-function mutations in genes in the homologous recombination pathway, especially BRCA1 and BRCA2, predict higher rates of platinum sensitivity, better overall survival (OS), and better response to PARPi in women with OC.	Platinum	129-137	BRCA2 DNA repair associated	Homo sapiens	98-103
27673289-1	2016	Poly(adenosine diphosphate-ribose) polymerase (PARP) inhibitors have shown clinical activity in epithelial ovarian cancer, leading both the US Food and Drug Administration (FDA) and the European Medicines Agency to approve olaparib for tumors characterized by BRCA1 and BRCA2 mutations.	olaparib	223-231	BRCA2 DNA repair associated	Homo sapiens	270-275
27488020-6	2016	Mutation testing by Caris molecular intelligence demonstrated a breast cancer 2 gene mutation and further treatment with carboplatin and veliparib achieved disease stabilisation.	veliparib	137-146	BRCA2 DNA repair associated	Homo sapiens	64-79
27060066-7	2016	cDNA representing BRCA2 alternate splice sites was amplified and visualised using capillary or agarose gel electrophoresis, followed by sequencing.	Sepharose	95-102	BRCA2 DNA repair associated	Homo sapiens	18-23
27465688-9	2016	MK-2206 prevented cisplatin- and olaparib-induced AKT activation in the BRCA2-deficient PEO1 cells.	MK 2206	0-7	BRCA2 DNA repair associated	Homo sapiens	72-77
27465688-9	2016	MK-2206 prevented cisplatin- and olaparib-induced AKT activation in the BRCA2-deficient PEO1 cells.	Cisplatin	18-27	BRCA2 DNA repair associated	Homo sapiens	72-77
27465688-9	2016	MK-2206 prevented cisplatin- and olaparib-induced AKT activation in the BRCA2-deficient PEO1 cells.	olaparib	33-41	BRCA2 DNA repair associated	Homo sapiens	72-77
27385701-3	2016	Olaparib is indicated for use in treating certain patients with advanced, recurrent ovarian cancer who have mutations of the breast cancer 1 gene (BRCA1) or breast cancer 2 gene (BRCA2).	olaparib	0-8	BRCA2 DNA repair associated	Homo sapiens	179-184
27443740-1	2016	Cells deficient in the Brca1 and Brca2 genes have reduced capacity to repair DNA double-strand breaks by homologous recombination and consequently are hypersensitive to DNA-damaging agents, including cisplatin and poly(ADP-ribose) polymerase (PARP) inhibitors.	Cisplatin	200-209	BRCA2 DNA repair associated	Homo sapiens	33-38
27443740-5	2016	More generally, acquisition of PARP inhibitors and cisplatin resistance is associated with replication fork protection in Brca2-deficient tumour cells that do not develop Brca2 reversion mutations.	Cisplatin	51-60	BRCA2 DNA repair associated	Homo sapiens	122-127
27303922-7	2016	We further found that pyrvinium pamoate dramatically downregulated several key DNA repair genes in genotoxically-stressed cells, including DNA ligase IV and BRCA2, leading to unbearable genomic instability and cell death.	pyrvinium	22-39	BRCA2 DNA repair associated	Homo sapiens	157-162
27385701-5	2016	In Phase II clinical trials including patients with platinum-sensitive, platinum-resistant, and platinum-refractory ovarian cancers, olaparib significantly improved progression-free survival, with similar rates of response reported in patients with BRCA1- and BRCA2-mutated disease.	olaparib	133-141	BRCA2 DNA repair associated	Homo sapiens	260-265
26387543-2	2016	This interaction is abrogated by cyclin A-CDK2-mediated phosphorylation of BRCA2 at serine 3291 (Ser3291).	Serine	84-90	BRCA2 DNA repair associated	Homo sapiens	75-80
27323902-14	2016	DISCUSSION: Results might be pivotal for registration of olaparib as standard first line treatment in advanced BRCA1- or BRCA2-mutated breast cancer.	olaparib	57-65	BRCA2 DNA repair associated	Homo sapiens	121-126
27165126-21	2016	Our data shows that BRCA2 is mutated in our PACC model, which could contribute to the oxaliplatin sensitivity observed.	Oxaliplatin	86-97	BRCA2 DNA repair associated	Homo sapiens	20-25
27272846-0	2016	Thyroid Hormones and Vitamin D in Patients with Breast Cancer with Mutations in BRCA1 or BRCA2 Genes.	Vitamin D	21-30	BRCA2 DNA repair associated	Homo sapiens	89-94
27272846-8	2016	A significantly increased level of vitamin D in BRCA2-mutation carriers compared to those without mutation (p=0.02) was detected.	Vitamin D	35-44	BRCA2 DNA repair associated	Homo sapiens	48-53
27272846-12	2016	Vitamin D was significantly elevated in BRCA2-mutation carriers and the observation of a better tumor grade in this group could be consistent with the ability of vitamin D to inhibit growth and induce differentiation.	Vitamin D	0-9	BRCA2 DNA repair associated	Homo sapiens	40-45
27272846-12	2016	Vitamin D was significantly elevated in BRCA2-mutation carriers and the observation of a better tumor grade in this group could be consistent with the ability of vitamin D to inhibit growth and induce differentiation.	Vitamin D	162-171	BRCA2 DNA repair associated	Homo sapiens	40-45
26724258-0	2016	Biallelic Inactivation of BRCA2 in Platinum-sensitive Metastatic Castration-resistant Prostate Cancer.	Platinum	35-43	BRCA2 DNA repair associated	Homo sapiens	26-31
26724258-6	2016	Biallelic BRCA2 inactivation in mCRPC warrants further exploration as a predictive biomarker for sensitivity to platinum chemotherapy.	Platinum	112-120	BRCA2 DNA repair associated	Homo sapiens	10-15
27067391-6	2016	Custom oligonucleotide baits spanning the complete coding, non-coding, and intergenic regions 10 kb up- and downstream of ATM, BRCA1, BRCA2, CDH1, CHEK2, PALB2, and TP53 were synthesized for solution hybridization enrichment.	Oligonucleotides	7-22	BRCA2 DNA repair associated	Homo sapiens	134-139
26959114-0	2016	Reciprocal positive selection for weakness - preventing olaparib resistance by inhibiting BRCA2.	olaparib	56-64	BRCA2 DNA repair associated	Homo sapiens	90-95
26959114-2	2016	The PARP-1 inhibitor olaparib is approved for use in BRCA-mutated ovarian cancers but BRCA2-reversion mutations lead to functional homologous recombination repair (HRR) and olaparib resistance.	olaparib	173-181	BRCA2 DNA repair associated	Homo sapiens	86-91
26959114-5	2016	We report that BRCA2 downregulation sensitized multiple human tumor cell lines (but not non-cancer human kidney cells) to olaparib and, combined with olaparib, increased aneuploidy and chromosomal translocations in human tumor cells.	olaparib	122-130	BRCA2 DNA repair associated	Homo sapiens	15-20
26959114-5	2016	We report that BRCA2 downregulation sensitized multiple human tumor cell lines (but not non-cancer human kidney cells) to olaparib and, combined with olaparib, increased aneuploidy and chromosomal translocations in human tumor cells.	olaparib	150-158	BRCA2 DNA repair associated	Homo sapiens	15-20
26959114-9	2016	In vivo use of BRCA2 antisense oligonucleotides may be a viable option to expand clinical use of olaparib and prevent resistance.	Oligonucleotides	31-47	BRCA2 DNA repair associated	Homo sapiens	15-20
26959114-9	2016	In vivo use of BRCA2 antisense oligonucleotides may be a viable option to expand clinical use of olaparib and prevent resistance.	olaparib	97-105	BRCA2 DNA repair associated	Homo sapiens	15-20
26964893-5	2016	These signatures predict platinum-sensitivity and survival in EOC, as it was previously shown for germline mutations of BRCA1/BRCA2.	Platinum	25-33	BRCA2 DNA repair associated	Homo sapiens	126-131
26763880-0	2016	KOHBRA BRCA risk calculator (KOHCal): a model for predicting BRCA1 and BRCA2 mutations in Korean breast cancer patients.	kohbra	0-6	BRCA2 DNA repair associated	Homo sapiens	71-76
26748828-5	2016	Treatment with the G4-stabilizing compound pyridostatin (PDS) increases telomere fragility in BRCA2-deficient cells, suggesting that G4 formation drives telomere instability.	pyridostatin	43-55	BRCA2 DNA repair associated	Homo sapiens	94-99
26962171-0	2016	Complete Durable Response From Carboplatin and Olaparib in a Heavily Pretreated Triple-Negative Metastatic Breast Cancer With Germline BRCA2 and "BRCAness" Mutations.	Carboplatin	31-42	BRCA2 DNA repair associated	Homo sapiens	135-140
26962171-0	2016	Complete Durable Response From Carboplatin and Olaparib in a Heavily Pretreated Triple-Negative Metastatic Breast Cancer With Germline BRCA2 and "BRCAness" Mutations.	olaparib	47-55	BRCA2 DNA repair associated	Homo sapiens	135-140
26784987-6	2016	In addition, one of the 9 active compounds, adenosine 5"-monophosphate (A5MP), and also its mimic 5-aminoimidazole-4-carboxamide ribonucleotide (AICAR) 5" phosphate (ZMP) inhibited RAD52 activity in vivo and exerted synthetic lethality against BRCA1 and BRCA2-mutated carcinomas.	adenosine 5"-monophosphate	44-70	BRCA2 DNA repair associated	Homo sapiens	254-259
26745694-1	2016	OBJECTIVE: The aim of the study was to evaluate the activity and tolerability of iniparib monotherapy in women with BRCA1 or BRCA2-associated advanced epithelial ovarian, fallopian tube, or primary peritoneal cancer.	iniparib	81-89	BRCA2 DNA repair associated	Homo sapiens	125-130
26893716-0	2016	Polymorphic variants in the vitamin D pathway genes and the risk of ovarian cancer among non-carriers of BRCA1/BRCA2 mutations.	Vitamin D	28-37	BRCA2 DNA repair associated	Homo sapiens	111-116
26784987-6	2016	In addition, one of the 9 active compounds, adenosine 5"-monophosphate (A5MP), and also its mimic 5-aminoimidazole-4-carboxamide ribonucleotide (AICAR) 5" phosphate (ZMP) inhibited RAD52 activity in vivo and exerted synthetic lethality against BRCA1 and BRCA2-mutated carcinomas.	Adenosine Monophosphate	72-76	BRCA2 DNA repair associated	Homo sapiens	254-259
26784987-6	2016	In addition, one of the 9 active compounds, adenosine 5"-monophosphate (A5MP), and also its mimic 5-aminoimidazole-4-carboxamide ribonucleotide (AICAR) 5" phosphate (ZMP) inhibited RAD52 activity in vivo and exerted synthetic lethality against BRCA1 and BRCA2-mutated carcinomas.	AICA ribonucleotide	98-143	BRCA2 DNA repair associated	Homo sapiens	254-259
26784987-6	2016	In addition, one of the 9 active compounds, adenosine 5"-monophosphate (A5MP), and also its mimic 5-aminoimidazole-4-carboxamide ribonucleotide (AICAR) 5" phosphate (ZMP) inhibited RAD52 activity in vivo and exerted synthetic lethality against BRCA1 and BRCA2-mutated carcinomas.	AICA ribonucleotide	145-150	BRCA2 DNA repair associated	Homo sapiens	254-259
26784987-6	2016	In addition, one of the 9 active compounds, adenosine 5"-monophosphate (A5MP), and also its mimic 5-aminoimidazole-4-carboxamide ribonucleotide (AICAR) 5" phosphate (ZMP) inhibited RAD52 activity in vivo and exerted synthetic lethality against BRCA1 and BRCA2-mutated carcinomas.	5" phosphate	152-164	BRCA2 DNA repair associated	Homo sapiens	254-259
26961668-3	2016	In the United States, Olaparib, a PARP inhibitor, has been recently approved for ovarian cancer patients treated with three or more lines of prior chemotherapy who harbor germline mutations in BRCA1 or BRCA2.	olaparib	22-30	BRCA2 DNA repair associated	Homo sapiens	202-207
26712194-5	2016	PFTC has been described in high-risk breast-ovarian cancer families with germ-line BRCA-1 and BRCA-2 mutations.	pftc	0-4	BRCA2 DNA repair associated	Homo sapiens	94-100
26590714-4	2015	The recent approval of olaparib (Lynparza), the poly (ADP-ribose) polymerase (PARP) inhibitor for treating tumors harboring BRCA1 or BRCA2 mutations, represents the first medicine based on this principle, exploiting an underlying cause of tumor formation that also represents an Achilles" heel.	olaparib	23-31	BRCA2 DNA repair associated	Homo sapiens	133-138
26446551-5	2016	However, plasma levels of vitamin D binding protein isotype 1 and alpha1-antitrypsin isotypes 2, 3 and 4 were significantly decreased in BRCA2 mutation carriers compared to controls.	Vitamin D	26-35	BRCA2 DNA repair associated	Homo sapiens	137-142
26319584-6	2015	Loss of BRCA1 or BRCA2 gene function has long been associated with inherited susceptibility to breast cancer but these results suggest that exposure to aluminium-based antiperspirant salts may also reduce levels of these key components of DNA repair in breast epithelial cells.	Aluminum	152-161	BRCA2 DNA repair associated	Homo sapiens	17-22
26844277-2	2015	Our goal was to compare the effectiveness of different PAC screening strategies in BRCA2 mutation carriers, from the standpoint of life expectancy.	pac	55-58	BRCA2 DNA repair associated	Homo sapiens	83-88
26210103-5	2015	In addition, it was recently shown that aberrations in DNA repair genes, such as BRCA2 and ATM, are present in both somatic and germline form in a significant minority of prostate cancer; these abnormalities can be targeted by drugs such as platinums and PARP inhibitors.	Platinum	241-250	BRCA2 DNA repair associated	Homo sapiens	81-86
26510020-9	2015	Of these 16 patients, 14 (88%) had a response to olaparib, including all 7 patients with BRCA2 loss (4 with biallelic somatic loss, and 3 with germline mutations) and 4 of 5 with ATM aberrations.	olaparib	49-57	BRCA2 DNA repair associated	Homo sapiens	89-94
26585231-4	2015	We found that AZD1775 sensitized to gemcitabine-radiation in BRCA2 wild-type but not BRCA2 mutant pancreatic cancer cells.	adavosertib	14-21	BRCA2 DNA repair associated	Homo sapiens	61-66
26489468-0	2015	Poly(ADP-Ribose) Mediates the BRCA2-Dependent Early DNA Damage Response.	Poly Adenosine Diphosphate Ribose	0-16	BRCA2 DNA repair associated	Homo sapiens	30-35
26489468-2	2015	Previous studies have shown that BRCA2 contains three tandem oligonucleotide/oligosaccharide binding folds (OB-folds) that are involved in DNA binding during DNA double-strand break repair.	Oligonucleotides	61-76	BRCA2 DNA repair associated	Homo sapiens	33-38
26489468-2	2015	Previous studies have shown that BRCA2 contains three tandem oligonucleotide/oligosaccharide binding folds (OB-folds) that are involved in DNA binding during DNA double-strand break repair.	Oligosaccharides	77-92	BRCA2 DNA repair associated	Homo sapiens	33-38
26489468-4	2015	Unexpectedly, we found that the OB-folds of BRCA2 recognize poly(ADP-ribose) (PAR) and mediate the fast recruitment of BRCA2 to DNA lesions, which is suppressed by PARP inhibitor treatment.	Poly Adenosine Diphosphate Ribose	60-76	BRCA2 DNA repair associated	Homo sapiens	44-49
26489468-4	2015	Unexpectedly, we found that the OB-folds of BRCA2 recognize poly(ADP-ribose) (PAR) and mediate the fast recruitment of BRCA2 to DNA lesions, which is suppressed by PARP inhibitor treatment.	Poly Adenosine Diphosphate Ribose	60-76	BRCA2 DNA repair associated	Homo sapiens	119-124
26496295-3	2015	We report successful treatment of a metastatic TNBC in a woman with a BRCA2 germline mutation using combined bevacizumab/paclitaxel/carboplatin (BPC) therapy.	Paclitaxel	121-131	BRCA2 DNA repair associated	Homo sapiens	70-75
26496295-3	2015	We report successful treatment of a metastatic TNBC in a woman with a BRCA2 germline mutation using combined bevacizumab/paclitaxel/carboplatin (BPC) therapy.	Carboplatin	132-143	BRCA2 DNA repair associated	Homo sapiens	70-75
26496295-3	2015	We report successful treatment of a metastatic TNBC in a woman with a BRCA2 germline mutation using combined bevacizumab/paclitaxel/carboplatin (BPC) therapy.	bpc	145-148	BRCA2 DNA repair associated	Homo sapiens	70-75
26496295-8	2015	At the most recent (5-year) follow-up, the patient was alive with good quality of life and no evidence of metastases.This finding suggests that BPC therapy might be considered a good therapeutic option for the treatment of metastatic TNBC in a woman with a BRCA2 germline mutation.	bpc	144-147	BRCA2 DNA repair associated	Homo sapiens	257-262
26585231-4	2015	We found that AZD1775 sensitized to gemcitabine-radiation in BRCA2 wild-type but not BRCA2 mutant pancreatic cancer cells.	gemcitabine	36-47	BRCA2 DNA repair associated	Homo sapiens	61-66
26585231-7	2015	In HR-proficient (BRCA2 wild-type) or -deficient (BRAC2 null) isogenic cells, AZD1775 sensitized to gemcitabine-radiation in BRCA2 wild-type, but not in BRCA2 null cells, despite significant G2 checkpoint abrogation.	adavosertib	78-85	BRCA2 DNA repair associated	Homo sapiens	18-23
26585231-7	2015	In HR-proficient (BRCA2 wild-type) or -deficient (BRAC2 null) isogenic cells, AZD1775 sensitized to gemcitabine-radiation in BRCA2 wild-type, but not in BRCA2 null cells, despite significant G2 checkpoint abrogation.	adavosertib	78-85	BRCA2 DNA repair associated	Homo sapiens	125-130
26585231-7	2015	In HR-proficient (BRCA2 wild-type) or -deficient (BRAC2 null) isogenic cells, AZD1775 sensitized to gemcitabine-radiation in BRCA2 wild-type, but not in BRCA2 null cells, despite significant G2 checkpoint abrogation.	adavosertib	78-85	BRCA2 DNA repair associated	Homo sapiens	125-130
26585231-7	2015	In HR-proficient (BRCA2 wild-type) or -deficient (BRAC2 null) isogenic cells, AZD1775 sensitized to gemcitabine-radiation in BRCA2 wild-type, but not in BRCA2 null cells, despite significant G2 checkpoint abrogation.	gemcitabine	100-111	BRCA2 DNA repair associated	Homo sapiens	125-130
26585231-7	2015	In HR-proficient (BRCA2 wild-type) or -deficient (BRAC2 null) isogenic cells, AZD1775 sensitized to gemcitabine-radiation in BRCA2 wild-type, but not in BRCA2 null cells, despite significant G2 checkpoint abrogation.	gemcitabine	100-111	BRCA2 DNA repair associated	Homo sapiens	125-130
26320393-11	2015	A modeling of the wild-type and mutated BRC5-BRC6 domain revealed that the deletion of the 2 Serine residues might affect the structure of this BRCA2 domain.	Serine	93-99	BRCA2 DNA repair associated	Homo sapiens	144-149
26310895-5	2015	In addition, these compounds exacerbate DNA damage and cell death in response to the PARP inhibitor olaparib in BRCA2-deficient Capan-1 cells and cooperate with gemcitabine to the killing of pancreatic cancer cells.	olaparib	100-108	BRCA2 DNA repair associated	Homo sapiens	112-117
26180923-4	2015	METHODS: We tested gemcitabine and cisplatin sensitivity of four BRCA1 and BRCA2 mutant and three BRCA1 and BRCA2 wild-type (WT) patient-derived pancreatic cancer xenografts.	Cisplatin	35-44	BRCA2 DNA repair associated	Homo sapiens	75-80
25864590-4	2015	We provide further support for this observation by showing that shRNA-mediated BRCA2 knockdown in PANC-1, a BRCA2-proficient cell line, induces sensitization to cisplatin and BMN 673 but not to veliparib.	Cisplatin	161-170	BRCA2 DNA repair associated	Homo sapiens	79-84
26180923-6	2015	The BRCA1 and BRCA2 mutant xenografts were significantly more sensitive to cisplatin although these models also showed sensitivity to gemcitabine.	Cisplatin	75-84	BRCA2 DNA repair associated	Homo sapiens	14-19
26180923-6	2015	The BRCA1 and BRCA2 mutant xenografts were significantly more sensitive to cisplatin although these models also showed sensitivity to gemcitabine.	gemcitabine	134-145	BRCA2 DNA repair associated	Homo sapiens	14-19
26180923-7	2015	The BRCA1 and BRCA2 WT models showed sensitivity to gemcitabine but not cisplatin.	gemcitabine	52-63	BRCA2 DNA repair associated	Homo sapiens	14-19
25975349-5	2015	Knocking down of BRCA1 or BRCA2 in TNBC cells with BRCA1 allelic loss by RNA interference significantly enhanced AZD2281-induced growth inhibition and induced significant autophagy that was associated with mitophagy in cells with BRCA mutations.	olaparib	113-120	BRCA2 DNA repair associated	Homo sapiens	26-31
26022977-0	2015	Tamoxifen and risk of contralateral breast cancer among women with inherited mutations in BRCA1 and BRCA2: a meta-analysis.	Tamoxifen	0-9	BRCA2 DNA repair associated	Homo sapiens	100-105
25827330-2	2015	Specifically, these 5-deazaflavins lack the single electron reactivity with O2 of riboflavin-derived coenzymes (FMN and FAD), and, in general, have a more negative redox potential than NAD(P)(+).	5-deazaflavin	20-34	BRCA2 DNA repair associated	Homo sapiens	120-123
25935583-0	2015	Prospective evaluation of alcohol consumption and the risk of breast cancer in BRCA1 and BRCA2 mutation carriers.	Alcohols	26-33	BRCA2 DNA repair associated	Homo sapiens	89-94
25836596-3	2015	BRCA1- or BRCA2-deficient cells were found to be more sensitive to oxidative stress, modeled by treatment with patho-physiologic concentrations of hydrogen peroxide.	Hydrogen Peroxide	147-164	BRCA2 DNA repair associated	Homo sapiens	10-15
25836596-5	2015	In addition, after hydrogen peroxide treatment, BRCA deficient cells showed impaired Rad51 foci which are dependent on an intact BRCA1-BRCA2 pathway.	Hydrogen Peroxide	19-36	BRCA2 DNA repair associated	Homo sapiens	135-140
25818403-0	2015	A phase II evaluation of the potent, highly selective PARP inhibitor veliparib in the treatment of persistent or recurrent epithelial ovarian, fallopian tube, or primary peritoneal cancer in patients who carry a germline BRCA1 or BRCA2 mutation - An NRG Oncology/Gynecologic Oncology Group study.	veliparib	69-78	BRCA2 DNA repair associated	Homo sapiens	230-235
25818403-1	2015	BACKGROUND: Veliparib is a potent small molecule inhibitor of PARP-1/2, which is cytotoxic in tumor cells with deficiencies in BRCA1 or BRCA2.	veliparib	12-21	BRCA2 DNA repair associated	Homo sapiens	136-141
25975349-0	2015	The PARP inhibitor AZD2281 (Olaparib) induces autophagy/mitophagy in BRCA1 and BRCA2 mutant breast cancer cells.	olaparib	19-26	BRCA2 DNA repair associated	Homo sapiens	79-84
25975349-0	2015	The PARP inhibitor AZD2281 (Olaparib) induces autophagy/mitophagy in BRCA1 and BRCA2 mutant breast cancer cells.	olaparib	28-36	BRCA2 DNA repair associated	Homo sapiens	79-84
25975349-3	2015	We found that AZD2281 was the most potent in the PARP inhibitors and induces significant growth inhibition (~95%) in BRCA1 mutant (HCC-1937, MDA-MB-436, and SUM-149PT) and BRCA2 mutant (HCC-1428) cell lines.	olaparib	14-21	BRCA2 DNA repair associated	Homo sapiens	172-177
25960189-0	2015	Folic acid supplementation in vitro induces cell type-specific changes in BRCA1 and BRCA 2 mRNA expression, but does not alter DNA methylation of their promoters or DNA repair.	Folic Acid	0-10	BRCA2 DNA repair associated	Homo sapiens	84-90
25734415-10	2015	Metabolite levels in the BRCA2 cohort showed increased unsaturation of 21% (P = .030) relative to triglycerides level.	Triglycerides	98-111	BRCA2 DNA repair associated	Homo sapiens	25-30
25734415-11	2015	Comparison of the BRCA1 and BRCA2 cohorts showed a 47% (P = .002) increase in cholesterol level in the BRCA2 cohort when compared with diallylic lipid level and a 52% (P = .003) increase when compared with triglycerides level.	Cholesterol	78-89	BRCA2 DNA repair associated	Homo sapiens	28-33
25734415-11	2015	Comparison of the BRCA1 and BRCA2 cohorts showed a 47% (P = .002) increase in cholesterol level in the BRCA2 cohort when compared with diallylic lipid level and a 52% (P = .003) increase when compared with triglycerides level.	Cholesterol	78-89	BRCA2 DNA repair associated	Homo sapiens	103-108
25734415-11	2015	Comparison of the BRCA1 and BRCA2 cohorts showed a 47% (P = .002) increase in cholesterol level in the BRCA2 cohort when compared with diallylic lipid level and a 52% (P = .003) increase when compared with triglycerides level.	Triglycerides	206-219	BRCA2 DNA repair associated	Homo sapiens	28-33
25734415-11	2015	Comparison of the BRCA1 and BRCA2 cohorts showed a 47% (P = .002) increase in cholesterol level in the BRCA2 cohort when compared with diallylic lipid level and a 52% (P = .003) increase when compared with triglycerides level.	Triglycerides	206-219	BRCA2 DNA repair associated	Homo sapiens	103-108
25741641-4	2015	We used a novel protocol to evaluate the effectiveness of BRCA2 inhibition as a means to sensitize tumor cells to the DNA damaging drug cisplatin.	Cisplatin	136-145	BRCA2 DNA repair associated	Homo sapiens	58-63
25883215-1	2015	Based on a series of basic, preclinical and clinical studies, the Poly (ADP-ribose) Polymerase 1 (PARP1) inhibitor, olaparib, has recently been approved for use in ovarian cancer patients with BRCA1 or BRCA2 mutations.	olaparib	116-124	BRCA2 DNA repair associated	Homo sapiens	202-207
26015868-1	2015	BACKGROUND: Ovarian and triple-negative breast cancers with BRCA1 or BRCA2 loss are highly sensitive to treatment with PARP inhibitors and platinum-based cytotoxic agents and show an accumulation of genomic scars in the form of gross DNA copy number aberrations.	Platinum	139-147	BRCA2 DNA repair associated	Homo sapiens	69-74
26015868-2	2015	Cancers without BRCA1 or BRCA2 loss but with accumulation of similar genomic scars also show increased sensitivity to platinum-based chemotherapy.	Platinum	118-126	BRCA2 DNA repair associated	Homo sapiens	25-30
25708226-3	2015	Olaparib, a highly potent PARP inhibitor, has recently been the approved for ovarian cancer therapy by the FDA and European commission in patients with platinum-sensitive, recurrent, high-grade serous ovarian cancer with BRCA1 or BRCA2 mutations.	olaparib	0-8	BRCA2 DNA repair associated	Homo sapiens	230-235
25925750-2	2015	BRCA1 and BRCA2 are involved in DNA double-strand break repair, DNA alterations that can be caused by exposure to reactive oxygen species, a main source of which are mitochondria.	Reactive Oxygen Species	114-137	BRCA2 DNA repair associated	Homo sapiens	10-15
25743105-10	2015	One patient with a BRCA2-mutated tumor experienced complete remission of liver metastasis following cisplatinum chemotherapy.	Cisplatin	100-111	BRCA2 DNA repair associated	Homo sapiens	19-24
25737278-5	2015	However, in BRCA2 mutant cancers, cisplatin resistance can occur independently of restored HR by a mechanism that remains unknown.	Cisplatin	34-43	BRCA2 DNA repair associated	Homo sapiens	12-17
25737278-8	2015	Suggesting clinical relevance, cisplatin-resistant clones lacking genetic reversion of BRCA2 show de novo loss of CHD4 expression in vitro.	Cisplatin	31-40	BRCA2 DNA repair associated	Homo sapiens	87-92
25537514-6	2015	Our work highlights that a proportion of patients with wild-type BRCA1/2 ovarian cancers benefit from platinum-based chemotherapy and that the patients who benefit could be predicted from BRCA1/2-directed miRNA signature.	Platinum	102-110	BRCA2 DNA repair associated	Homo sapiens	65-72
25366685-0	2015	Olaparib monotherapy in patients with advanced cancer and a germline BRCA1/2 mutation.	olaparib	0-8	BRCA2 DNA repair associated	Homo sapiens	69-76
25502281-5	2015	A large observational study has provided evidence that the SERM tamoxifen may be efficacious for breast cancer prevention in women who carry mutations in the breast cancer predisposition genes, BRCA1 and BRCA2.	Tamoxifen	64-73	BRCA2 DNA repair associated	Homo sapiens	204-209
25366685-1	2015	PURPOSE: Olaparib is an oral poly (ADP-ribose) polymerase inhibitor with activity in germline BRCA1 and BRCA2 (BRCA1/2) -associated breast and ovarian cancers.	olaparib	9-17	BRCA2 DNA repair associated	Homo sapiens	104-109
25366685-1	2015	PURPOSE: Olaparib is an oral poly (ADP-ribose) polymerase inhibitor with activity in germline BRCA1 and BRCA2 (BRCA1/2) -associated breast and ovarian cancers.	olaparib	9-17	BRCA2 DNA repair associated	Homo sapiens	111-118
25366685-2	2015	We evaluated the efficacy and safety of olaparib in a spectrum of BRCA1/2-associated cancers.	olaparib	40-48	BRCA2 DNA repair associated	Homo sapiens	66-73
25366685-12	2015	CONCLUSION: Responses to olaparib were observed across different tumor types associated with germline BRCA1/2 mutations.	olaparib	25-33	BRCA2 DNA repair associated	Homo sapiens	102-109
25993149-1	2015	Retrospective studies have shown an improved prognosis, higher response rates to platinum-containing regimens, and longer treatment-free intervals between relapses in patients with BRCA 1 and BRCA 2 (BRCA1/2)-mutated ovarian cancer (BMOC) compared with patients who are not carriers of this mutation.	Platinum	81-89	BRCA2 DNA repair associated	Homo sapiens	192-198
25583815-1	2015	In a phase II study, researchers found that the PARP inhibitor olaparib led to stable disease or tumor regressions in patients with advanced breast, ovarian, pancreatic, and prostate cancers who had germline mutations in BRCA1 or BRCA2.	olaparib	63-71	BRCA2 DNA repair associated	Homo sapiens	230-235
25481791-1	2015	BACKGROUND: The poly(ADP-ribose) polymerase inhibitor olaparib has shown antitumour activity in patients with platinum-sensitive, recurrent, high-grade serous ovarian cancer with or without BRCA1 or BRCA2 mutations.	olaparib	54-62	BRCA2 DNA repair associated	Homo sapiens	199-204
25238946-1	2015	Women with germline mutations in the cancer susceptibility genes, BRCA1 or BRCA2, associated with Hereditary Breast & Ovarian Cancer syndrome, have up to an 85% lifetime risk of breast cancer and up to a 46% lifetime risk of ovarian, tubal, and peritoneal cancers.	Adenosine Monophosphate	117-120	BRCA2 DNA repair associated	Homo sapiens	75-80
24974076-0	2014	BRCA2 inhibition enhances cisplatin-mediated alterations in tumor cell proliferation, metabolism, and metastasis.	Cisplatin	26-35	BRCA2 DNA repair associated	Homo sapiens	0-5
24974076-7	2014	We developed a BRCA2-targeting second-generation antisense oligonucleotide (ASO), which sensitized human lung, ovarian, and breast cancer cells to cisplatin by as much as 60%.	Oligonucleotides	59-74	BRCA2 DNA repair associated	Homo sapiens	15-20
24974076-7	2014	We developed a BRCA2-targeting second-generation antisense oligonucleotide (ASO), which sensitized human lung, ovarian, and breast cancer cells to cisplatin by as much as 60%.	Oligonucleotides, Antisense	76-79	BRCA2 DNA repair associated	Homo sapiens	15-20
24974076-7	2014	We developed a BRCA2-targeting second-generation antisense oligonucleotide (ASO), which sensitized human lung, ovarian, and breast cancer cells to cisplatin by as much as 60%.	Cisplatin	147-156	BRCA2 DNA repair associated	Homo sapiens	15-20
24974076-8	2014	BRCA2 ASO treatment overcame acquired cisplatin resistance in head and neck cancer cells, but induced minimal cisplatin sensitivity in non-tumor cells.	Cisplatin	38-47	BRCA2 DNA repair associated	Homo sapiens	0-5
24974076-9	2014	BRCA2 ASO plus cisplatin reduced respiration as an early event preceding cell death, concurrent with increased glucose uptake without a difference in glycolysis.	Glucose	111-118	BRCA2 DNA repair associated	Homo sapiens	0-5
24974076-11	2014	These results implicate BRCA2 as a regulator of metastatic frequency and cellular metabolic response following cisplatin treatment.	Cisplatin	111-120	BRCA2 DNA repair associated	Homo sapiens	24-29
25193512-9	2014	Furthermore, knockout of BRCA2 markedly sensitized DLD-1 cells to the clinical nitrogen mustard prodrugs TH-302 and PR-104 and significantly augmented sterilization of clonogens by these agents in xenografts, both as monotherapy and in combination with radiotherapy, but had less effect on activity of the benzotriazine di-N-oxide SN30000.	Nitrogen	79-87	BRCA2 DNA repair associated	Homo sapiens	25-30
25337721-4	2014	Homologous recombination (HR)-dependent DNA repair-associated genes (i.e. BRCA1, BRCA2, RAD51 and FANCD2) were also increased in U251 and A172 cells after treatment with TMZ.	Temozolomide	170-173	BRCA2 DNA repair associated	Homo sapiens	81-86
25193512-9	2014	Furthermore, knockout of BRCA2 markedly sensitized DLD-1 cells to the clinical nitrogen mustard prodrugs TH-302 and PR-104 and significantly augmented sterilization of clonogens by these agents in xenografts, both as monotherapy and in combination with radiotherapy, but had less effect on activity of the benzotriazine di-N-oxide SN30000.	Triazines	306-319	BRCA2 DNA repair associated	Homo sapiens	25-30
25193512-9	2014	Furthermore, knockout of BRCA2 markedly sensitized DLD-1 cells to the clinical nitrogen mustard prodrugs TH-302 and PR-104 and significantly augmented sterilization of clonogens by these agents in xenografts, both as monotherapy and in combination with radiotherapy, but had less effect on activity of the benzotriazine di-N-oxide SN30000.	di-n-oxide	320-330	BRCA2 DNA repair associated	Homo sapiens	25-30
25193512-10	2014	PR-104 monotherapy was more effective than cisplatin at inhibiting growth of BRCA2-knockout tumors at equitoxic doses.	Cisplatin	43-52	BRCA2 DNA repair associated	Homo sapiens	77-82
24902638-0	2014	Silencing of BRCA2 decreases anoikis and its heterologous expression sensitizes yeast cells to acetic acid-induced programmed cell death.	Acetic Acid	95-106	BRCA2 DNA repair associated	Homo sapiens	13-18
25194416-2	2014	Both FAD and FMN flavin groups mediate the transfer of NADPH derived electrons to NOS.	NADP	55-60	BRCA2 DNA repair associated	Homo sapiens	5-8
25186150-1	2014	Ovarian carcinomas (OC) arising in BRCA1 and BRCA2 mutation carriers demonstrate pronounced sensitivity to platinum-based therapy due to deficiency of double-strand break DNA repair.	Platinum	107-115	BRCA2 DNA repair associated	Homo sapiens	45-50
25053826-0	2014	BRCA2 and RAD51 promote double-strand break formation and cell death in response to gemcitabine.	gemcitabine	84-95	BRCA2 DNA repair associated	Homo sapiens	0-5
25053826-4	2014	Gemcitabine is a potent replication inhibitor used to treat cancers with mutations in HR genes such as BRCA2.	gemcitabine	0-11	BRCA2 DNA repair associated	Homo sapiens	103-108
24902638-10	2014	Treatment with the antioxidants N-acetylcysteine or ascorbic acid reduced sensitivity to anoikis in human cells and inhibited AA-PCD in yeast cells expressing BRCA2.	Ascorbic Acid	52-65	BRCA2 DNA repair associated	Homo sapiens	159-164
24902638-6	2014	Using yeast as a model, we assessed that expression of human BRCA2 does not induce cell death by itself but it can promote acetic acid-induced PCD (AA-PCD).	Acetic Acid	123-134	BRCA2 DNA repair associated	Homo sapiens	61-66
24902638-11	2014	Taken together, these results show a new function of BRCA2 protein as modulator of anoikis sensitivity through an evolutionarily-conserved molecular mechanism involving regulation of ROS production and/or detoxification by BRCA2 during PCD processes.	ros	183-186	BRCA2 DNA repair associated	Homo sapiens	53-58
24902638-11	2014	Taken together, these results show a new function of BRCA2 protein as modulator of anoikis sensitivity through an evolutionarily-conserved molecular mechanism involving regulation of ROS production and/or detoxification by BRCA2 during PCD processes.	ros	183-186	BRCA2 DNA repair associated	Homo sapiens	223-228
24902638-8	2014	A higher increase in ROS levels occurred in the early phase of AA-PCD in BRCA2-expressing yeast cells compared with non-expressing cells.	ros	21-24	BRCA2 DNA repair associated	Homo sapiens	73-78
24902638-9	2014	Accordingly, a delay in the initial burst of ROS levels was observed in BRCA2-knockdown anoikis-resistant human cells.	ros	45-48	BRCA2 DNA repair associated	Homo sapiens	72-77
24902638-10	2014	Treatment with the antioxidants N-acetylcysteine or ascorbic acid reduced sensitivity to anoikis in human cells and inhibited AA-PCD in yeast cells expressing BRCA2.	Acetylcysteine	32-48	BRCA2 DNA repair associated	Homo sapiens	159-164
25076338-1	2014	Recent data suggests that treating patients with pancreatic cancer that express mutations in BRCA1, BRCA2, and PALB2 with chemotherapy which targets the DNA repair defect in these cells, such as platinum based therapies or PARPi [poly (ADP-ribose) polymerase inhibitor], may be more beneficial in these patients.	Platinum	195-203	BRCA2 DNA repair associated	Homo sapiens	100-105
24951267-0	2014	Duration of tamoxifen use and the risk of contralateral breast cancer in BRCA1 and BRCA2 mutation carriers.	Tamoxifen	12-21	BRCA2 DNA repair associated	Homo sapiens	83-88
24951267-10	2014	Short-term use of tamoxifen for chemoprevention in BRCA1 and BRCA2 mutation carriers may be as effective as a conventional 5-year course of treatment.	Tamoxifen	18-27	BRCA2 DNA repair associated	Homo sapiens	61-66
24965603-7	2014	Treatment with the PARPi AZD2281 +/- temozolomide induced DNA damage in CyclinA2+ cells in both primary AML cells and cell lines and distngiushed cell lines deficient (BRCA2-/-) or impaired (BRCA1+/-) in HRR activity from BRCA1+/+ cell lines based on p-H2AX induction.	olaparib	25-32	BRCA2 DNA repair associated	Homo sapiens	168-173
24965603-7	2014	Treatment with the PARPi AZD2281 +/- temozolomide induced DNA damage in CyclinA2+ cells in both primary AML cells and cell lines and distngiushed cell lines deficient (BRCA2-/-) or impaired (BRCA1+/-) in HRR activity from BRCA1+/+ cell lines based on p-H2AX induction.	Temozolomide	37-49	BRCA2 DNA repair associated	Homo sapiens	168-173
25093514-1	2014	Poly (ADP-ribose) polymerase (PARP) inhibitors and platinum-based chemotherapies have been found to be particularly effective in tumors that harbor deleterious germline or somatic mutations in the BRCA1 or BRCA2 genes, the products of which contribute to the conservative homologous recombination repair of DNA double-strand breaks.	Platinum	51-59	BRCA2 DNA repair associated	Homo sapiens	206-211
24842883-0	2014	Phase I/Ib study of olaparib and carboplatin in BRCA1 or BRCA2 mutation-associated breast or ovarian cancer with biomarker analyses.	olaparib	20-28	BRCA2 DNA repair associated	Homo sapiens	57-62
24728577-1	2014	Variants of uncertain clinical significance (VUS) in the high-penetrance breast cancer susceptibility genes BRCA1 and BRCA2 represent a major obstacle in genetic counseling of high-risk breast cancer families.	3-[(3~{a}~{S},4~{S},6~{a}~{R})-4-carboxy-2,3,4,5,6,6~{a}-hexahydro-1~{H}-pyrrolo[2,3-c]pyrrol-3~{a}-yl]propyl-$l^{3}-oxidanyl-bis(oxidanyl)boranuide	45-48	BRCA2 DNA repair associated	Homo sapiens	118-123
24728577-2	2014	We analyzed a missense VUS located in BRCA2 (p.Asn3124Ile; HGVS: BRCA2 c.9371A > T) present in seven independent high-risk breast cancer families that were counseled and genetically tested in South-West Germany.	3-[(3~{a}~{S},4~{S},6~{a}~{R})-4-carboxy-2,3,4,5,6,6~{a}-hexahydro-1~{H}-pyrrolo[2,3-c]pyrrol-3~{a}-yl]propyl-$l^{3}-oxidanyl-bis(oxidanyl)boranuide	23-26	BRCA2 DNA repair associated	Homo sapiens	38-43
24728577-2	2014	We analyzed a missense VUS located in BRCA2 (p.Asn3124Ile; HGVS: BRCA2 c.9371A > T) present in seven independent high-risk breast cancer families that were counseled and genetically tested in South-West Germany.	3-[(3~{a}~{S},4~{S},6~{a}~{R})-4-carboxy-2,3,4,5,6,6~{a}-hexahydro-1~{H}-pyrrolo[2,3-c]pyrrol-3~{a}-yl]propyl-$l^{3}-oxidanyl-bis(oxidanyl)boranuide	23-26	BRCA2 DNA repair associated	Homo sapiens	65-70
24842883-0	2014	Phase I/Ib study of olaparib and carboplatin in BRCA1 or BRCA2 mutation-associated breast or ovarian cancer with biomarker analyses.	Carboplatin	33-44	BRCA2 DNA repair associated	Homo sapiens	57-62
24842883-1	2014	BACKGROUND: Olaparib has single-agent activity against breast/ovarian cancer (BrCa/OvCa) in germline BRCA1 or BRCA2 mutation carriers (gBRCAm).	olaparib	12-20	BRCA2 DNA repair associated	Homo sapiens	110-115
24627472-2	2014	The protein RAP80 plays a central role in the damage response by targeting BRCA1/BRCA2 tumor suppressors to DNA damage foci through multivalent binding of Lys-63-linked polyubiquitin chains.	Lysine	155-158	BRCA2 DNA repair associated	Homo sapiens	81-86
24887359-0	2014	Genomic patterns resembling BRCA1- and BRCA2-mutated breast cancers predict benefit of intensified carboplatin-based chemotherapy.	Carboplatin	99-110	BRCA2 DNA repair associated	Homo sapiens	39-44
24784564-5	2014	Antisense-mediated reduction of IDO, alone and (in a synthetic lethal approach) in combination with antisense to the DNA repair protein BRCA2 sensitizes human lung cancer cells to olaparib and cisplatin.	olaparib	180-188	BRCA2 DNA repair associated	Homo sapiens	136-141
24784564-5	2014	Antisense-mediated reduction of IDO, alone and (in a synthetic lethal approach) in combination with antisense to the DNA repair protein BRCA2 sensitizes human lung cancer cells to olaparib and cisplatin.	Cisplatin	193-202	BRCA2 DNA repair associated	Homo sapiens	136-141
24627472-7	2014	Loss of this single glutamate residue disrupts favorable electrostatic interactions between RAP80 and ubiquitin, establishing a plausible molecular basis for a potential predisposition to cancer unrelated to mutations within BRCA1/BRCA2 genes.	Glutamic Acid	20-29	BRCA2 DNA repair associated	Homo sapiens	231-236
24772314-9	2014	Two pathological/presumably pathological variants were detected in the breast cancer patient group: a mutation in BRCA2 at the chromosomal (chr) position chr13:32890665, which affected the first position of the 5" splice region following exon 2; and a mutation in BRCA1 at chr17:41219635, causing an in-frame triple nucleotide deletion of valine 1688 (8.3%).	Valine	339-345	BRCA2 DNA repair associated	Homo sapiens	114-119
24384087-3	2014	Mass spectrometry mapping revealed that the MT1-MMP cleavage site of human BRCA2 is between Asn-2135 and Leu-2136 ((2132)LSNN/LNVEGG(2141)), and the point mutation L2136D abrogated MT1-MMP cleavage.	Asparagine	92-95	BRCA2 DNA repair associated	Homo sapiens	75-80
24627042-0	2014	The BRCA2 gene is a potential molecular target during 5-fluorouracil therapy in human oral cancer cells.	Fluorouracil	54-68	BRCA2 DNA repair associated	Homo sapiens	4-9
24627042-7	2014	It was found that BRCA2 was involved in such repair, and may be effectively targeted to inhibit the repair of 5-FU-induced damage.	Fluorouracil	110-114	BRCA2 DNA repair associated	Homo sapiens	18-23
24627042-8	2014	Observations showed that knockdown of BRCA2 using small interference RNA suppression increased the sensitivity to 5-FU of human oral cancer cell lines (SAS and HSC3).	Fluorouracil	114-118	BRCA2 DNA repair associated	Homo sapiens	38-43
24627042-9	2014	These findings suggest that downregulation of BRCA2 may be useful for sensitizing tumor cells during 5-FU chemotherapy.	Fluorouracil	101-105	BRCA2 DNA repair associated	Homo sapiens	46-51
24624361-2	2014	Genetic and functional evidence points to the homologous recombination (HR) DNA repair system, and BRCA1 and BRCA2 in particular, as main determinants of response to platinum therapy.	Platinum	166-174	BRCA2 DNA repair associated	Homo sapiens	109-114
24624361-4	2014	Here, we discuss a therapeutic concept that seeks to disrupt HR capacity via targeting of BRCA1 and BRCA2 functionality in order to reverse platinum resistance in BRCA-proficient high-grade serous ovarian cancers (HGSOC).	Platinum	140-148	BRCA2 DNA repair associated	Homo sapiens	100-105
24485656-4	2014	PALB2, BRCA2, and Poleta colocalize at stalled or collapsed replication forks after hydroxyurea treatment.	Hydroxyurea	84-95	BRCA2 DNA repair associated	Homo sapiens	7-12
24285729-1	2014	BRCA1, BRCA2, and PALB2 are key players in cellular tolerance to chemotherapeutic agents, including camptothecin, cisplatin, and PARP inhibitor.	Camptothecin	100-112	BRCA2 DNA repair associated	Homo sapiens	7-12
24285729-1	2014	BRCA1, BRCA2, and PALB2 are key players in cellular tolerance to chemotherapeutic agents, including camptothecin, cisplatin, and PARP inhibitor.	Cisplatin	114-123	BRCA2 DNA repair associated	Homo sapiens	7-12
24384087-3	2014	Mass spectrometry mapping revealed that the MT1-MMP cleavage site of human BRCA2 is between Asn-2135 and Leu-2136 ((2132)LSNN/LNVEGG(2141)), and the point mutation L2136D abrogated MT1-MMP cleavage.	Leucine	105-108	BRCA2 DNA repair associated	Homo sapiens	75-80
24336406-4	2013	Decreasing the intracellular calcium levels using BAPTA, or direct reconstitution of BRCA2 protein levels either by recombinant expression or by small molecule inhibition of both Skp2 and miR-1245 restored sensitivity to rucaparib to wild-type levels.	rucaparib	221-230	BRCA2 DNA repair associated	Homo sapiens	85-90
23859469-5	2014	Respondents recommended prophylactic oophorectomy more often than prophylactic mastectomy or tamoxifen for women with a BRCA1 or BRCA2 mutation (p < 0.0001).	Tamoxifen	93-102	BRCA2 DNA repair associated	Homo sapiens	129-134
24240700-1	2014	Small-molecule inhibitors of PARP1/2, such as olaparib, have been proposed to serve as a synthetic lethal therapy for cancers that harbor BRCA1 or BRCA2 mutations.	olaparib	46-54	BRCA2 DNA repair associated	Homo sapiens	147-152
23980083-10	2013	CONCLUSION: Age at treatment and use of tamoxifen are important predictors of chemotherapy-induced amenorrhea in women who carry a BRCA1 or BRCA2 mutation.	Tamoxifen	40-49	BRCA2 DNA repair associated	Homo sapiens	140-145
24140203-10	2013	INTERPRETATION: Carriers of BRCA1/BRCA2 mutations are exposed to higher titres of oestradiol and progesterone-known risk-factors for breast cancer.	Estradiol	82-92	BRCA2 DNA repair associated	Homo sapiens	34-39
24140203-10	2013	INTERPRETATION: Carriers of BRCA1/BRCA2 mutations are exposed to higher titres of oestradiol and progesterone-known risk-factors for breast cancer.	Progesterone	97-109	BRCA2 DNA repair associated	Homo sapiens	34-39
23918944-0	2013	Tamoxifen and risk of contralateral breast cancer for BRCA1 and BRCA2 mutation carriers.	Tamoxifen	0-9	BRCA2 DNA repair associated	Homo sapiens	64-69
23678008-7	2013	Pull down assays demonstrated the occurrence of complex comprising of all three proteins and DNA, where p53 tends to compete out hRAD51 and BRCA2(BRC1-8), leading to not only the decline in ATP hydrolysis but also the strand exchange function of hRAD51 that was stimulated by BRCA2(BRC1-8).	Adenosine Triphosphate	190-193	BRCA2 DNA repair associated	Homo sapiens	140-145
23918944-1	2013	PURPOSE: To determine whether adjuvant tamoxifen treatment for breast cancer (BC) is associated with reduced contralateral breast cancer (CBC) risk for BRCA1 and/or BRCA2 mutation carriers.	Tamoxifen	39-48	BRCA2 DNA repair associated	Homo sapiens	165-170
23918944-5	2013	RESULTS: Of 1,583 BRCA1 and 881 BRCA2 mutation carriers, 383 (24%) and 454 (52%), respectively, took tamoxifen after first BC diagnosis.	Tamoxifen	101-110	BRCA2 DNA repair associated	Homo sapiens	32-37
23918944-10	2013	CONCLUSION: This study provides evidence that tamoxifen use is associated with a reduction in CBC risk for BRCA1 and BRCA2 mutation carriers.	Tamoxifen	46-55	BRCA2 DNA repair associated	Homo sapiens	117-122
23964347-0	2013	Assessment of the Prognostic Value of Two Common Variants of BRCA1 and BRCA2 Genes in Ovarian Cancer Patients Treated with Cisplatin and Paclitaxel: A Gynecologic Oncology Group Study.	Cisplatin	123-132	BRCA2 DNA repair associated	Homo sapiens	71-76
23964347-0	2013	Assessment of the Prognostic Value of Two Common Variants of BRCA1 and BRCA2 Genes in Ovarian Cancer Patients Treated with Cisplatin and Paclitaxel: A Gynecologic Oncology Group Study.	Paclitaxel	137-147	BRCA2 DNA repair associated	Homo sapiens	71-76
23964347-1	2013	PURPOSE: BRCA1/BRCA2 germline mutations appear to enhance the platinum-sensitivity, but little is known about the prognostic relevance of polymorphisms in BRCA1/BRCA2 in epithelial ovarian cancer (EOC).	Platinum	62-70	BRCA2 DNA repair associated	Homo sapiens	15-20
23562522-5	2013	We estimated the impact of tamoxifen and hormone replacement therapy on the incidence of endometrial cancer in BRCA1 and BRCA2 carriers.	Tamoxifen	27-36	BRCA2 DNA repair associated	Homo sapiens	121-126
23696131-8	2013	Importantly, across six different PDA cell lines, two with defects in the Fanconi anemia/BRCA2 pathway (Hs766T and Capan-1), mitoxantrone is 40- to 20,000-fold more potent than GEM, with increased endogenous USP11 mRNA levels associated with increased sensitivity to mitoxantrone.	Mitoxantrone	125-137	BRCA2 DNA repair associated	Homo sapiens	89-94
23658460-8	2013	A high prevalence of BRCA1 185delAG (8.1%; P < 0.001) and BRCA2 6174delT (10.8%; P < 0.001) in Ashkenazi Jewish patients with PDAC was shown.	pdac	132-136	BRCA2 DNA repair associated	Homo sapiens	61-66
23940574-5	2013	Transcripts associated with BRCA1, BRCA2, ATM and CHEK2 showed altered expression in melanoma cell lines after cisplatin treatment.	Cisplatin	111-120	BRCA2 DNA repair associated	Homo sapiens	35-40
23847380-1	2013	A phase II study of the PARP inhibitor olaparib (AstraZeneca) for cancer patients with inherited BRCA1 and BRCA2 gene mutations confirmed earlier results showing clinical benefit for advanced breast and ovarian cancers, and demonstrated evidence of effectiveness against pancreatic and prostate cancers.	olaparib	39-47	BRCA2 DNA repair associated	Homo sapiens	107-112
23833673-0	2013	BRCA2 affects the efficiency of DNA double-strand break repair in response to N-nitroso compounds with differing carcinogenic potentials.	n-nitroso compounds	78-97	BRCA2 DNA repair associated	Homo sapiens	0-5
23833673-7	2013	The expression of BRCA2 and RAD51 was demonstrated to be inhibited by NDEA treatment but upregulated by NDELA or NDPA treatment.	Diethylnitrosamine	70-74	BRCA2 DNA repair associated	Homo sapiens	18-23
23833673-7	2013	The expression of BRCA2 and RAD51 was demonstrated to be inhibited by NDEA treatment but upregulated by NDELA or NDPA treatment.	N-nitrosodiethanolamine	104-109	BRCA2 DNA repair associated	Homo sapiens	18-23
23833673-7	2013	The expression of BRCA2 and RAD51 was demonstrated to be inhibited by NDEA treatment but upregulated by NDELA or NDPA treatment.	N-nitroso(di-n-propyl)amine	113-117	BRCA2 DNA repair associated	Homo sapiens	18-23
23474559-4	2013	In another study (Abstract #147), substantial responses were observed in both patients with BRCA2-associated pancreatic cancer treated with the poly-(ADP-ribose) polymerase (PARP) inhibitor ABT-888 (veliparib).	veliparib	190-197	BRCA2 DNA repair associated	Homo sapiens	92-97
23473053-4	2013	Mechanistic studies revealed that the new PARP1 inhibitors significantly inhibited H2O2-triggered PARylation in SKOV3 cells, induced cellular accumulation of DNA double-strand breaks, and impaired cell-cycle progression in BRCA2-deficient cells.	Hydrogen Peroxide	83-87	BRCA2 DNA repair associated	Homo sapiens	223-228
23265709-0	2013	Implications of BRCA1 and BRCA2 mutations for the efficacy of paclitaxel monotherapy in advanced ovarian cancer.	Paclitaxel	62-72	BRCA2 DNA repair associated	Homo sapiens	26-31
23265709-1	2013	INTRODUCTION: Preclinical data suggest that BRCA1 and BRCA2 (BRCA1/2)-mutated ovarian cancers (BMOC) are exquisitely sensitive to platinum-salts, but resistant to microtubule-stabilizing anticancer agents.	Platinum	130-138	BRCA2 DNA repair associated	Homo sapiens	54-59
23265709-1	2013	INTRODUCTION: Preclinical data suggest that BRCA1 and BRCA2 (BRCA1/2)-mutated ovarian cancers (BMOC) are exquisitely sensitive to platinum-salts, but resistant to microtubule-stabilizing anticancer agents.	Platinum	130-138	BRCA2 DNA repair associated	Homo sapiens	61-68
23481354-7	2013	We determined that antisense downregulation of BRCA2 synergistically potentiated drugs with mechanisms of action related to BRCA2 function (cisplatin, melphalan), a phenomenon we named "complementary lethality."	Cisplatin	140-149	BRCA2 DNA repair associated	Homo sapiens	47-52
23481354-7	2013	We determined that antisense downregulation of BRCA2 synergistically potentiated drugs with mechanisms of action related to BRCA2 function (cisplatin, melphalan), a phenomenon we named "complementary lethality."	Cisplatin	140-149	BRCA2 DNA repair associated	Homo sapiens	124-129
23481354-7	2013	We determined that antisense downregulation of BRCA2 synergistically potentiated drugs with mechanisms of action related to BRCA2 function (cisplatin, melphalan), a phenomenon we named "complementary lethality."	Melphalan	151-160	BRCA2 DNA repair associated	Homo sapiens	47-52
23481354-7	2013	We determined that antisense downregulation of BRCA2 synergistically potentiated drugs with mechanisms of action related to BRCA2 function (cisplatin, melphalan), a phenomenon we named "complementary lethality."	Melphalan	151-160	BRCA2 DNA repair associated	Homo sapiens	124-129
23481354-12	2013	This work has contributed to the development of a BRCA2-targeting antisense oligdeoxynucleotide (ASO) "BR-1" which we will test in vivo in combination with our TS-targeting ASO "SARI 83" and attempt early clinical trials in the future.Molecular Therapy - Nucleic Acids (2013) 2, e78; doi:10.1038/mtna.2013.7 published online 12 March 2013.	oligdeoxynucleotide	76-95	BRCA2 DNA repair associated	Homo sapiens	50-55
23481354-12	2013	This work has contributed to the development of a BRCA2-targeting antisense oligdeoxynucleotide (ASO) "BR-1" which we will test in vivo in combination with our TS-targeting ASO "SARI 83" and attempt early clinical trials in the future.Molecular Therapy - Nucleic Acids (2013) 2, e78; doi:10.1038/mtna.2013.7 published online 12 March 2013.	1,5-anhydroglucitol	97-100	BRCA2 DNA repair associated	Homo sapiens	50-55
23474559-4	2013	In another study (Abstract #147), substantial responses were observed in both patients with BRCA2-associated pancreatic cancer treated with the poly-(ADP-ribose) polymerase (PARP) inhibitor ABT-888 (veliparib).	veliparib	199-208	BRCA2 DNA repair associated	Homo sapiens	92-97
23106910-11	2012	Cisplatin-induced DNA damage response showed negative relationship between SET overexpression and BRCA2 recruitment.	Cisplatin	0-9	BRCA2 DNA repair associated	Homo sapiens	98-103
24371674-0	2013	Unexpected long-term survival in a BRCA2 patient with metastatic carcinosarcoma associated with tamoxifen.	Tamoxifen	96-105	BRCA2 DNA repair associated	Homo sapiens	35-40
23881989-9	2013	In contrast, there is emerging evidence of relative resistance of tumors containing BRCA1 or BRCA2 mutations (or BRCAness) to taxanes.	Taxoids	126-133	BRCA2 DNA repair associated	Homo sapiens	93-98
23344974-6	2013	The initial fragment hits were thoroughly validated biophysically by isothermal titration calorimetry (ITC) and NMR techniques and observed by X-ray crystallography to bind in a shallow surface pocket that is occupied in the native complex by the side chain of a phenylalanine from the conserved FxxA interaction motif found in BRCA2.	Phenylalanine	263-276	BRCA2 DNA repair associated	Homo sapiens	328-333
23165508-4	2013	Massively parallel DNA sequencing of treatment-naive and post-olaparib treatment biopsies identified tumour-specific BRCA2 secondary mutations in olaparib-resistant metastases.	olaparib	62-70	BRCA2 DNA repair associated	Homo sapiens	117-122
23165508-4	2013	Massively parallel DNA sequencing of treatment-naive and post-olaparib treatment biopsies identified tumour-specific BRCA2 secondary mutations in olaparib-resistant metastases.	olaparib	146-154	BRCA2 DNA repair associated	Homo sapiens	117-122
23165508-5	2013	These secondary mutations restored full-length BRCA2 protein, and most likely cause olaparib resistance by re-establishing BRCA2 function in the tumour cells.	olaparib	84-92	BRCA2 DNA repair associated	Homo sapiens	123-128
23762568-2	2013	Despite the fact that women who inherited mutations in the BRCA1 and BRCA2 genes have a high risk of developing breast cancer, studies have also shown that significant exposure to certain metal compounds and organic solvents also increases the risks of mammary gland carcinogenesis.	Metals	188-193	BRCA2 DNA repair associated	Homo sapiens	69-74
23483928-9	2013	The overall RR estimates of 29/29 poly-Q repeats on risk of BC in BRCA1/2, BRCA1, and BRCA2, were always greater than 1.00; however, this effect was not statistically significant.	polyglutamine	34-40	BRCA2 DNA repair associated	Homo sapiens	86-91
22843497-3	2012	We developed bisulfite pyrosequencing assays to screen >600 affected BRCA1/BRCA2 mutation-negative patients from the German Consortium for Hereditary Breast and Ovarian Cancer for constitutive hypermethylation of ATM, BRCA1, BRCA2, RAD51C, PTEN and TP53 in blood cells.	hydrogen sulfite	13-22	BRCA2 DNA repair associated	Homo sapiens	78-83
22430443-6	2012	A significant interaction was also observed between occupational exposure to benzene and BRCA2 (rs144848) for NHL overall (Pfor interaction=0.0042).	Benzene	77-84	BRCA2 DNA repair associated	Homo sapiens	89-94
22579622-5	2012	Cells expressing high levels of BRCA2 feature normal growth, increased sensitivity to mitomycin C, and increased illegitimate recombination.	Mitomycin	86-97	BRCA2 DNA repair associated	Homo sapiens	32-37
22217331-4	2012	We demonstrated by quantitative analysis of methylated alleles a significant decrease in the methylation of the cytosine phosphate guanine (CpG) islands in the promoters of BRCA1 and BRCA2 after the S-equol treatment in MCF-7 and MDA-MB-231 cells and a trend in MCF-10a cells.	cytosine phosphate guanine	112-138	BRCA2 DNA repair associated	Homo sapiens	183-188
22833573-4	2012	Here we show that depleting ATR, BRCA1, BRCA2, or RAD51 sensitized to ABT-888 (veliparib) alone, FdUrd alone, and FdUrd + ABT-888 (F+A), suggesting that homologous recombination (HR) repair protects cells exposed to these agents.	2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid	70-73	BRCA2 DNA repair associated	Homo sapiens	40-45
22833573-4	2012	Here we show that depleting ATR, BRCA1, BRCA2, or RAD51 sensitized to ABT-888 (veliparib) alone, FdUrd alone, and FdUrd + ABT-888 (F+A), suggesting that homologous recombination (HR) repair protects cells exposed to these agents.	2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid	122-125	BRCA2 DNA repair associated	Homo sapiens	40-45
22778154-8	2012	Moreover, the ABT-888/carboplatin combination delayed tumor growth in Brca2 xenografts.	2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid	14-17	BRCA2 DNA repair associated	Homo sapiens	70-75
22778154-8	2012	Moreover, the ABT-888/carboplatin combination delayed tumor growth in Brca2 xenografts.	Carboplatin	22-33	BRCA2 DNA repair associated	Homo sapiens	70-75
22449149-8	2012	Correlative studies demonstrated decreased expression of BRCA2 (P = 0 0072) and FANCF (P = 0 0458) mRNA following bortezomib treatment.	Bortezomib	114-124	BRCA2 DNA repair associated	Homo sapiens	57-62
22562176-1	2012	Synthetic lethal therapeutic strategy using poly(adenosine diphosphate [ADP]-ribose) polymerase (PARP) inhibitor olaparib in carriers of BRCA1 or BRCA2 mutation has shown promise in clinical settings.	olaparib	113-121	BRCA2 DNA repair associated	Homo sapiens	146-151
22576693-8	2012	These results suggest that the breast tissue of women with BRCA1 or BRCA2 mutations could be more susceptible to the effects of BPA.	bisphenol A	128-131	BRCA2 DNA repair associated	Homo sapiens	68-73
22339411-2	2012	We investigated the putative effects on DNA methylation by two naturally occurring isoflavones, genistein and daidzein, in a study of the BRCA1 and BRCA2 oncosuppressor genes in breast cancer cell lines (MCF-7, MDA-MB 231, and MCF10a).	Genistein	96-105	BRCA2 DNA repair associated	Homo sapiens	148-153
22339411-2	2012	We investigated the putative effects on DNA methylation by two naturally occurring isoflavones, genistein and daidzein, in a study of the BRCA1 and BRCA2 oncosuppressor genes in breast cancer cell lines (MCF-7, MDA-MB 231, and MCF10a).	daidzein	110-118	BRCA2 DNA repair associated	Homo sapiens	148-153
21756279-11	2012	One BRCA2 carrier treated with docetaxel plus platinum survived 37 months.	Docetaxel	31-40	BRCA2 DNA repair associated	Homo sapiens	4-9
22452356-1	2012	BACKGROUND: Olaparib (AZD2281) is an oral poly(adenosine diphosphate [ADP]-ribose) polymerase inhibitor that has shown antitumor activity in patients with high-grade serous ovarian cancer with or without BRCA1 or BRCA2 germline mutations.	olaparib	12-20	BRCA2 DNA repair associated	Homo sapiens	213-218
22452356-1	2012	BACKGROUND: Olaparib (AZD2281) is an oral poly(adenosine diphosphate [ADP]-ribose) polymerase inhibitor that has shown antitumor activity in patients with high-grade serous ovarian cancer with or without BRCA1 or BRCA2 germline mutations.	olaparib	22-29	BRCA2 DNA repair associated	Homo sapiens	213-218
20960027-6	2012	In this study sensitivity to the inhibitor ZM447439 was tested on a panel of 15 non-malignant and malignant epithelial cell lines that differed with respect to BRCA2 and p53 status and related to level of Aurora kinase expression.	4-(4-(N-benzoylamino)anilino)-6-methoxy-7-(3-(1-morpholino)propoxy)quinazoline	43-51	BRCA2 DNA repair associated	Homo sapiens	160-165
22293751-3	2012	After exposure of cells to hydroxyurea or aphidicolin, APRIN and other cohesin components associate with BRCA2 in early S-phase.	Hydroxyurea	27-38	BRCA2 DNA repair associated	Homo sapiens	105-110
22293751-3	2012	After exposure of cells to hydroxyurea or aphidicolin, APRIN and other cohesin components associate with BRCA2 in early S-phase.	Aphidicolin	42-53	BRCA2 DNA repair associated	Homo sapiens	105-110
22670552-5	2012	This report presents such a case, in which a 52-year-old woman carrier of the BRCA2 mutation gene was successfully treated with hyperbaric oxygen therapy.	Oxygen	139-145	BRCA2 DNA repair associated	Homo sapiens	78-83
22291137-5	2012	RESULTS: Consistent with earlier reports, olaparib and veliparib selectively induced apoptosis and inhibited colony formation in cells lacking BRCA2 or ATM.	olaparib	42-50	BRCA2 DNA repair associated	Homo sapiens	143-148
22291137-5	2012	RESULTS: Consistent with earlier reports, olaparib and veliparib selectively induced apoptosis and inhibited colony formation in cells lacking BRCA2 or ATM.	veliparib	55-64	BRCA2 DNA repair associated	Homo sapiens	143-148
21756279-11	2012	One BRCA2 carrier treated with docetaxel plus platinum survived 37 months.	Platinum	46-54	BRCA2 DNA repair associated	Homo sapiens	4-9
22101337-3	2011	Using gene expression microarray analysis, we find that DNA damage response (DDR) pathways elicited by veliparib (ABT-888), a PARP inhibitor, plus topotecan comprise the G1/S checkpoint, ATM, and p53 signaling pathways in p53-wildtype cancer cell lines and BRCA1, BRCA2 and ATR pathway in p53-mutant lines.	veliparib	103-112	BRCA2 DNA repair associated	Homo sapiens	264-269
22076253-0	2012	Uptake of a randomized breast cancer prevention trial comparing letrozole to placebo in BRCA1/2 mutations carriers: the LIBER trial.	Letrozole	64-73	BRCA2 DNA repair associated	Homo sapiens	88-95
22076253-4	2012	LIBER is an ongoing double-blind, randomized phase III trial to evaluate the efficacy of 5-year letrozole versus placebo to decrease breast cancer incidence in post-menopausal BRCA1/2 mutation carriers (NCT00673335).	Letrozole	96-105	BRCA2 DNA repair associated	Homo sapiens	176-183
22203755-1	2012	PURPOSE: Olaparib (AZD2281), an orally active poly (ADP-ribose) polymerase inhibitor that induces synthetic lethality in BRCA1- or BRCA2-deficient cells, has shown promising clinical efficacy in nonrandomized phase II trials in patients with ovarian cancer with BRCA1 or BRCA2 deficiency.	olaparib	9-17	BRCA2 DNA repair associated	Homo sapiens	131-136
22203755-1	2012	PURPOSE: Olaparib (AZD2281), an orally active poly (ADP-ribose) polymerase inhibitor that induces synthetic lethality in BRCA1- or BRCA2-deficient cells, has shown promising clinical efficacy in nonrandomized phase II trials in patients with ovarian cancer with BRCA1 or BRCA2 deficiency.	olaparib	19-26	BRCA2 DNA repair associated	Homo sapiens	131-136
22901131-3	2012	METHODS: The methylation type of the BRCA2 promoter was evaluated using bisulfate-modified DNA in methylation- specific PCR and the MTHFRa1278c polymorphism was assessed by PCR-RFLP.	hydrogen sulfate	72-81	BRCA2 DNA repair associated	Homo sapiens	37-42
22019631-2	2012	In this review the tumor suppressor genes p53, FoxO, retinoblastoma (RB), p21, p16, and breast cancer susceptibility genes 1 and 2 (BRCA1 and BRCA2) and their roles in oxidative stress are summarized with a focus on the links and interplay between their pathways and reactive oxygen species (ROS).	Reactive Oxygen Species	267-290	BRCA2 DNA repair associated	Homo sapiens	142-147
22019631-2	2012	In this review the tumor suppressor genes p53, FoxO, retinoblastoma (RB), p21, p16, and breast cancer susceptibility genes 1 and 2 (BRCA1 and BRCA2) and their roles in oxidative stress are summarized with a focus on the links and interplay between their pathways and reactive oxygen species (ROS).	Reactive Oxygen Species	292-295	BRCA2 DNA repair associated	Homo sapiens	142-147
21761396-0	2012	The efficacy of taxane chemotherapy for metastatic breast cancer in BRCA1 and BRCA2 mutation carriers.	taxane	16-22	BRCA2 DNA repair associated	Homo sapiens	78-83
21761396-1	2012	BACKGROUND: We assessed the efficacy of taxane chemotherapy in BRCA1- and BRCA2-associated patients compared with sporadic metastatic breast cancer patients.	taxane	40-46	BRCA2 DNA repair associated	Homo sapiens	74-79
21761396-9	2012	HRec-positive BRCA1- and BRCA2-associated patients had a sensitivity to taxane chemotherapy similar to that of sporadic patients.	taxane	72-78	BRCA2 DNA repair associated	Homo sapiens	25-30
22176776-2	2012	Recent studies in the Cancer Genome Atlas project have demonstrated that BRCA2 mutation carriers are more responsive to platinum-based chemotherapy among high-grade serous ovarian cancer patients.	Platinum	120-128	BRCA2 DNA repair associated	Homo sapiens	73-78
22101337-3	2011	Using gene expression microarray analysis, we find that DNA damage response (DDR) pathways elicited by veliparib (ABT-888), a PARP inhibitor, plus topotecan comprise the G1/S checkpoint, ATM, and p53 signaling pathways in p53-wildtype cancer cell lines and BRCA1, BRCA2 and ATR pathway in p53-mutant lines.	2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid	114-117	BRCA2 DNA repair associated	Homo sapiens	264-269
22101337-3	2011	Using gene expression microarray analysis, we find that DNA damage response (DDR) pathways elicited by veliparib (ABT-888), a PARP inhibitor, plus topotecan comprise the G1/S checkpoint, ATM, and p53 signaling pathways in p53-wildtype cancer cell lines and BRCA1, BRCA2 and ATR pathway in p53-mutant lines.	Topotecan	147-156	BRCA2 DNA repair associated	Homo sapiens	264-269
21839586-2	2011	An example of this may be the increased susceptibility of BRCA1 or BRCA2 mutation carriers to the carcinogen formaldehyde.	Formaldehyde	109-121	BRCA2 DNA repair associated	Homo sapiens	67-72
22044372-6	2011	An Asn372His homozygous variation was noted in the BRCA2 gene in the patient with medulloblastoma whereas the variation was heterozygous in the healthy father.	asn372his	3-12	BRCA2 DNA repair associated	Homo sapiens	51-56
21839586-6	2011	It is known that some types of formaldehyde-associated DNA damage require error-free DNA repairs mediated by pathways containing BRCA1 and BRCA2 proteins.	Formaldehyde	31-43	BRCA2 DNA repair associated	Homo sapiens	139-144
21990299-6	2011	Moreover, BRCA2 mutations were associated with a significantly higher primary chemotherapy sensitivity rate (100% for BRCA2-mutated vs 82% [P = .02] and 80% [P = .05] for BRCA wild-type and BRCA1-mutated cases, respectively) and longer platinum-free duration (median platinum-free duration, 18.0 months for BRCA2-mutated vs 11.7 [P = .02] and 12.5 [P = .04] months for BRCA wild-type and BRCA1-mutated cases, respectively).	Platinum	267-275	BRCA2 DNA repair associated	Homo sapiens	10-15
21378390-3	2011	Here we report a remarkable case of cure following platinum-resistant stage III ovarian carcinoma in a woman with a BRCA2 mutation.	Platinum	51-59	BRCA2 DNA repair associated	Homo sapiens	116-121
21990299-6	2011	Moreover, BRCA2 mutations were associated with a significantly higher primary chemotherapy sensitivity rate (100% for BRCA2-mutated vs 82% [P = .02] and 80% [P = .05] for BRCA wild-type and BRCA1-mutated cases, respectively) and longer platinum-free duration (median platinum-free duration, 18.0 months for BRCA2-mutated vs 11.7 [P = .02] and 12.5 [P = .04] months for BRCA wild-type and BRCA1-mutated cases, respectively).	Platinum	236-244	BRCA2 DNA repair associated	Homo sapiens	10-15
21741379-0	2011	A new assay for functional screening of BRCA2 linker region mutations identifies variants that alter chemoresistance to cisplatin.	Cisplatin	120-129	BRCA2 DNA repair associated	Homo sapiens	40-45
20625817-0	2011	Ionizing radiation or mitomycin-induced micronuclei in lymphocytes of BRCA1 or BRCA2 mutation carriers.	Mitomycin	22-31	BRCA2 DNA repair associated	Homo sapiens	79-84
21819606-2	2011	Breast and ovarian neoplasms from BRCA1 or BRCA2 mutation carriers are characterized by deficient homologous recombination (HR) of DNA, that makes them particularly sensitive to platinum compounds or inhibitors of poly (ADP-ribose) polymerase (PARP).	Platinum	178-186	BRCA2 DNA repair associated	Homo sapiens	43-48
21613821-0	2011	Complete remission, in BRCA2 mutation carrier with metastatic pancreatic adenocarcinoma, treated with cisplatin based therapy.	Cisplatin	102-111	BRCA2 DNA repair associated	Homo sapiens	23-28
21762248-7	2011	Consumption of alcohol other than wine interacted significantly with BRCA2 mutations (COR = 2.15, 95% CI: 1.03-4.49).	Alcohols	15-22	BRCA2 DNA repair associated	Homo sapiens	69-74
21762248-8	2011	Consumption of wine may protect against BRCA1-associated tumors, while women with BRCA2 mutations may be at greater risk of alcohol-induced breast cancer.	Alcohols	124-131	BRCA2 DNA repair associated	Homo sapiens	82-87
21709188-2	2011	In cell lines, BRCA2 restoration mediates resistance to platinum chemotherapy and poly (ADP-ribose) polymerase (PARP) inhibitors.	Platinum	56-64	BRCA2 DNA repair associated	Homo sapiens	15-20
21523855-1	2011	Variants of uncertain significance (VUS) in the BRCA1 and BRCA2 genes potentially affecting coding sequence as well as normal splicing activity have confounded predisposition testing in breast cancer.	3-[(3~{a}~{S},4~{S},6~{a}~{R})-4-carboxy-2,3,4,5,6,6~{a}-hexahydro-1~{H}-pyrrolo[2,3-c]pyrrol-3~{a}-yl]propyl-$l^{3}-oxidanyl-bis(oxidanyl)boranuide	36-39	BRCA2 DNA repair associated	Homo sapiens	58-63
21601571-0	2011	Valine 1532 of human BRC repeat 4 plays an important role in the interaction between BRCA2 and RAD51.	Valine	0-6	BRCA2 DNA repair associated	Homo sapiens	85-90
20625817-3	2011	We investigated whether lymphocytes carrying BRCA1 or BRCA2 mutations displayed an increased sensitivity to radiation or mitomycin C (MMC) in vitro treatments.	Mitomycin	121-132	BRCA2 DNA repair associated	Homo sapiens	54-59
20625817-3	2011	We investigated whether lymphocytes carrying BRCA1 or BRCA2 mutations displayed an increased sensitivity to radiation or mitomycin C (MMC) in vitro treatments.	Mitomycin	134-137	BRCA2 DNA repair associated	Homo sapiens	54-59
21438617-2	2011	We observed that oxidized FAD (FAD(ox)) in solution readily aggregates at submillimolar concentration.	Flavin-Adenine Dinucleotide	26-29	BRCA2 DNA repair associated	Homo sapiens	31-38
21573016-8	2011	However, FANCG and FANCD1/BRCA2 played notably important roles in the repair of TMZ-induced DNA damage.	Temozolomide	80-83	BRCA2 DNA repair associated	Homo sapiens	19-25
21573016-8	2011	However, FANCG and FANCD1/BRCA2 played notably important roles in the repair of TMZ-induced DNA damage.	Temozolomide	80-83	BRCA2 DNA repair associated	Homo sapiens	26-31
22073281-7	2011	The data show that knockdown of Rad51 or BRCA2 greatly sensitizes cells to DSBs and the induction of cell death following temozolomide and nimustine (ACNU).	dsbs	75-79	BRCA2 DNA repair associated	Homo sapiens	41-46
21425892-1	2011	There is evidence that tamoxifen treatment of BRCA1 and BRCA2 carriers for prior breast cancer increases risk of endometrioid subtype endometrial cancer (EC), and suggestive evidence that BRCA1 and BRCA2 mutation carriers may be predisposed to EC in the absence of tamoxifen exposure.	Tamoxifen	23-32	BRCA2 DNA repair associated	Homo sapiens	56-61
21425892-1	2011	There is evidence that tamoxifen treatment of BRCA1 and BRCA2 carriers for prior breast cancer increases risk of endometrioid subtype endometrial cancer (EC), and suggestive evidence that BRCA1 and BRCA2 mutation carriers may be predisposed to EC in the absence of tamoxifen exposure.	Tamoxifen	265-274	BRCA2 DNA repair associated	Homo sapiens	56-61
21425892-1	2011	There is evidence that tamoxifen treatment of BRCA1 and BRCA2 carriers for prior breast cancer increases risk of endometrioid subtype endometrial cancer (EC), and suggestive evidence that BRCA1 and BRCA2 mutation carriers may be predisposed to EC in the absence of tamoxifen exposure.	Tamoxifen	265-274	BRCA2 DNA repair associated	Homo sapiens	198-203
21385444-9	2011	On the contrary, downregulation of BRCA2, a critical protein for homologous recombination repair (HRR), significantly enhanced the efficacy of cisplatin in killing ovarian cancer cell line PEO4.	Cisplatin	143-152	BRCA2 DNA repair associated	Homo sapiens	35-40
21385444-9	2011	On the contrary, downregulation of BRCA2, a critical protein for homologous recombination repair (HRR), significantly enhanced the efficacy of cisplatin in killing ovarian cancer cell line PEO4.	peo4	189-193	BRCA2 DNA repair associated	Homo sapiens	35-40
21097693-0	2011	Tumor growth inhibition by olaparib in BRCA2 germline-mutated patient-derived ovarian cancer tissue xenografts.	olaparib	27-35	BRCA2 DNA repair associated	Homo sapiens	39-44
21097693-4	2011	RESULTS: We show that olaparib alone and in combination with carboplatin greatly inhibit growth in BRCA2-mutated ovarian serous carcinoma.	olaparib	22-30	BRCA2 DNA repair associated	Homo sapiens	99-104
21097693-4	2011	RESULTS: We show that olaparib alone and in combination with carboplatin greatly inhibit growth in BRCA2-mutated ovarian serous carcinoma.	Carboplatin	61-72	BRCA2 DNA repair associated	Homo sapiens	99-104
21368455-8	2011	In additional studies, the PARP inhibitor has shown remarkable activity in BRCA1- or BRCA2-mutant tumors when used in combination with gemcitabine and carboplatin.	gemcitabine	135-146	BRCA2 DNA repair associated	Homo sapiens	85-90
21508395-0	2011	Evidence for the efficacy of Iniparib, a PARP-1 inhibitor, in BRCA2-associated pancreatic cancer.	iniparib	29-37	BRCA2 DNA repair associated	Homo sapiens	62-67
21508395-5	2011	This report describes the case of a patient with a germline BRCA2 mutation and an associated pancreatic cancer treated with iniparib (BSI-201), a PARP inhibitor, who demonstrated a complete pathologic response to this agent.	iniparib	124-132	BRCA2 DNA repair associated	Homo sapiens	60-65
21470549-0	2011	The therapeutic ratio is preserved for radiotherapy or cisplatin treatment in BRCA2-mutated prostate cancers.	Cisplatin	55-64	BRCA2 DNA repair associated	Homo sapiens	78-83
21289082-7	2011	Thus, the growth-suppressive effect of CHK1 inhibition in BRCA2-mutant tumors can be opposed by concurrent KRAS activation and TP53 mutations typical of pancreatic adenocarcinoma, and CHK1i resistance in this setting can be overcome by gemcitabine.	gemcitabine	236-247	BRCA2 DNA repair associated	Homo sapiens	58-63
22866093-8	2011	The third family carried the known BRCA2 mutation c.5073dupA/p.trp1692metfsX3.	trp1692metfsx3	63-77	BRCA2 DNA repair associated	Homo sapiens	35-40
21183737-0	2011	Therapeutic potential of poly(ADP-ribose) polymerase inhibitor AG014699 in human cancers with mutated or methylated BRCA1 or BRCA2.	rucaparib	63-71	BRCA2 DNA repair associated	Homo sapiens	125-130
21183737-11	2011	Growth of xenograft tumors with BRCA1/2 mutations or with epigenetically silenced BRCA1 was reduced by AG014699 treatment, and combination treatment with AG014699 plus carboplatin was more effective than either drug alone.	rucaparib	103-111	BRCA2 DNA repair associated	Homo sapiens	32-39
21183737-13	2011	CONCLUSION: Human cancer cells or xenograft tumors with mutated or epigenetically silenced BRCA1/2 were sensitive to AG014699 monotherapy, indicating a potential role for PARP inhibitors in sporadic human cancers.	rucaparib	117-125	BRCA2 DNA repair associated	Homo sapiens	91-98
22073281-7	2011	The data show that knockdown of Rad51 or BRCA2 greatly sensitizes cells to DSBs and the induction of cell death following temozolomide and nimustine (ACNU).	Temozolomide	122-134	BRCA2 DNA repair associated	Homo sapiens	41-46
22073281-7	2011	The data show that knockdown of Rad51 or BRCA2 greatly sensitizes cells to DSBs and the induction of cell death following temozolomide and nimustine (ACNU).	Nimustine	139-148	BRCA2 DNA repair associated	Homo sapiens	41-46
22073281-7	2011	The data show that knockdown of Rad51 or BRCA2 greatly sensitizes cells to DSBs and the induction of cell death following temozolomide and nimustine (ACNU).	Nimustine	150-154	BRCA2 DNA repair associated	Homo sapiens	41-46
22073281-9	2011	The expression of O(6)-methylguanine-DNA methyltransferase (MGMT) abolished all these effects, indicating that O(6)-alkylguanine induced by these drugs is the primary lesion responsible for the formation of DSBs and increased sensitivity of glioma cells following knockdown of Rad51 and BRCA2.	o(6)-alkylguanine	111-128	BRCA2 DNA repair associated	Homo sapiens	287-292
22073281-9	2011	The expression of O(6)-methylguanine-DNA methyltransferase (MGMT) abolished all these effects, indicating that O(6)-alkylguanine induced by these drugs is the primary lesion responsible for the formation of DSBs and increased sensitivity of glioma cells following knockdown of Rad51 and BRCA2.	dsbs	207-211	BRCA2 DNA repair associated	Homo sapiens	287-292
22073281-12	2011	The data provides evidence that down-regulation of Rad51 or BRCA2 is a reasonable strategy for sensitizing glioma cells to killing by O(6)-alkylating anti-cancer drugs.	o(6)	134-138	BRCA2 DNA repair associated	Homo sapiens	60-65
21056012-4	2010	Correspondingly, three out of four PDACs from patients inheriting BRCA2(999del5) did not exhibit loss-of-heterozygosity (LOH).	pdacs	35-40	BRCA2 DNA repair associated	Homo sapiens	66-71
20541936-0	2010	Alcohol consumption and the risk of breast cancer among BRCA1 and BRCA2 mutation carriers.	Alcohols	0-7	BRCA2 DNA repair associated	Homo sapiens	66-71
21159167-4	2010	RESULTS: U0126 significantly modulated endogenous expression of several important drug resistance (BCL2, ABCB1, ABCC3), prosurvival (BCL2), DNA repair (BRCA1, BRCA2), hormone receptor (AR, ESR2, PPARgamma) and drug metabolism (CYP3A4) genes newly identified in MM cells.	U 0126	9-14	BRCA2 DNA repair associated	Homo sapiens	159-164
20921464-0	2010	Compliance with tamoxifen in women with breast cancer and a BRCA1 or BRCA2 mutation.	Tamoxifen	16-25	BRCA2 DNA repair associated	Homo sapiens	69-74
20309627-7	2010	Our data suggest that the risk for breast cancer among BRCA1 or BRCA2 carriers may be modified by reproductive characteristics and alcohol use.	Alcohols	131-138	BRCA2 DNA repair associated	Homo sapiens	64-69
20708982-5	2010	We show that HR defective cells (BRCA2, Rad51D and XRCC3 mutants) are dramatically more sensitive to MMS-induced DNA damage as measured by colony formation, apoptosis and chromosomal aberrations, while NHEJ defective cells (Ku80 and DNA-PK(CS) mutants) are only mildly sensitive to the killing, apoptosis-inducing and clastogenic effects of MMS.	Methyl Methanesulfonate	101-104	BRCA2 DNA repair associated	Homo sapiens	33-38
20729832-4	2010	BRCA2 acts by targeting RAD51 to ssDNA over double-stranded DNA, enabling RAD51 to displace replication protein-A (RPA) from ssDNA and stabilizing RAD51-ssDNA filaments by blocking ATP hydrolysis.	Adenosine Triphosphate	181-184	BRCA2 DNA repair associated	Homo sapiens	0-5
20135344-5	2010	Conditional logistic regression was used to compare the risk of CBC associated with chemotherapy and tamoxifen in BRCA1/BRCA2 mutation carriers and non-carriers.	Tamoxifen	101-110	BRCA2 DNA repair associated	Homo sapiens	120-125
20922827-0	2010	Targeted therapies: PARP inhibitor olaparib is safe and effective in patients with BRCA1 and BRCA2 mutations.	olaparib	35-43	BRCA2 DNA repair associated	Homo sapiens	93-98
20485165-3	2010	RECENT FINDINGS: Preclinical recognition that BRCA1 and BRCA2-associated tumours are very sensitive to inhibition of poly-ADP ribose polymerase (PARP), a key molecule in DNA repair, led to ovarian cancer patients with germline BRCA1 and BRCA2 mutations being treated with the PARP inhibitor olaparib (AZD2281, KU-0059436; KuDOS/Astra-Zeneca).	olaparib	291-299	BRCA2 DNA repair associated	Homo sapiens	237-242
20485165-3	2010	RECENT FINDINGS: Preclinical recognition that BRCA1 and BRCA2-associated tumours are very sensitive to inhibition of poly-ADP ribose polymerase (PARP), a key molecule in DNA repair, led to ovarian cancer patients with germline BRCA1 and BRCA2 mutations being treated with the PARP inhibitor olaparib (AZD2281, KU-0059436; KuDOS/Astra-Zeneca).	olaparib	301-308	BRCA2 DNA repair associated	Homo sapiens	56-61
20485165-3	2010	RECENT FINDINGS: Preclinical recognition that BRCA1 and BRCA2-associated tumours are very sensitive to inhibition of poly-ADP ribose polymerase (PARP), a key molecule in DNA repair, led to ovarian cancer patients with germline BRCA1 and BRCA2 mutations being treated with the PARP inhibitor olaparib (AZD2281, KU-0059436; KuDOS/Astra-Zeneca).	olaparib	291-299	BRCA2 DNA repair associated	Homo sapiens	56-61
20485165-3	2010	RECENT FINDINGS: Preclinical recognition that BRCA1 and BRCA2-associated tumours are very sensitive to inhibition of poly-ADP ribose polymerase (PARP), a key molecule in DNA repair, led to ovarian cancer patients with germline BRCA1 and BRCA2 mutations being treated with the PARP inhibitor olaparib (AZD2281, KU-0059436; KuDOS/Astra-Zeneca).	olaparib	301-308	BRCA2 DNA repair associated	Homo sapiens	237-242
20631063-3	2010	In a screen for novel drugs that selectively kill BRCA2-defective cells, we identified 6-thioguanine (6TG), which induces DNA double-strand breaks (DSB) that are repaired by HR.	Thioguanine	87-100	BRCA2 DNA repair associated	Homo sapiens	50-55
20631063-3	2010	In a screen for novel drugs that selectively kill BRCA2-defective cells, we identified 6-thioguanine (6TG), which induces DNA double-strand breaks (DSB) that are repaired by HR.	Thioguanine	102-105	BRCA2 DNA repair associated	Homo sapiens	50-55
20631063-7	2010	We also show that 6TG could kill cells and tumors that have gained resistance to PARP inhibitors or cisplatin through genetic reversion of the BRCA2 gene.	Thioguanine	18-21	BRCA2 DNA repair associated	Homo sapiens	143-148
20631063-10	2010	We show that BRCA2 is also required for survival from mismatch repair-independent lesions formed by 6TG, which do not include DSBs.	1,2-di-(4-sulfamidophenyl)-4-butylpyrazolidine-3,5-dione	126-130	BRCA2 DNA repair associated	Homo sapiens	13-18
20609468-0	2010	Oral poly(ADP-ribose) polymerase inhibitor olaparib in patients with BRCA1 or BRCA2 mutations and recurrent ovarian cancer: a proof-of-concept trial.	olaparib	43-51	BRCA2 DNA repair associated	Homo sapiens	78-83
20609468-2	2010	We aimed to assess the efficacy and safety of olaparib for treatment of advanced ovarian cancer in patients with BRCA1 or BRCA2 mutations.	olaparib	46-54	BRCA2 DNA repair associated	Homo sapiens	122-127
20609467-0	2010	Oral poly(ADP-ribose) polymerase inhibitor olaparib in patients with BRCA1 or BRCA2 mutations and advanced breast cancer: a proof-of-concept trial.	olaparib	43-51	BRCA2 DNA repair associated	Homo sapiens	78-83
20450923-0	2010	Several tetratricopeptide repeat (TPR) motifs of FANCG are required for assembly of the BRCA2/D1-D2-G-X3 complex, FANCD2 monoubiquitylation and phleomycin resistance.	Phleomycins	144-154	BRCA2 DNA repair associated	Homo sapiens	88-93
20033769-3	2010	BRCA1 and BRCA2 genes were screened for germline mutations in 131 patients with a family history of breast and/or ovarian cancer who had undergone BCT and radiotherapy.	Bicarbonates	147-150	BRCA2 DNA repair associated	Homo sapiens	10-15
20421506-3	2010	We found that the transactivation domain of p53 made specific interactions with the C-terminal oligonucleotide/oligosaccharide-binding-fold domains of BRCA2 (BRCA2(CTD)).	Oligonucleotides	95-110	BRCA2 DNA repair associated	Homo sapiens	151-156
20421506-3	2010	We found that the transactivation domain of p53 made specific interactions with the C-terminal oligonucleotide/oligosaccharide-binding-fold domains of BRCA2 (BRCA2(CTD)).	Oligosaccharides	111-126	BRCA2 DNA repair associated	Homo sapiens	151-156
20442529-0	2010	Mitomycin-induced interstitial pneumonitis in a patient with BRCA2 associated metastatic pancreatic carcinoma.	Mitomycin	0-9	BRCA2 DNA repair associated	Homo sapiens	61-66
20127002-8	2010	After genistein or daidzein treatments, BRCA1 was found to be up-regulated when knocked down with BRCA2-siRNA MCF-7 and BRCA2 was found to be up-regulated when knocked down with BRCA2-siRNA MDA-MB 231 cells.	Genistein	6-15	BRCA2 DNA repair associated	Homo sapiens	98-103
20127002-8	2010	After genistein or daidzein treatments, BRCA1 was found to be up-regulated when knocked down with BRCA2-siRNA MCF-7 and BRCA2 was found to be up-regulated when knocked down with BRCA2-siRNA MDA-MB 231 cells.	Genistein	6-15	BRCA2 DNA repair associated	Homo sapiens	120-125
20127002-8	2010	After genistein or daidzein treatments, BRCA1 was found to be up-regulated when knocked down with BRCA2-siRNA MCF-7 and BRCA2 was found to be up-regulated when knocked down with BRCA2-siRNA MDA-MB 231 cells.	Genistein	6-15	BRCA2 DNA repair associated	Homo sapiens	120-125
20127002-8	2010	After genistein or daidzein treatments, BRCA1 was found to be up-regulated when knocked down with BRCA2-siRNA MCF-7 and BRCA2 was found to be up-regulated when knocked down with BRCA2-siRNA MDA-MB 231 cells.	daidzein	19-27	BRCA2 DNA repair associated	Homo sapiens	98-103
20127002-8	2010	After genistein or daidzein treatments, BRCA1 was found to be up-regulated when knocked down with BRCA2-siRNA MCF-7 and BRCA2 was found to be up-regulated when knocked down with BRCA2-siRNA MDA-MB 231 cells.	daidzein	19-27	BRCA2 DNA repair associated	Homo sapiens	120-125
20127002-8	2010	After genistein or daidzein treatments, BRCA1 was found to be up-regulated when knocked down with BRCA2-siRNA MCF-7 and BRCA2 was found to be up-regulated when knocked down with BRCA2-siRNA MDA-MB 231 cells.	daidzein	19-27	BRCA2 DNA repair associated	Homo sapiens	120-125
20174566-3	2010	To identify predictors of pathogenic mutation status in familial breast cancer patients, we explored the use of gene expression arrays to assess the effect of two DNA-damaging agents (irradiation and mitomycin C) on cellular response in relation to BRCA1 and BRCA2 mutation status.	Mitomycin	200-211	BRCA2 DNA repair associated	Homo sapiens	259-264
20174566-5	2010	Using an RNA-pooling strategy, we found that treating LCLs with 1.2 microM mitomycin C and measuring the gene expression profiles 1 hour post-treatment had the greatest potential to discriminate BRCA1, BRCA2, and BRCAX mutation status.	Mitomycin	75-86	BRCA2 DNA repair associated	Homo sapiens	202-207
19861535-0	2009	Fanconi anemia complementation group FANCD2 protein serine 331 phosphorylation is important for fanconi anemia pathway function and BRCA2 interaction.	Serine	52-58	BRCA2 DNA repair associated	Homo sapiens	132-137
20028873-0	2010	Potentiation of temozolomide cytotoxicity by inhibition of DNA polymerase beta is accentuated by BRCA2 mutation.	Temozolomide	16-28	BRCA2 DNA repair associated	Homo sapiens	97-102
20028873-5	2010	Cytotoxicity assays based on colony formation revealed that LCA exhibits synergism with the alkylating agent temozolomide, which engages BER through DNA methylation, and that the degree of synergism is increased in cells lacking functional BRCA2.	Lithocholic Acid	60-63	BRCA2 DNA repair associated	Homo sapiens	240-245
20028873-6	2010	BRCA2-deficient cells also showed heightened susceptibility to both LCA and temozolomide individually.	Lithocholic Acid	68-71	BRCA2 DNA repair associated	Homo sapiens	0-5
20028873-6	2010	BRCA2-deficient cells also showed heightened susceptibility to both LCA and temozolomide individually.	Temozolomide	76-88	BRCA2 DNA repair associated	Homo sapiens	0-5
19959799-0	2010	Detection of BRCA1 and BRCA2 Ashkenazi Jewish founder mutations in formalin-fixed paraffin-embedded tissues using conventional PCR and heteroduplex/amplicon size differences.	Formaldehyde	67-75	BRCA2 DNA repair associated	Homo sapiens	23-28
19959799-0	2010	Detection of BRCA1 and BRCA2 Ashkenazi Jewish founder mutations in formalin-fixed paraffin-embedded tissues using conventional PCR and heteroduplex/amplicon size differences.	Paraffin	82-90	BRCA2 DNA repair associated	Homo sapiens	23-28
19578754-0	2009	CBP-mediated post-translational N-glycosylation of BRCA2.	Nitrogen	32-33	BRCA2 DNA repair associated	Homo sapiens	51-56
19654294-5	2009	PEO1 was BRCA2 deficient and sensitive to cisplatin and a poly(ADP-ribose) polymerase inhibitor, AG14361, whereas PEO4 was resistant.	Cisplatin	42-51	BRCA2 DNA repair associated	Homo sapiens	9-14
19654294-5	2009	PEO1 was BRCA2 deficient and sensitive to cisplatin and a poly(ADP-ribose) polymerase inhibitor, AG14361, whereas PEO4 was resistant.	1-(4-dimethylaminomethylphenyl)-8,9-dihydro-7H-2,7,9a-benzo(cd)azulen-6-one	97-104	BRCA2 DNA repair associated	Homo sapiens	9-14
19654294-7	2009	In vitro cisplatin/AG14361 selection of PEO1 led to restoration of BRCA2 due to another secondary BRCA2 mutation.	Cisplatin	9-18	BRCA2 DNA repair associated	Homo sapiens	67-72
19654294-7	2009	In vitro cisplatin/AG14361 selection of PEO1 led to restoration of BRCA2 due to another secondary BRCA2 mutation.	Cisplatin	9-18	BRCA2 DNA repair associated	Homo sapiens	98-103
19654294-7	2009	In vitro cisplatin/AG14361 selection of PEO1 led to restoration of BRCA2 due to another secondary BRCA2 mutation.	1-(4-dimethylaminomethylphenyl)-8,9-dihydro-7H-2,7,9a-benzo(cd)azulen-6-one	19-26	BRCA2 DNA repair associated	Homo sapiens	67-72
19654294-7	2009	In vitro cisplatin/AG14361 selection of PEO1 led to restoration of BRCA2 due to another secondary BRCA2 mutation.	1-(4-dimethylaminomethylphenyl)-8,9-dihydro-7H-2,7,9a-benzo(cd)azulen-6-one	19-26	BRCA2 DNA repair associated	Homo sapiens	98-103
19654294-8	2009	BRCA2 depletion sensitized BRCA2-restored PEO1 clones and PEO4 to cisplatin/AG14361.	Cisplatin	66-75	BRCA2 DNA repair associated	Homo sapiens	0-5
19654294-8	2009	BRCA2 depletion sensitized BRCA2-restored PEO1 clones and PEO4 to cisplatin/AG14361.	Cisplatin	66-75	BRCA2 DNA repair associated	Homo sapiens	27-32
19564533-8	2009	CONCLUSION: BRCA2-associated breast cancer is more sensitive to standard first-line chemotherapy for metastatic breast cancer in comparison with sporadic breast cancer, especially to anthracyclines.	Anthracyclines	183-197	BRCA2 DNA repair associated	Homo sapiens	12-17
19647219-2	2009	A recent report in the New England Journal of Medicine on the early clinical evaluation of Olaparib in cancers lacking the BRCA1 or BRCA2 genes exemplifies this promising new trend.	olaparib	91-99	BRCA2 DNA repair associated	Homo sapiens	132-137
19433978-0	2009	Prolonged survival in a patient with BRCA2 associated metastatic pancreatic cancer after exposure to camptothecin: a case report and review of literature.	Camptothecin	101-113	BRCA2 DNA repair associated	Homo sapiens	37-42
19433978-3	2009	There is evidence of in vivo therapeutic response to the cross-linking agents; such as mitomycin C (MMC) in BRCA2 mutated pancreatic cell lines.	Mitomycin	87-98	BRCA2 DNA repair associated	Homo sapiens	108-113
19433978-3	2009	There is evidence of in vivo therapeutic response to the cross-linking agents; such as mitomycin C (MMC) in BRCA2 mutated pancreatic cell lines.	Mitomycin	100-103	BRCA2 DNA repair associated	Homo sapiens	108-113
19433978-17	2009	Our case is the first clinical piece of evidence that demonstrates an increased sensitivity to camptothecin-11 and a reduced topoisomerase I relaxation activity in BRCA2 associated pancreatic cancer.	Irinotecan	95-110	BRCA2 DNA repair associated	Homo sapiens	164-169
19574032-0	2009	Dramatic response to platinum in a patient with cancer with a germline BRCA2 mutation.	Platinum	21-29	BRCA2 DNA repair associated	Homo sapiens	71-76
19574032-1	2009	We present a case of dramatic response of poor prognosis cancer in a lady with a germline mutation in the BRCA2 gene who was exposed to platinum containing chemotherapy.	Platinum	136-144	BRCA2 DNA repair associated	Homo sapiens	106-111
19578754-4	2009	Digestion with peptide N-glycosidase F indicates that the glycosylation of BRCA2 is N-linked.	Nitrogen	23-24	BRCA2 DNA repair associated	Homo sapiens	75-80
19602291-2	2009	Restoration of BRCA1 and BRCA2 mediates resistance to platinum chemotherapy in recurrent BRCA1 and BRCA2 mutated hereditary ovarian carcinomas.	Platinum	54-62	BRCA2 DNA repair associated	Homo sapiens	25-30
19671736-6	2009	17-AAG down-regulated Rad51 and BRCA2 protein levels, abrogated induction of Rad51 foci by radiation, and inhibited HR measured by the I-Sce1 assay.	tanespimycin	0-6	BRCA2 DNA repair associated	Homo sapiens	32-37
19553191-0	2009	BRCA2-dependent homologous recombination is required for repair of Arsenite-induced replication lesions in mammalian cells.	arsenite	67-75	BRCA2 DNA repair associated	Homo sapiens	0-5
19572662-3	2009	The reduction of NAD+ and FAD is complimented by an enthalpy transfer between organic functional components (aromatic ring, amide and olefinic functionalities), yet the sum of the overall energy values (the total system) remains nearly constant, irrespective of which direction the redox reaction proceeds.	Amides	124-129	BRCA2 DNA repair associated	Homo sapiens	26-29
19572662-3	2009	The reduction of NAD+ and FAD is complimented by an enthalpy transfer between organic functional components (aromatic ring, amide and olefinic functionalities), yet the sum of the overall energy values (the total system) remains nearly constant, irrespective of which direction the redox reaction proceeds.	olefinic	134-142	BRCA2 DNA repair associated	Homo sapiens	26-29
19602291-2	2009	Restoration of BRCA1 and BRCA2 mediates resistance to platinum chemotherapy in recurrent BRCA1 and BRCA2 mutated hereditary ovarian carcinomas.	Platinum	54-62	BRCA2 DNA repair associated	Homo sapiens	99-104
19553641-13	2009	CONCLUSIONS: Olaparib has few of the adverse effects of conventional chemotherapy, inhibits PARP, and has antitumor activity in cancer associated with the BRCA1 or BRCA2 mutation.	olaparib	13-21	BRCA2 DNA repair associated	Homo sapiens	164-169
19602291-13	2009	Recurrent ovarian carcinomas commonly have increased BRCA1 and/or BRCA2 protein expression post chemotherapy exposure which could mediate resistance to platinum based therapies.	Platinum	152-160	BRCA2 DNA repair associated	Homo sapiens	66-71
19584259-10	2009	Resistance to mitomycin C and the repair of DNA double-strand breaks by homologous recombination require the interaction of PALB2 with both BRCA1 and BRCA2.	Mitomycin	14-25	BRCA2 DNA repair associated	Homo sapiens	150-155
19589159-16	2009	The importance of these findings lies in the potential benefit from targeted therapy, through the use of agents leading to DNA double-strand breaks such as PARP inhibitors (olaparib) and cisplatin, for a much larger group of patients than the few BRCA1 and BRCA2 germline mutation carriers.	olaparib	173-181	BRCA2 DNA repair associated	Homo sapiens	257-262
18553220-5	2009	Carriers of the BRCA2 rs1799944 variant (991 Asp) were found to have an increased risk of breast cancer (OR = 1.41, 95% CI 1.08-1.83, P = 0.01) with P (trend) = 0.0076.	Aspartic Acid	45-48	BRCA2 DNA repair associated	Homo sapiens	16-21
19016568-5	2009	We found that a rapid increase in BRCA2 S3291 phosphorylation occurs following 17-beta-oestradiol (E2) treatment.	Estradiol	79-97	BRCA2 DNA repair associated	Homo sapiens	34-39
19016568-5	2009	We found that a rapid increase in BRCA2 S3291 phosphorylation occurs following 17-beta-oestradiol (E2) treatment.	Estradiol	99-101	BRCA2 DNA repair associated	Homo sapiens	34-39
19016568-6	2009	This increase seen in BRCA2 total and phospho-S3291 protein levels was found to be unaffected with cycloheximide pre-treatment, but decreased following tamoxifen, ICI 182,780 or roscovitine treatment.	Cycloheximide	99-112	BRCA2 DNA repair associated	Homo sapiens	22-27
19016568-6	2009	This increase seen in BRCA2 total and phospho-S3291 protein levels was found to be unaffected with cycloheximide pre-treatment, but decreased following tamoxifen, ICI 182,780 or roscovitine treatment.	Tamoxifen	152-161	BRCA2 DNA repair associated	Homo sapiens	22-27
19016568-6	2009	This increase seen in BRCA2 total and phospho-S3291 protein levels was found to be unaffected with cycloheximide pre-treatment, but decreased following tamoxifen, ICI 182,780 or roscovitine treatment.	Roscovitine	178-189	BRCA2 DNA repair associated	Homo sapiens	22-27
19324993-0	2009	A rapid and reliable test for BRCA1 and BRCA2 founder mutation analysis in paraffin tissue using pyrosequencing.	Paraffin	75-83	BRCA2 DNA repair associated	Homo sapiens	40-45
19074863-4	2008	Furthermore, a similar mechanism seems to be associated with carboplatin resistance in some BRCA2 mutation carriers with ovarian cancer.	Carboplatin	61-72	BRCA2 DNA repair associated	Homo sapiens	92-97
18840549-0	2009	Brca2/Xrcc2 dependent HR, but not NHEJ, is required for protection against O(6)-methylguanine triggered apoptosis, DSBs and chromosomal aberrations by a process leading to SCEs.	O-(6)-methylguanine	75-93	BRCA2 DNA repair associated	Homo sapiens	0-5
18990703-9	2008	Inhibition of Parp-1 activity (by 3-AB) reduced histone 3 lysine 9 acetylation and blocked Parp-1 binding to the BRCA2 promoter.	Lysine	58-64	BRCA2 DNA repair associated	Homo sapiens	113-118
18678871-5	2008	In addition, based on a structural model of PuO(Rh) that was built using the crystal structure of human monoamine oxidase B (MAO-B), we constructed an active mutant enzyme, PuO(Rh) A394C, that contains covalently bound FAD.	puo	44-47	BRCA2 DNA repair associated	Homo sapiens	219-222
19047179-3	2008	Here, we describe the involvement of BRCA2 in O6-alkylguanine DNA alkyltransferase (AGT)-mediated repair of O6-methylguanine adducts.	O-(6)-methylguanine	108-124	BRCA2 DNA repair associated	Homo sapiens	37-42
19047179-6	2008	We show that O6-benzylguanine (O6BG), a nontoxic inhibitor of AGT, can also induce BRCA2 degradation.	O(6)-benzylguanine	13-29	BRCA2 DNA repair associated	Homo sapiens	83-88
19047179-6	2008	We show that O6-benzylguanine (O6BG), a nontoxic inhibitor of AGT, can also induce BRCA2 degradation.	O(6)-benzylguanine	31-35	BRCA2 DNA repair associated	Homo sapiens	83-88
18951438-7	2008	In this article we discuss how LSDBs can accomplish these goals, using existing databases for BRCA1, BRCA2, MSH2, MLH1, TP53, and CDKN2A to illustrate the progress and remaining challenges in this field.	lsdbs	31-36	BRCA2 DNA repair associated	Homo sapiens	101-106
18951447-8	2008	Here we describe the advantages and disadvantages of using the tumor characteristics of patients carrying germline variants of uncertain significance (VUS) in BRCA1, BRCA2, or in one of the mismatch repair (MMR) genes, MLH1, MSH2, or MSH6, to infer pathogenicity.	3-[(3~{a}~{S},4~{S},6~{a}~{R})-4-carboxy-2,3,4,5,6,6~{a}-hexahydro-1~{H}-pyrrolo[2,3-c]pyrrol-3~{a}-yl]propyl-$l^{3}-oxidanyl-bis(oxidanyl)boranuide	151-154	BRCA2 DNA repair associated	Homo sapiens	166-171
18678871-3	2008	Here we show that this low FAD/protein ratio is the result of tight binding of ADP, thereby competing with FAD binding.	Adenosine Diphosphate	79-82	BRCA2 DNA repair associated	Homo sapiens	27-30
18678871-5	2008	In addition, based on a structural model of PuO(Rh) that was built using the crystal structure of human monoamine oxidase B (MAO-B), we constructed an active mutant enzyme, PuO(Rh) A394C, that contains covalently bound FAD.	Rhodium	48-50	BRCA2 DNA repair associated	Homo sapiens	219-222
18678871-3	2008	Here we show that this low FAD/protein ratio is the result of tight binding of ADP, thereby competing with FAD binding.	Adenosine Diphosphate	79-82	BRCA2 DNA repair associated	Homo sapiens	107-110
18678871-6	2008	These findings show that the covalent FAD-protein linkage can be formed autocatalytically and hint to a new-found rationale for covalent flavinylation: covalent flavinylation may have evolved to prevent binding of ADP or related cellular compounds, which would prohibit formation of flavinylated and functional enzyme.	Adenosine Diphosphate	214-217	BRCA2 DNA repair associated	Homo sapiens	38-41
18426226-4	2008	Phenylethylhydrazine stoichiometrically reduces the covalent FAD moieties of MAO A and of MAO B.	Phenelzine	0-20	BRCA2 DNA repair associated	Homo sapiens	61-64
18593900-5	2008	We found that the null states BRCA2(Deltaex11/Deltaex11) and BRCA2(Deltaex11/Y3308X) were deleterious as assessed by a loss of RAD51 focus formation on genotoxic damage and by acquisition of toxic hypersensitivity to mitomycin C and etoposide, whereas BRCA2(Deltaex11/Y3308Y), BRCA2(Deltaex11/P3292L), and BRCA2(Deltaex11/P3280H) had wild-type function.	Mitomycin	217-228	BRCA2 DNA repair associated	Homo sapiens	30-35
18593900-5	2008	We found that the null states BRCA2(Deltaex11/Deltaex11) and BRCA2(Deltaex11/Y3308X) were deleterious as assessed by a loss of RAD51 focus formation on genotoxic damage and by acquisition of toxic hypersensitivity to mitomycin C and etoposide, whereas BRCA2(Deltaex11/Y3308Y), BRCA2(Deltaex11/P3292L), and BRCA2(Deltaex11/P3280H) had wild-type function.	Mitomycin	217-228	BRCA2 DNA repair associated	Homo sapiens	61-66
18593900-5	2008	We found that the null states BRCA2(Deltaex11/Deltaex11) and BRCA2(Deltaex11/Y3308X) were deleterious as assessed by a loss of RAD51 focus formation on genotoxic damage and by acquisition of toxic hypersensitivity to mitomycin C and etoposide, whereas BRCA2(Deltaex11/Y3308Y), BRCA2(Deltaex11/P3292L), and BRCA2(Deltaex11/P3280H) had wild-type function.	Mitomycin	217-228	BRCA2 DNA repair associated	Homo sapiens	61-66
18593900-5	2008	We found that the null states BRCA2(Deltaex11/Deltaex11) and BRCA2(Deltaex11/Y3308X) were deleterious as assessed by a loss of RAD51 focus formation on genotoxic damage and by acquisition of toxic hypersensitivity to mitomycin C and etoposide, whereas BRCA2(Deltaex11/Y3308Y), BRCA2(Deltaex11/P3292L), and BRCA2(Deltaex11/P3280H) had wild-type function.	Mitomycin	217-228	BRCA2 DNA repair associated	Homo sapiens	61-66
18593900-5	2008	We found that the null states BRCA2(Deltaex11/Deltaex11) and BRCA2(Deltaex11/Y3308X) were deleterious as assessed by a loss of RAD51 focus formation on genotoxic damage and by acquisition of toxic hypersensitivity to mitomycin C and etoposide, whereas BRCA2(Deltaex11/Y3308Y), BRCA2(Deltaex11/P3292L), and BRCA2(Deltaex11/P3280H) had wild-type function.	Mitomycin	217-228	BRCA2 DNA repair associated	Homo sapiens	61-66
18593900-5	2008	We found that the null states BRCA2(Deltaex11/Deltaex11) and BRCA2(Deltaex11/Y3308X) were deleterious as assessed by a loss of RAD51 focus formation on genotoxic damage and by acquisition of toxic hypersensitivity to mitomycin C and etoposide, whereas BRCA2(Deltaex11/Y3308Y), BRCA2(Deltaex11/P3292L), and BRCA2(Deltaex11/P3280H) had wild-type function.	Etoposide	233-242	BRCA2 DNA repair associated	Homo sapiens	30-35
18593900-5	2008	We found that the null states BRCA2(Deltaex11/Deltaex11) and BRCA2(Deltaex11/Y3308X) were deleterious as assessed by a loss of RAD51 focus formation on genotoxic damage and by acquisition of toxic hypersensitivity to mitomycin C and etoposide, whereas BRCA2(Deltaex11/Y3308Y), BRCA2(Deltaex11/P3292L), and BRCA2(Deltaex11/P3280H) had wild-type function.	Etoposide	233-242	BRCA2 DNA repair associated	Homo sapiens	61-66
18593900-5	2008	We found that the null states BRCA2(Deltaex11/Deltaex11) and BRCA2(Deltaex11/Y3308X) were deleterious as assessed by a loss of RAD51 focus formation on genotoxic damage and by acquisition of toxic hypersensitivity to mitomycin C and etoposide, whereas BRCA2(Deltaex11/Y3308Y), BRCA2(Deltaex11/P3292L), and BRCA2(Deltaex11/P3280H) had wild-type function.	Etoposide	233-242	BRCA2 DNA repair associated	Homo sapiens	61-66
18593900-5	2008	We found that the null states BRCA2(Deltaex11/Deltaex11) and BRCA2(Deltaex11/Y3308X) were deleterious as assessed by a loss of RAD51 focus formation on genotoxic damage and by acquisition of toxic hypersensitivity to mitomycin C and etoposide, whereas BRCA2(Deltaex11/Y3308Y), BRCA2(Deltaex11/P3292L), and BRCA2(Deltaex11/P3280H) had wild-type function.	Etoposide	233-242	BRCA2 DNA repair associated	Homo sapiens	61-66
18593900-5	2008	We found that the null states BRCA2(Deltaex11/Deltaex11) and BRCA2(Deltaex11/Y3308X) were deleterious as assessed by a loss of RAD51 focus formation on genotoxic damage and by acquisition of toxic hypersensitivity to mitomycin C and etoposide, whereas BRCA2(Deltaex11/Y3308Y), BRCA2(Deltaex11/P3292L), and BRCA2(Deltaex11/P3280H) had wild-type function.	Etoposide	233-242	BRCA2 DNA repair associated	Homo sapiens	61-66
18593900-6	2008	A proposed phosphorylation site at codon 3291 affecting function was confirmed by substitution of an acidic residue (glutamate, BRCA2(Deltaex11/S3291E)) for the native serine, but in contrast to a prior report, phosphorylation was dispensable (alanine, BRCA2(Deltaex11/S3291A)) for BRCA2-governed cellular phenotypes.	Glutamic Acid	117-126	BRCA2 DNA repair associated	Homo sapiens	128-133
18593900-6	2008	A proposed phosphorylation site at codon 3291 affecting function was confirmed by substitution of an acidic residue (glutamate, BRCA2(Deltaex11/S3291E)) for the native serine, but in contrast to a prior report, phosphorylation was dispensable (alanine, BRCA2(Deltaex11/S3291A)) for BRCA2-governed cellular phenotypes.	Glutamic Acid	117-126	BRCA2 DNA repair associated	Homo sapiens	253-258
18593900-6	2008	A proposed phosphorylation site at codon 3291 affecting function was confirmed by substitution of an acidic residue (glutamate, BRCA2(Deltaex11/S3291E)) for the native serine, but in contrast to a prior report, phosphorylation was dispensable (alanine, BRCA2(Deltaex11/S3291A)) for BRCA2-governed cellular phenotypes.	Glutamic Acid	117-126	BRCA2 DNA repair associated	Homo sapiens	253-258
18593900-6	2008	A proposed phosphorylation site at codon 3291 affecting function was confirmed by substitution of an acidic residue (glutamate, BRCA2(Deltaex11/S3291E)) for the native serine, but in contrast to a prior report, phosphorylation was dispensable (alanine, BRCA2(Deltaex11/S3291A)) for BRCA2-governed cellular phenotypes.	Serine	168-174	BRCA2 DNA repair associated	Homo sapiens	128-133
18593900-6	2008	A proposed phosphorylation site at codon 3291 affecting function was confirmed by substitution of an acidic residue (glutamate, BRCA2(Deltaex11/S3291E)) for the native serine, but in contrast to a prior report, phosphorylation was dispensable (alanine, BRCA2(Deltaex11/S3291A)) for BRCA2-governed cellular phenotypes.	Serine	168-174	BRCA2 DNA repair associated	Homo sapiens	253-258
18593900-6	2008	A proposed phosphorylation site at codon 3291 affecting function was confirmed by substitution of an acidic residue (glutamate, BRCA2(Deltaex11/S3291E)) for the native serine, but in contrast to a prior report, phosphorylation was dispensable (alanine, BRCA2(Deltaex11/S3291A)) for BRCA2-governed cellular phenotypes.	Serine	168-174	BRCA2 DNA repair associated	Homo sapiens	253-258
18593900-6	2008	A proposed phosphorylation site at codon 3291 affecting function was confirmed by substitution of an acidic residue (glutamate, BRCA2(Deltaex11/S3291E)) for the native serine, but in contrast to a prior report, phosphorylation was dispensable (alanine, BRCA2(Deltaex11/S3291A)) for BRCA2-governed cellular phenotypes.	Alanine	244-251	BRCA2 DNA repair associated	Homo sapiens	128-133
18593900-6	2008	A proposed phosphorylation site at codon 3291 affecting function was confirmed by substitution of an acidic residue (glutamate, BRCA2(Deltaex11/S3291E)) for the native serine, but in contrast to a prior report, phosphorylation was dispensable (alanine, BRCA2(Deltaex11/S3291A)) for BRCA2-governed cellular phenotypes.	Alanine	244-251	BRCA2 DNA repair associated	Homo sapiens	253-258
18593900-6	2008	A proposed phosphorylation site at codon 3291 affecting function was confirmed by substitution of an acidic residue (glutamate, BRCA2(Deltaex11/S3291E)) for the native serine, but in contrast to a prior report, phosphorylation was dispensable (alanine, BRCA2(Deltaex11/S3291A)) for BRCA2-governed cellular phenotypes.	Alanine	244-251	BRCA2 DNA repair associated	Homo sapiens	253-258
18212739-6	2008	We also show that phosphorylation of FANCG serine 7 is required for its co-precipitation with BRCA2, XRCC3 and FANCD2, as well as the direct interaction of BRCA2-FANCD2.	Serine	43-49	BRCA2 DNA repair associated	Homo sapiens	94-99
18212739-6	2008	We also show that phosphorylation of FANCG serine 7 is required for its co-precipitation with BRCA2, XRCC3 and FANCD2, as well as the direct interaction of BRCA2-FANCD2.	Serine	43-49	BRCA2 DNA repair associated	Homo sapiens	156-161
18212739-7	2008	These results argue that FANCG has a role independent of the FA core complex, and we propose that phosphorylation of serine 7 is the signalling event required for forming a discrete complex comprising FANCD1/BRCA2-FANCD2-FANCG-XRCC3 (D1-D2-G-X3).	serine 7	117-125	BRCA2 DNA repair associated	Homo sapiens	201-207
18212739-7	2008	These results argue that FANCG has a role independent of the FA core complex, and we propose that phosphorylation of serine 7 is the signalling event required for forming a discrete complex comprising FANCD1/BRCA2-FANCD2-FANCG-XRCC3 (D1-D2-G-X3).	serine 7	117-125	BRCA2 DNA repair associated	Homo sapiens	208-213
18842997-0	2008	Methionine-dependence phenotype in the de novo pathway in BRCA1 and BRCA2 mutation carriers with and without breast cancer.	Methionine	0-10	BRCA2 DNA repair associated	Homo sapiens	68-73
18842997-8	2008	The results of this study support the hypothesis that defects in methionine metabolism may be associated with breast cancer risk in BRCA carriers.	Methionine	65-75	BRCA2 DNA repair associated	Homo sapiens	132-136
18720553-7	2008	Three recent studies demonstrated that acquired resistance to platinum analogues or PARP inhibitors in tumors carrying frame-shift BRCA1/2 mutations came from restored BRCA1/2 expression and HR function due to secondary intragenic mutations that corrected the open reading frames of mutated BRCA1/2.	Platinum	62-70	BRCA2 DNA repair associated	Homo sapiens	131-138
18720553-7	2008	Three recent studies demonstrated that acquired resistance to platinum analogues or PARP inhibitors in tumors carrying frame-shift BRCA1/2 mutations came from restored BRCA1/2 expression and HR function due to secondary intragenic mutations that corrected the open reading frames of mutated BRCA1/2.	Platinum	62-70	BRCA2 DNA repair associated	Homo sapiens	168-175
18720553-7	2008	Three recent studies demonstrated that acquired resistance to platinum analogues or PARP inhibitors in tumors carrying frame-shift BRCA1/2 mutations came from restored BRCA1/2 expression and HR function due to secondary intragenic mutations that corrected the open reading frames of mutated BRCA1/2.	Platinum	62-70	BRCA2 DNA repair associated	Homo sapiens	168-175
18429825-0	2008	Dinucleotide repeat polymorphisms of RAD51, BRCA1, BRCA2 gene regions in breast cancer.	Dinucleoside Phosphates	0-12	BRCA2 DNA repair associated	Homo sapiens	51-56
18059333-6	2008	Mutation of a leucine residue in the NES1 motif to alanine (L1384A) resulted in both cytoplasmic and nuclear localization of the GFP-NES1 fusion protein and a nuclear accumulation of ectopic full-length BRCA2-FLAG.	Leucine	14-21	BRCA2 DNA repair associated	Homo sapiens	203-208
18059333-6	2008	Mutation of a leucine residue in the NES1 motif to alanine (L1384A) resulted in both cytoplasmic and nuclear localization of the GFP-NES1 fusion protein and a nuclear accumulation of ectopic full-length BRCA2-FLAG.	Alanine	51-58	BRCA2 DNA repair associated	Homo sapiens	203-208
18059333-7	2008	Moreover, treatment of cells with leptomycin B decreased centrosomal localization of BRCA2.	leptomycin B	34-46	BRCA2 DNA repair associated	Homo sapiens	85-90
18469443-0	2008	Response to a third-line mitomycin C (MMC)-based chemotherapy in a patient with metastatic pancreatic adenocarcinoma carrying germline BRCA2 mutation.	Mitomycin	25-36	BRCA2 DNA repair associated	Homo sapiens	135-140
18469443-0	2008	Response to a third-line mitomycin C (MMC)-based chemotherapy in a patient with metastatic pancreatic adenocarcinoma carrying germline BRCA2 mutation.	Mitomycin	38-41	BRCA2 DNA repair associated	Homo sapiens	135-140
18469443-6	2008	CONCLUSION: We feel that this is of interest because of preclinical reports of increased sensitivity of pancreatic cells carrying BRCA2 mutations to DNA-intercalating agents such as mitomycin C.	Mitomycin	182-193	BRCA2 DNA repair associated	Homo sapiens	130-135
18196574-13	2008	However, only the minority of women with a BRCA1 or BRCA2 mutation opt for prophylactic mastectomy or take tamoxifen for the prevention of hereditary breast cancer.	Tamoxifen	107-116	BRCA2 DNA repair associated	Homo sapiens	52-57
18429825-4	2008	Dinucleotide polymorphism repeats in the 15q14-21, 17q21 and 13q12-13 regions, where the RAD51, BRCA1 and BRCA2 genes are located, respectively, have been evaluated.	Dinucleoside Phosphates	0-12	BRCA2 DNA repair associated	Homo sapiens	106-111
18429825-8	2008	The results indicate that dinucleotide CA repeat polymorphism at RAD51 and BRCA2 gene regions might be associated with genetic susceptibility to breast cancer.	dinucleotide ca	26-41	BRCA2 DNA repair associated	Homo sapiens	75-80
18413725-1	2008	Although ovarian carcinomas with mutated BRCA1 or BRCA2 are sensitive to platinum compounds, such carcinomas eventually develop platinum resistance.	Platinum	73-81	BRCA2 DNA repair associated	Homo sapiens	50-55
18413725-2	2008	Previously, we showed that acquired resistance to cisplatin in BRCA2-mutated tumors can be mediated by secondary intragenic mutations in BRCA2 that restore the wild-type BRCA2 reading frame.	Cisplatin	50-59	BRCA2 DNA repair associated	Homo sapiens	63-68
18413725-2	2008	Previously, we showed that acquired resistance to cisplatin in BRCA2-mutated tumors can be mediated by secondary intragenic mutations in BRCA2 that restore the wild-type BRCA2 reading frame.	Cisplatin	50-59	BRCA2 DNA repair associated	Homo sapiens	137-142
18413725-2	2008	Previously, we showed that acquired resistance to cisplatin in BRCA2-mutated tumors can be mediated by secondary intragenic mutations in BRCA2 that restore the wild-type BRCA2 reading frame.	Cisplatin	50-59	BRCA2 DNA repair associated	Homo sapiens	137-142
18264087-0	2008	Secondary mutations as a mechanism of cisplatin resistance in BRCA2-mutated cancers.	Cisplatin	38-47	BRCA2 DNA repair associated	Homo sapiens	62-67
18167127-5	2008	In BRCA2-overexpressing PC-3 cells, transient transfection with a constitutively active PI3-kinase mutant or treatment with the MAPK/ERK inhibitor PD98059 rescued MMP-9 levels and restored the migratory and invasive capabilities.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	147-154	BRCA2 DNA repair associated	Homo sapiens	3-8
18264087-1	2008	Ovarian carcinomas with mutations in the tumour suppressor BRCA2 are particularly sensitive to platinum compounds.	Platinum	95-103	BRCA2 DNA repair associated	Homo sapiens	59-64
18264087-8	2008	Finally, we evaluated recurrent cancers from patients whose primary BRCA2-mutated ovarian carcinomas were treated with cisplatin.	Cisplatin	119-128	BRCA2 DNA repair associated	Homo sapiens	68-73
18264087-9	2008	The recurrent tumour that acquired cisplatin resistance had undergone reversion of its BRCA2 mutation.	Cisplatin	35-44	BRCA2 DNA repair associated	Homo sapiens	87-92
18264087-4	2008	Here we show that acquired resistance to cisplatin can be mediated by secondary intragenic mutations in BRCA2 that restore the wild-type BRCA2 reading frame.	Cisplatin	41-50	BRCA2 DNA repair associated	Homo sapiens	104-109
18264087-10	2008	Our results suggest that secondary mutations that restore the wild-type BRCA2 reading frame may be a major clinical mediator of acquired resistance to platinum-based chemotherapy.	Platinum	151-159	BRCA2 DNA repair associated	Homo sapiens	72-77
18264087-4	2008	Here we show that acquired resistance to cisplatin can be mediated by secondary intragenic mutations in BRCA2 that restore the wild-type BRCA2 reading frame.	Cisplatin	41-50	BRCA2 DNA repair associated	Homo sapiens	137-142
18264087-5	2008	First, in a cisplatin-resistant BRCA2-mutated breast-cancer cell line, HCC1428, a secondary genetic change in BRCA2 rescued BRCA2 function.	Cisplatin	12-21	BRCA2 DNA repair associated	Homo sapiens	32-37
18264087-5	2008	First, in a cisplatin-resistant BRCA2-mutated breast-cancer cell line, HCC1428, a secondary genetic change in BRCA2 rescued BRCA2 function.	Cisplatin	12-21	BRCA2 DNA repair associated	Homo sapiens	110-115
18264087-5	2008	First, in a cisplatin-resistant BRCA2-mutated breast-cancer cell line, HCC1428, a secondary genetic change in BRCA2 rescued BRCA2 function.	Cisplatin	12-21	BRCA2 DNA repair associated	Homo sapiens	110-115
18264087-6	2008	Second, cisplatin selection of a BRCA2-mutated pancreatic cancer cell line, Capan-1 (refs 3, 4), led to five different secondary mutations that restored the wild-type BRCA2 reading frame.	Cisplatin	8-17	BRCA2 DNA repair associated	Homo sapiens	33-38
18264087-6	2008	Second, cisplatin selection of a BRCA2-mutated pancreatic cancer cell line, Capan-1 (refs 3, 4), led to five different secondary mutations that restored the wild-type BRCA2 reading frame.	Cisplatin	8-17	BRCA2 DNA repair associated	Homo sapiens	167-172
18172318-3	2008	We show that homologous recombination plays a critical role in repair of tirapazamine-induced damage because cells defective in homologous recombination proteins XRCC2, XRCC3, Rad51D, BRCA1, or BRCA2 are particularly sensitive to tirapazamine.	Tirapazamine	73-85	BRCA2 DNA repair associated	Homo sapiens	194-199
17855454-5	2007	A role for variation in NER and BRCA2/FA pathway genes as determinants of OS was provided by an analysis restricted to the 456 patients treated with platinum-based agents.	Platinum	149-157	BRCA2 DNA repair associated	Homo sapiens	32-37
18086758-2	2007	We have genotyped nine putative functional single-nucleotide polymorphisms (SNP) in genes involved in steroid hormone synthesis (SRD5A2, CYP19A1, HSB17B1, and HSD17B4) and DNA repair (XRCC2, XRCC3, BRCA2, and RAD52) using two Australian ovarian cancer case-control studies, comprising a total of 1,466 cases and 1,821 controls of Caucasian origin.	Steroids	102-117	BRCA2 DNA repair associated	Homo sapiens	198-203
17846587-4	2007	The enzyme preferred FAD as a cofactor and NADH rather than NADPH as an electron donor.	NAD	43-47	BRCA2 DNA repair associated	Homo sapiens	21-24
17671173-0	2007	BRCA1- and BRCA2-deficient cells are sensitive to etoposide-induced DNA double-strand breaks via topoisomerase II.	Etoposide	50-59	BRCA2 DNA repair associated	Homo sapiens	11-16
17671173-3	2007	Here, we show that both BRCA1 and BRCA2 determine the sensitivity to the cytotoxic drug, etoposide, using genetic complementation of BRCA-deficient cells.	Etoposide	89-98	BRCA2 DNA repair associated	Homo sapiens	34-39
17898808-5	2007	Tamoxifen is an alternative approach only for BRCA2 mutation carriers.	Tamoxifen	0-9	BRCA2 DNA repair associated	Homo sapiens	46-51
17101782-6	2007	This phosphorylation of FoxM1 on serine residue 361 caused increased stability of the FoxM1 protein with corresponding increased transcription of XRCC1 and BRCA2 genes, both of which are required for repair of DNA damage.	Serine	33-39	BRCA2 DNA repair associated	Homo sapiens	156-161
17634835-5	2007	Tamoxifen may offer benefit to women who are carriers of BRCA2 mutations, although no prospective trials have been conducted.	Tamoxifen	0-9	BRCA2 DNA repair associated	Homo sapiens	57-62
17289874-9	2007	5-Aza-2"-deoxycytidine treatment of NSCLC cells showed demethylation and reexpression of the BRCA1 and BRCA2 genes and reduced anchorage-independent growth.	Decitabine	0-22	BRCA2 DNA repair associated	Homo sapiens	103-108
17466083-5	2007	Initial efforts by CIMBA to identify modifiers of breast cancer risk for BRCA1 and BRCA2 mutation carriers have focused on validation of common genetic variants previously associated with risk in smaller studies of carriers or unselected breast cancers.	cimba	19-24	BRCA2 DNA repair associated	Homo sapiens	83-88
17106252-1	2006	Fanconi anemia (FA) results from mutations in a group of genes whose products, including BRCA2 and BACH1/BRIP1, are known to function in one common pathway (the FA-BRCA pathway) to guard genome integrity, especially when challenged by DNA crosslinking agents, such as Cisplatin and mitomycin C (MMC).	Cisplatin	268-277	BRCA2 DNA repair associated	Homo sapiens	89-94
17143532-6	2007	Disruption of MAPK/ERK with PD98059 prevented any BRCA2 upregulation inhibiting DNA synthesis below basal levels.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	28-35	BRCA2 DNA repair associated	Homo sapiens	50-55
17945002-0	2007	Implication of BRCA2 -26G>A 5" untranslated region polymorphism in susceptibility to sporadic breast cancer and its modulation by p53 codon 72 Arg>Pro polymorphism.	Arginine	146-149	BRCA2 DNA repair associated	Homo sapiens	15-20
17106252-1	2006	Fanconi anemia (FA) results from mutations in a group of genes whose products, including BRCA2 and BACH1/BRIP1, are known to function in one common pathway (the FA-BRCA pathway) to guard genome integrity, especially when challenged by DNA crosslinking agents, such as Cisplatin and mitomycin C (MMC).	Mitomycin	282-293	BRCA2 DNA repair associated	Homo sapiens	89-94
17106252-1	2006	Fanconi anemia (FA) results from mutations in a group of genes whose products, including BRCA2 and BACH1/BRIP1, are known to function in one common pathway (the FA-BRCA pathway) to guard genome integrity, especially when challenged by DNA crosslinking agents, such as Cisplatin and mitomycin C (MMC).	Mitomycin	295-298	BRCA2 DNA repair associated	Homo sapiens	89-94
16920162-3	2006	FANCD1/BRCA2-deficient fibroblasts appeared hypersensitive to mitomycin C (MMC), slightly sensitive to methyl methane sulfonate (MMS), and like cells derived from other FA complementation groups, not sensitive to X-ray irradiation.	Mitomycin	62-73	BRCA2 DNA repair associated	Homo sapiens	0-6
16920162-3	2006	FANCD1/BRCA2-deficient fibroblasts appeared hypersensitive to mitomycin C (MMC), slightly sensitive to methyl methane sulfonate (MMS), and like cells derived from other FA complementation groups, not sensitive to X-ray irradiation.	Mitomycin	62-73	BRCA2 DNA repair associated	Homo sapiens	7-12
16920162-3	2006	FANCD1/BRCA2-deficient fibroblasts appeared hypersensitive to mitomycin C (MMC), slightly sensitive to methyl methane sulfonate (MMS), and like cells derived from other FA complementation groups, not sensitive to X-ray irradiation.	Mitomycin	75-78	BRCA2 DNA repair associated	Homo sapiens	0-6
16920162-3	2006	FANCD1/BRCA2-deficient fibroblasts appeared hypersensitive to mitomycin C (MMC), slightly sensitive to methyl methane sulfonate (MMS), and like cells derived from other FA complementation groups, not sensitive to X-ray irradiation.	Mitomycin	75-78	BRCA2 DNA repair associated	Homo sapiens	7-12
16920162-3	2006	FANCD1/BRCA2-deficient fibroblasts appeared hypersensitive to mitomycin C (MMC), slightly sensitive to methyl methane sulfonate (MMS), and like cells derived from other FA complementation groups, not sensitive to X-ray irradiation.	Methyl Methanesulfonate	103-127	BRCA2 DNA repair associated	Homo sapiens	0-6
16920162-3	2006	FANCD1/BRCA2-deficient fibroblasts appeared hypersensitive to mitomycin C (MMC), slightly sensitive to methyl methane sulfonate (MMS), and like cells derived from other FA complementation groups, not sensitive to X-ray irradiation.	Methyl Methanesulfonate	103-127	BRCA2 DNA repair associated	Homo sapiens	7-12
16920162-3	2006	FANCD1/BRCA2-deficient fibroblasts appeared hypersensitive to mitomycin C (MMC), slightly sensitive to methyl methane sulfonate (MMS), and like cells derived from other FA complementation groups, not sensitive to X-ray irradiation.	Methyl Methanesulfonate	129-132	BRCA2 DNA repair associated	Homo sapiens	0-6
16920162-3	2006	FANCD1/BRCA2-deficient fibroblasts appeared hypersensitive to mitomycin C (MMC), slightly sensitive to methyl methane sulfonate (MMS), and like cells derived from other FA complementation groups, not sensitive to X-ray irradiation.	Methyl Methanesulfonate	129-132	BRCA2 DNA repair associated	Homo sapiens	7-12
16920162-7	2006	In contrast to Brca2-deficient rodent cells, FA-D1/BRCA2 cells showed normal sister chromatid exchange (SCE) levels, both spontaneous as well as after MMC treatment.	Mitomycin	151-154	BRCA2 DNA repair associated	Homo sapiens	45-50
16564059-4	2006	Here, we show that HR deficient cell lines irs1SF and V-C8, deficient in XRCC3 and BRCA2, respectively, are hypersensitive to Cr[VI], implicating this repair pathway in repair of Cr[VI] damage.	Chromium	126-128	BRCA2 DNA repair associated	Homo sapiens	83-88
16728435-12	2006	These results suggest that genetic polymorphisms in WRN, TP53 and BRCA2 that maintain genomic stability impact benzene-induced hematotoxicity.	Benzene	111-118	BRCA2 DNA repair associated	Homo sapiens	66-71
16687415-4	2006	Here we show that BRCA2-dependent chromatin loading of Rad51 after mitomycin C treatment was not compromised by disruption of FANCC or FANCD2.	Mitomycin	67-78	BRCA2 DNA repair associated	Homo sapiens	18-23
16331614-0	2006	Tamoxifen and contralateral breast cancer in BRCA1 and BRCA2 carriers: an update.	Tamoxifen	0-9	BRCA2 DNA repair associated	Homo sapiens	55-60
16331614-7	2006	The multivariate odds ratio for contralateral breast cancer associated with tamoxifen use was 0.50 for carriers of BRCA1 mutations (95% CI, 0.30-0.85) and was 0.42 for carriers of BRCA2 mutations (95% CI, 0.17-1.02).	Tamoxifen	76-85	BRCA2 DNA repair associated	Homo sapiens	180-185
15648188-11	2005	For example, a 40-year-old BRCA2 carrier may only have a 10% and 50% lifetime risk of ovarian and breast cancer, respectively, and interventions including tamoxifen and breast MRI screening may significantly reduce the risk of both getting breast cancer and dying from it, thereby obviating the need for early screening or prophylactic surgeries, permitting these women to defer the quality of life struggles until they are older.	Tamoxifen	155-164	BRCA2 DNA repair associated	Homo sapiens	27-32
16605249-11	2006	Folates have been shown to protect both human and bacterial enzymes from loss of FAD.	Folic Acid	0-7	BRCA2 DNA repair associated	Homo sapiens	81-84
16605249-13	2006	Here we report the structures of the Ala177Val mutant of E. coli MTHFR and of its complex with the 5,10-dideazafolate analogue, LY309887, and suggest mechanisms by which the mutation may perturb FAD binding.	5,10-dideazafolate	99-117	BRCA2 DNA repair associated	Homo sapiens	195-198
16605249-13	2006	Here we report the structures of the Ala177Val mutant of E. coli MTHFR and of its complex with the 5,10-dideazafolate analogue, LY309887, and suggest mechanisms by which the mutation may perturb FAD binding.	6R-2',5'-thienyl-5,10-dideazatetrahydrofolic acid	128-136	BRCA2 DNA repair associated	Homo sapiens	195-198
16605249-17	2006	The direct interactions of bound folate with the cofactor provide one mechanism for linkage between binding of FAD and folate binding that could account in part for the protective action of folates.	Folic Acid	33-39	BRCA2 DNA repair associated	Homo sapiens	111-114
16605249-17	2006	The direct interactions of bound folate with the cofactor provide one mechanism for linkage between binding of FAD and folate binding that could account in part for the protective action of folates.	Folic Acid	119-125	BRCA2 DNA repair associated	Homo sapiens	111-114
16605249-17	2006	The direct interactions of bound folate with the cofactor provide one mechanism for linkage between binding of FAD and folate binding that could account in part for the protective action of folates.	Folic Acid	190-197	BRCA2 DNA repair associated	Homo sapiens	111-114
16550498-0	2006	Improving sensitivity of electrophoretic heteroduplex analysis using nucleosides as additives: Application to the breast cancer predisposition gene BRCA2.	Nucleosides	69-80	BRCA2 DNA repair associated	Homo sapiens	148-153
16261408-4	2005	Gene-gene interaction between the BRCA2-Met1915Thr Thr/Thr and BRCA2-Met784Val Met/Met homozygous variants increased the risk.	Threonine	47-50	BRCA2 DNA repair associated	Homo sapiens	34-39
16261408-4	2005	Gene-gene interaction between the BRCA2-Met1915Thr Thr/Thr and BRCA2-Met784Val Met/Met homozygous variants increased the risk.	Threonine	47-50	BRCA2 DNA repair associated	Homo sapiens	63-68
16261408-4	2005	Gene-gene interaction between the BRCA2-Met1915Thr Thr/Thr and BRCA2-Met784Val Met/Met homozygous variants increased the risk.	Threonine	51-54	BRCA2 DNA repair associated	Homo sapiens	34-39
16261408-4	2005	Gene-gene interaction between the BRCA2-Met1915Thr Thr/Thr and BRCA2-Met784Val Met/Met homozygous variants increased the risk.	Threonine	51-54	BRCA2 DNA repair associated	Homo sapiens	63-68
16026872-8	2005	Hypoxia (48-72 h of 0.2% O2) decreased RNA expression of a number of HR-related genes (e.g. Rad51, Rad52, Rad54, BRCA1, BRCA2) in both normal and malignant cultures.	Oxygen	25-27	BRCA2 DNA repair associated	Homo sapiens	120-125
15951253-0	2005	Quantification by affinity perfusion chromatography of phosphorylated BRCAl and BRCA2 proteins from tumor cells after lycopene treatment.	Lycopene	118-126	BRCA2 DNA repair associated	Homo sapiens	80-85
15951253-8	2005	Treatment with 10 microM lycopene increased P-BRCA1 and P-BRCA2 in the breast tumor cell line MCF7 but not in MDA-MB-231 or MCF-10a, breast tumor or fibrocystic cell lines, respectively.	Lycopene	25-33	BRCA2 DNA repair associated	Homo sapiens	58-63
15671039-2	2005	Cells defective in BRCA2.FANCD1 are extremely sensitive to mitomycin C (MMC) similarly to cells deficient in any of the Fanconi anemia (FA) complementation group proteins (FANC).	Mitomycin	59-70	BRCA2 DNA repair associated	Homo sapiens	19-24
15671039-2	2005	Cells defective in BRCA2.FANCD1 are extremely sensitive to mitomycin C (MMC) similarly to cells deficient in any of the Fanconi anemia (FA) complementation group proteins (FANC).	Mitomycin	59-70	BRCA2 DNA repair associated	Homo sapiens	25-31
15671039-2	2005	Cells defective in BRCA2.FANCD1 are extremely sensitive to mitomycin C (MMC) similarly to cells deficient in any of the Fanconi anemia (FA) complementation group proteins (FANC).	Mitomycin	59-70	BRCA2 DNA repair associated	Homo sapiens	25-29
15671039-2	2005	Cells defective in BRCA2.FANCD1 are extremely sensitive to mitomycin C (MMC) similarly to cells deficient in any of the Fanconi anemia (FA) complementation group proteins (FANC).	Mitomycin	72-75	BRCA2 DNA repair associated	Homo sapiens	19-24
15671039-2	2005	Cells defective in BRCA2.FANCD1 are extremely sensitive to mitomycin C (MMC) similarly to cells deficient in any of the Fanconi anemia (FA) complementation group proteins (FANC).	Mitomycin	72-75	BRCA2 DNA repair associated	Homo sapiens	25-31
15671039-2	2005	Cells defective in BRCA2.FANCD1 are extremely sensitive to mitomycin C (MMC) similarly to cells deficient in any of the Fanconi anemia (FA) complementation group proteins (FANC).	Mitomycin	72-75	BRCA2 DNA repair associated	Homo sapiens	25-29
15721786-4	2005	The fragment consisting of amino acids 290-456 BRCA2 was found predominantly in the soluble portion of the cell lysate and was purified by ion exchange and nickel-NTA affinity chromatography.	nickel-nta	156-166	BRCA2 DNA repair associated	Homo sapiens	47-52
15951959-12	2005	CONCLUSION: Although tamoxifen appears to be effective in preventing breast cancer in women with a BRCA1 or BRCA2 mutation, few women now take the drug compared to those who choose other preventive measures including surgery.	Tamoxifen	21-30	BRCA2 DNA repair associated	Homo sapiens	108-113
16605249-18	2006	Conformation changes induced by folate binding may also suppress dissociation of FAD.	Folic Acid	32-38	BRCA2 DNA repair associated	Homo sapiens	81-84
16648548-5	2006	The discovery of genetic factors of which the presence predisposes pancreatic cancer to successful targeting, such as the association of BRCA2/Fanconi anemia genes defects and sensitivity to mitomycin C, will eventually lead to a more individualized treatment approach.	Mitomycin	191-202	BRCA2 DNA repair associated	Homo sapiens	137-142
16510331-3	2006	We aimed to assess whether BPSO improves overall mortality or cancer-specific mortality in BRCA1 and BRCA2 mutation carriers.	bpso	27-31	BRCA2 DNA repair associated	Homo sapiens	101-106
16297086-4	2005	Tamoxifen reduces the risk of breast cancer in BRCA-2 mutation carriers, but not in BRCA-1 mutation carriers.	Tamoxifen	0-9	BRCA2 DNA repair associated	Homo sapiens	47-53
16304766-4	2005	In cells with BSCA1 and BRCA2 genes mutations the chromosome loci transference could not be induced by the X-radiation, but it could be induced by the RNA-polymerize II repression by alpha-amanitin.	Alpha-Amanitin	183-197	BRCA2 DNA repair associated	Homo sapiens	24-29
15800615-3	2005	Here we show that the carboxy-terminal region of BRCA2, which interacts directly with the essential recombination protein RAD51, contains a site (serine 3291; S3291) that is phosphorylated by cyclin-dependent kinases.	Serine	146-152	BRCA2 DNA repair associated	Homo sapiens	49-54
15258697-4	2004	At the lowest doses, the TGFbeta-RII-mutated and KRAS2-mutated cell line, TOV-21G, and the BRCA2-mutated cell line, TOV-81D, demonstrated a significantly higher sensitivity to cisplatin and gamma-irradiation than the TP53-mutated cell lines, TOV-112D and OV-90.	Cisplatin	176-185	BRCA2 DNA repair associated	Homo sapiens	91-96
15074178-2	2004	Part of the incidence of breast cancer can be explained by BRCA1 and BRCA2 germline mutations, which with current techniques can be retrospectively analysed in stored, paraffin-embedded tissue samples.	Paraffin	168-176	BRCA2 DNA repair associated	Homo sapiens	69-74
15382059-9	2004	Tamoxifen use was associated with breast cancer prevention among BRCA2 carriers (RR=0.38, 95%CI: 0.06-1.56).	Tamoxifen	0-9	BRCA2 DNA repair associated	Homo sapiens	65-70
15382059-10	2004	In BRCA1 or BRCA2 carriers with breast cancer, tamoxifen use was associated with the prevention of secondary breast cancer (OR= 0.50, 95% CI: 0.28-0.89).	Tamoxifen	47-56	BRCA2 DNA repair associated	Homo sapiens	12-17
15080686-9	2004	(Py)U- and (Py)C-containing oligodeoxynucleotides acted as effective reporter probes for homogeneous SNP typing of DNA samples containing c-Ha-ras and BRCA2 SNP sites.	Oligodeoxyribonucleotides	28-49	BRCA2 DNA repair associated	Homo sapiens	151-156
15314155-5	2004	Mitomycin C (MMC) led to decreased BRCA2 protein levels associated with increased ubiquitination, consistent with proteasome-dependent degradation.	Mitomycin	0-11	BRCA2 DNA repair associated	Homo sapiens	35-40
15314155-5	2004	Mitomycin C (MMC) led to decreased BRCA2 protein levels associated with increased ubiquitination, consistent with proteasome-dependent degradation.	Mitomycin	13-16	BRCA2 DNA repair associated	Homo sapiens	35-40
15280929-0	2004	Fludarabine, adriamycin and dexamethasone (FAD) in newly diagnosed advanced follicular lymphoma: a phase II study by the British National Lymphoma Investigation (BNLI).	Dexamethasone	28-41	BRCA2 DNA repair associated	Homo sapiens	43-46
15280929-3	2004	We here report the results of a phase II study of FAD (fludarabine, adriamycin, dexamethasone) regimen in 30 patients with advanced stage follicular lymphoma requiring treatment.	fludarabine	55-66	BRCA2 DNA repair associated	Homo sapiens	50-53
15280929-3	2004	We here report the results of a phase II study of FAD (fludarabine, adriamycin, dexamethasone) regimen in 30 patients with advanced stage follicular lymphoma requiring treatment.	Doxorubicin	68-78	BRCA2 DNA repair associated	Homo sapiens	50-53
15280929-3	2004	We here report the results of a phase II study of FAD (fludarabine, adriamycin, dexamethasone) regimen in 30 patients with advanced stage follicular lymphoma requiring treatment.	Dexamethasone	80-93	BRCA2 DNA repair associated	Homo sapiens	50-53
15251168-1	2004	The purpose of this study was to demonstrate the effects of lycopene, the major tomato carotenoid, on the expression of the BRCA1 and BRCA2 genes in three breast tumour cell lines, MCF-7, HBL-100, MDA-MB-231 and the fibrocystic breast cell line MCF-10a.	Lycopene	60-68	BRCA2 DNA repair associated	Homo sapiens	134-139
15251168-1	2004	The purpose of this study was to demonstrate the effects of lycopene, the major tomato carotenoid, on the expression of the BRCA1 and BRCA2 genes in three breast tumour cell lines, MCF-7, HBL-100, MDA-MB-231 and the fibrocystic breast cell line MCF-10a.	Carotenoids	87-97	BRCA2 DNA repair associated	Homo sapiens	134-139
15251168-6	2004	These preliminary results on the effects of lycopene on the expression of BRCA1 and BRCA2 oncosuppressor genes in breast cancer may reflect cross-talk between the oestrogen and retinoic acid receptor (RAR) pathways.	Lycopene	44-52	BRCA2 DNA repair associated	Homo sapiens	84-89
14732925-11	2004	This is likely to lead to changes in progesterone signaling in hormone-dependent tissues, which may be a factor in the increased risk of cancer in these tissues in women with germ-line BRCA1 or BRCA2 mutations.	Progesterone	37-49	BRCA2 DNA repair associated	Homo sapiens	194-199
14981540-7	2004	In vitro experiments showed that Brca2+/- mouse cells and Capan-1 cells, a human pancreatic cancer cell line deficient of BRCA2, were more sensitive to DMBA-induced apoptosis, than were Brca2+/+ mouse cells and a derivative of Capan-1 cells that expressed exogenous wild-type BRCA2, respectively.	9,10-Dimethyl-1,2-benzanthracene	152-156	BRCA2 DNA repair associated	Homo sapiens	122-127
14981540-7	2004	In vitro experiments showed that Brca2+/- mouse cells and Capan-1 cells, a human pancreatic cancer cell line deficient of BRCA2, were more sensitive to DMBA-induced apoptosis, than were Brca2+/+ mouse cells and a derivative of Capan-1 cells that expressed exogenous wild-type BRCA2, respectively.	9,10-Dimethyl-1,2-benzanthracene	152-156	BRCA2 DNA repair associated	Homo sapiens	276-281
14645421-0	2003	Tamoxifen as chemoprevention in BRCA1 and BRCA2 mutation carriers with breast cancer: a pilot survey of physicians.	Tamoxifen	0-9	BRCA2 DNA repair associated	Homo sapiens	42-47
20233484-6	2004	Tamoxifen has been shown to prevent contralateral breast cancers in BRCA1 and BRCA2 carriers but is not widely accepted as a means of primary prevention.	Tamoxifen	0-9	BRCA2 DNA repair associated	Homo sapiens	78-83
14647413-8	2004	Interestingly, Plk1-mediated modification of BRCA2 during the G2/M phases is inhibited by treatment with the radiomimetic agent, adriamycin.	Doxorubicin	129-139	BRCA2 DNA repair associated	Homo sapiens	45-50
15280184-5	2004	BRCA1/BRCA2 (BRCA1/2) gene analysis in women accrued in the NSABP-P1 trial who developed breast cancer showed that tamoxifen chemoprevention reduced breast cancer incidence in BRCA2 carriers.	Tamoxifen	115-124	BRCA2 DNA repair associated	Homo sapiens	6-11
15280184-5	2004	BRCA1/BRCA2 (BRCA1/2) gene analysis in women accrued in the NSABP-P1 trial who developed breast cancer showed that tamoxifen chemoprevention reduced breast cancer incidence in BRCA2 carriers.	Tamoxifen	115-124	BRCA2 DNA repair associated	Homo sapiens	176-181
14645421-1	2003	PURPOSE: To assess physician recommendations about the use of tamoxifen in premenopausal BRCA1 and BRCA2 mutation carriers.	Tamoxifen	62-71	BRCA2 DNA repair associated	Homo sapiens	99-104
14645421-7	2003	Physicians did not distinguish between BRCA1 and BRCA2 status in making recommendations about tamoxifen to breast cancer patients; however, in an unaffected woman, they were more likely to recommend tamoxifen to a BRCA2 mutation carrier than to a BRCA1 mutation carrier (73% v 57%; P <.0001).	Tamoxifen	199-208	BRCA2 DNA repair associated	Homo sapiens	214-219
12915460-7	2003	Furthermore, FANCG could be co-immunoprecipitated with BRCA2 from human cells, and FANCG co-localized in nuclear foci with both BRCA2 and RAD51 following DNA damage with mitomycin C.	Mitomycin	170-181	BRCA2 DNA repair associated	Homo sapiens	128-133
12457141-0	2002	[Explosive growth of uterine leiomyomas and carcinologic ovarian risk in a non-menopausal patient with BRCA1-BRCA2 mutation treated by tamoxifen].	Tamoxifen	135-144	BRCA2 DNA repair associated	Homo sapiens	109-114
12692539-3	2003	This pathway regulates cisplatin sensitivity and is governed by the coordinate activity of six genes associated with Fanconi anemia (FANCA, FANCC, FANCD2, FANCE, FANCF and FANCG) as well as BRCA1 and BRCA2 (FANCD1).	Cisplatin	23-32	BRCA2 DNA repair associated	Homo sapiens	200-205
12692539-3	2003	This pathway regulates cisplatin sensitivity and is governed by the coordinate activity of six genes associated with Fanconi anemia (FANCA, FANCC, FANCD2, FANCE, FANCF and FANCG) as well as BRCA1 and BRCA2 (FANCD1).	Cisplatin	23-32	BRCA2 DNA repair associated	Homo sapiens	207-213
12544504-10	2003	Tamoxifen may be considered as a chemopreventive agent in women with a high risk of breast cancer, including carriers of a BRCA2 mutation, but is probably not effective in BRCA1 carriers.	Tamoxifen	0-9	BRCA2 DNA repair associated	Homo sapiens	123-128
12815053-9	2003	Plk1 interacts with BRCA2 in vivo, and mutation of Ser193, Ser205/206, and Thr203/207 to Ala in BR-N1 abolished Plk1 phosphorylation, suggesting that BRCA2 is the substrate of Plk1.	Alanine	89-92	BRCA2 DNA repair associated	Homo sapiens	150-155
12838319-0	2003	Resveratrol increases BRCA1 and BRCA2 mRNA expression in breast tumour cell lines.	Resveratrol	0-11	BRCA2 DNA repair associated	Homo sapiens	32-37
12838319-2	2003	Resveratrol is also a phyto-oestrogen, binds to and activates oestrogen receptors that regulate the transcription of oestrogen-responsive target genes such as the breast cancer susceptibility genes BRCA1 and BRCA2.	Resveratrol	0-11	BRCA2 DNA repair associated	Homo sapiens	208-213
12838319-3	2003	We investigated the effects of resveratrol on BRCA1 and BRCA2 expression in human breast cancer cell lines (MCF7, HBL 100 and MDA-MB 231) using quantitative real-time RT-PCR, and by perfusion chromatography of the proteins.	Resveratrol	31-42	BRCA2 DNA repair associated	Homo sapiens	56-61
14507240-7	2003	This is the first study from South India, on BRCA1, BRCA2 & CHEK2 (1100 del C) mutations in patients with a family history of breast and/or ovarian cancer and early onset breast/ovarian cancer, using the sensitive DHPLC approach.	dhplc	218-223	BRCA2 DNA repair associated	Homo sapiens	52-57
12591928-1	2003	Adriamycin and other DNA-damaging agents have been shown to reduce BRCA2 mRNA levels in breast cancer cell lines, but the mechanism by which this occurs is unknown.	Doxorubicin	0-10	BRCA2 DNA repair associated	Homo sapiens	67-72
12591928-2	2003	In this study, we show that adriamycin and mitomycin C, but not other DNA-damaging agents, repress BRCA2 promoter activity in a dose- and time-dependent manner.	Doxorubicin	28-38	BRCA2 DNA repair associated	Homo sapiens	99-104
12591928-2	2003	In this study, we show that adriamycin and mitomycin C, but not other DNA-damaging agents, repress BRCA2 promoter activity in a dose- and time-dependent manner.	Mitomycin	43-54	BRCA2 DNA repair associated	Homo sapiens	99-104
12591928-3	2003	We demonstrate that the effect is dependent on wild type p53 and that adriamycin and p53 mediate repression of the BRCA2 promoter by inhibiting binding of an upstream stimulatory factor protein complex to the promoter.	Doxorubicin	70-80	BRCA2 DNA repair associated	Homo sapiens	115-120
12591928-4	2003	In addition, we present evidence indicating that adriamycin and other DNA-damaging agents reduce BRCA2 mRNA and protein levels by altering both BRCA2 mRNA stability and protein stability.	Doxorubicin	49-59	BRCA2 DNA repair associated	Homo sapiens	97-102
12591928-4	2003	In addition, we present evidence indicating that adriamycin and other DNA-damaging agents reduce BRCA2 mRNA and protein levels by altering both BRCA2 mRNA stability and protein stability.	Doxorubicin	49-59	BRCA2 DNA repair associated	Homo sapiens	144-149
12611456-1	2003	Clinical significance of BRCA1 and BRCA2 mRNA levels in tumor tissues as predictors of response to anthracycline-containing chemotherapy was studied in breast cancer patients.	Anthracyclines	99-112	BRCA2 DNA repair associated	Homo sapiens	35-40
12881020-2	2003	The aim of this study was to quantify BRCA2 tumor suppressor gene expression after treatment of cells with the phytoestrogens daidzein and genistein, the main compounds of soy.	daidzein	126-134	BRCA2 DNA repair associated	Homo sapiens	38-43
12881020-2	2003	The aim of this study was to quantify BRCA2 tumor suppressor gene expression after treatment of cells with the phytoestrogens daidzein and genistein, the main compounds of soy.	Genistein	139-148	BRCA2 DNA repair associated	Homo sapiens	38-43
12881020-3	2003	The effects of 5 microg/ml genistein and 20 microg/ml daidzein on BRCA2 expression were studied in two human mammary tumor cell lines, MCF7 and MDA-MB-231, and one normal human breast epithelial cell line, MCF10a.	daidzein	54-62	BRCA2 DNA repair associated	Homo sapiens	66-71
12881020-5	2003	With Genistein, we observed a 60% increase of BRCA2 mRNA in MDA-MB-231 and MCF10a, which are, respectively, estrogen receptors alpha-/beta+ and alpha-/beta-, and no variation in MCF7, which is ERalpha+/beta+.	Genistein	5-14	BRCA2 DNA repair associated	Homo sapiens	46-51
12881020-9	2003	Treatment with actinomycin D and cycloheximide demonstrated that the increase in BRCA2 mRNA was not blocked by cycloheximide, indicating that de novo protein synthesis was required in MDA-MB-23, although de novo synthesis was not required in MCF10a for the genistein.	Dactinomycin	15-28	BRCA2 DNA repair associated	Homo sapiens	81-86
12881020-9	2003	Treatment with actinomycin D and cycloheximide demonstrated that the increase in BRCA2 mRNA was not blocked by cycloheximide, indicating that de novo protein synthesis was required in MDA-MB-23, although de novo synthesis was not required in MCF10a for the genistein.	Cycloheximide	33-46	BRCA2 DNA repair associated	Homo sapiens	81-86
12881020-9	2003	Treatment with actinomycin D and cycloheximide demonstrated that the increase in BRCA2 mRNA was not blocked by cycloheximide, indicating that de novo protein synthesis was required in MDA-MB-23, although de novo synthesis was not required in MCF10a for the genistein.	Genistein	257-266	BRCA2 DNA repair associated	Homo sapiens	81-86
12881020-10	2003	With actinomycin D, genistein had a positive effect on the transcriptional level of BRCA2 mRNA in MDA-MB-231 and MCF10a.	Dactinomycin	5-18	BRCA2 DNA repair associated	Homo sapiens	84-89
12881020-10	2003	With actinomycin D, genistein had a positive effect on the transcriptional level of BRCA2 mRNA in MDA-MB-231 and MCF10a.	Genistein	20-29	BRCA2 DNA repair associated	Homo sapiens	84-89
12457141-5	2002	CONCLUSION: Use of tamoxifen in premenopausal woman with subjacent gynecological pathologies, whether BRCA1-BRCA2 mutation is present or not can prove to be delicate.	Tamoxifen	19-28	BRCA2 DNA repair associated	Homo sapiens	108-113
12228710-2	2002	Here, we present the 3.1 angstrom crystal structure of a approximately 90-kilodalton BRCA2 domain bound to DSS1, which reveals three oligonucleotide-binding (OB) folds and a helix-turn-helix (HTH) motif.	Oligonucleotides	133-148	BRCA2 DNA repair associated	Homo sapiens	85-90
12410562-6	2002	BRCA2 mRNA levels were upregulated in thymocytes treated with the DNA-damaging agent etoposide.	Etoposide	85-94	BRCA2 DNA repair associated	Homo sapiens	0-5
12070551-6	2002	This mutation is a 4-nucleotide deletion that creates a stop signal at codon 770 of the BRCA2 transcript.	4-nucleotide	19-31	BRCA2 DNA repair associated	Homo sapiens	88-93
12007633-1	2002	We have investigated the effects of chemotherapeutic agents such as adriamycin (ADR), camptothecin (CPT), mitomycin-C (MYC-C) and methotrexate (MTX) on the regulation of expression of the tumor susceptibility genes (BRCA1 and BRCA2), and the association of cell cycle progression in human breast cancer and normal breast epithelial cells.	Methotrexate	130-142	BRCA2 DNA repair associated	Homo sapiens	226-231
12065746-4	2002	Functional complementation of FA-D1 fibroblasts with wild-type BRCA2 complementary DNA restores MMC resistance.	Mitomycin	96-99	BRCA2 DNA repair associated	Homo sapiens	30-35
12065746-4	2002	Functional complementation of FA-D1 fibroblasts with wild-type BRCA2 complementary DNA restores MMC resistance.	Mitomycin	96-99	BRCA2 DNA repair associated	Homo sapiens	63-68
11710890-0	2001	Tamoxifen and breast cancer incidence among women with inherited mutations in BRCA1 and BRCA2: National Surgical Adjuvant Breast and Bowel Project (NSABP-P1) Breast Cancer Prevention Trial.	Tamoxifen	0-9	BRCA2 DNA repair associated	Homo sapiens	88-93
11890937-5	2002	We now investigated further cases heterozygous for a BRCA1 mutation and cases heterozygous for a BRCA2 mutation and show that enhanced micronucleus formation after gamma irradiation and H2O2-treatment is also a feature of lymphocytes carrying a BRCA2 mutation.	Hydrogen Peroxide	186-190	BRCA2 DNA repair associated	Homo sapiens	245-250
12064337-0	2002	Differential effects of n-3 and n-6 polyunsaturated fatty acids on BRCA1 and BRCA2 gene expression in breast cell lines.	n-6 polyunsaturated fatty acids	32-63	BRCA2 DNA repair associated	Homo sapiens	77-82
12064337-4	2002	Here, we examined the expression of BRCA1 and BRCA2 in breast cell lines after treatment with polyunsaturated fatty acids.	Fatty Acids, Unsaturated	94-121	BRCA2 DNA repair associated	Homo sapiens	46-51
12064337-5	2002	Real-time quantitative polymerase chain reaction determinations conclusively demonstrated increases in BRCA1 and BRCA2 mRNA expressions in MCF7 and MDA-MB 231 tumour cell lines after treatment with n-3 polyunsaturated fatty acids (eicosapentaenoic acid and docosahexaenoic acid), but no variation was noticed with the n-6 polyunsaturated fatty acid (arachidonic acid).	Fatty Acids, Omega-3	198-229	BRCA2 DNA repair associated	Homo sapiens	113-118
12064337-5	2002	Real-time quantitative polymerase chain reaction determinations conclusively demonstrated increases in BRCA1 and BRCA2 mRNA expressions in MCF7 and MDA-MB 231 tumour cell lines after treatment with n-3 polyunsaturated fatty acids (eicosapentaenoic acid and docosahexaenoic acid), but no variation was noticed with the n-6 polyunsaturated fatty acid (arachidonic acid).	Eicosapentaenoic Acid	231-252	BRCA2 DNA repair associated	Homo sapiens	113-118
12064337-5	2002	Real-time quantitative polymerase chain reaction determinations conclusively demonstrated increases in BRCA1 and BRCA2 mRNA expressions in MCF7 and MDA-MB 231 tumour cell lines after treatment with n-3 polyunsaturated fatty acids (eicosapentaenoic acid and docosahexaenoic acid), but no variation was noticed with the n-6 polyunsaturated fatty acid (arachidonic acid).	Docosahexaenoic Acids	257-277	BRCA2 DNA repair associated	Homo sapiens	113-118
12064337-5	2002	Real-time quantitative polymerase chain reaction determinations conclusively demonstrated increases in BRCA1 and BRCA2 mRNA expressions in MCF7 and MDA-MB 231 tumour cell lines after treatment with n-3 polyunsaturated fatty acids (eicosapentaenoic acid and docosahexaenoic acid), but no variation was noticed with the n-6 polyunsaturated fatty acid (arachidonic acid).	n-6 polyunsaturated fatty acid	318-348	BRCA2 DNA repair associated	Homo sapiens	113-118
12064337-5	2002	Real-time quantitative polymerase chain reaction determinations conclusively demonstrated increases in BRCA1 and BRCA2 mRNA expressions in MCF7 and MDA-MB 231 tumour cell lines after treatment with n-3 polyunsaturated fatty acids (eicosapentaenoic acid and docosahexaenoic acid), but no variation was noticed with the n-6 polyunsaturated fatty acid (arachidonic acid).	Arachidonic Acid	350-366	BRCA2 DNA repair associated	Homo sapiens	113-118
12064337-8	2002	We suggest the presence of a possible transcriptional or post-transcriptional regulation of BRCA1 and BRCA2 after n-3 polyunsaturated fatty acid treatment in breast tumour cells.	Fatty Acids, Omega-3	114-144	BRCA2 DNA repair associated	Homo sapiens	102-107
11890937-5	2002	We now investigated further cases heterozygous for a BRCA1 mutation and cases heterozygous for a BRCA2 mutation and show that enhanced micronucleus formation after gamma irradiation and H2O2-treatment is also a feature of lymphocytes carrying a BRCA2 mutation.	Hydrogen Peroxide	186-190	BRCA2 DNA repair associated	Homo sapiens	97-102
11870509-0	2002	Estimates of the likely prophylactic effect of tamoxifen in women with high risk BRCA1 and BRCA2 mutations.	Tamoxifen	47-56	BRCA2 DNA repair associated	Homo sapiens	91-96
12846491-13	2002	Using these, the effect of tamoxifen on the relative risk of developing breast cancer in women with a mutation in the BRCA1 gene is estimated to be 0.90 95% confidence interval (CI) (0.52, 1.61), and for the BRCA2 gene 0.71 95% CI (0.45, 1.21).	Tamoxifen	27-36	BRCA2 DNA repair associated	Homo sapiens	208-213
11710890-3	2001	OBJECTIVE: To evaluate the effect of tamoxifen on incidence of breast cancer among cancer-free women with inherited BRCA1 or BRCA2 mutations.	Tamoxifen	37-46	BRCA2 DNA repair associated	Homo sapiens	125-130
11710890-5	2001	MAIN OUTCOME MEASURE: Among women with BRCA1 or BRCA2 mutations, incidence of breast cancer among those who were receiving tamoxifen vs incidence of breast cancer among those receiving placebo.	Tamoxifen	123-132	BRCA2 DNA repair associated	Homo sapiens	48-53
11710890-8	2001	Of 11 patients with BRCA2 mutations, 3 received tamoxifen and 8 received placebo (risk ratio, 0.38; 95% confidence interval, 0.06-1.56).	Tamoxifen	48-57	BRCA2 DNA repair associated	Homo sapiens	20-25
11710890-10	2001	CONCLUSION: Tamoxifen reduced breast cancer incidence among healthy BRCA2 carriers by 62%, similar to the reduction in incidence of ER-positive breast cancer among all women in the Breast Cancer Prevention Trial.	Tamoxifen	12-21	BRCA2 DNA repair associated	Homo sapiens	68-73
11532935-5	2001	Furthermore, loss of Brca2 causes a large increase in genome-wide error-prone repair of both spontaneous DNA damage and mitomycin C-induced DNA cross-links at the expense of error-free repair by sister chromatid recombination.	Mitomycin	120-131	BRCA2 DNA repair associated	Homo sapiens	21-26
11560980-5	2001	Women who carry mutations in either the BRCA1 or BRCA2 gene will also experience reduced incidence of breast cancer with tamoxifen.	Tamoxifen	121-130	BRCA2 DNA repair associated	Homo sapiens	49-54
11694309-6	2001	This procedure allows the determination of the percentage of BRCA2 among the DNA-binding proteins and the quantitation of the difference of expression of BRCA2 oncosuppressor protein in breast carcinoma cells and in normal breast cells treated or untreated with phytoestrogens, such as daidzein or genistein.	daidzein	286-294	BRCA2 DNA repair associated	Homo sapiens	154-159
11694309-6	2001	This procedure allows the determination of the percentage of BRCA2 among the DNA-binding proteins and the quantitation of the difference of expression of BRCA2 oncosuppressor protein in breast carcinoma cells and in normal breast cells treated or untreated with phytoestrogens, such as daidzein or genistein.	Genistein	298-307	BRCA2 DNA repair associated	Homo sapiens	154-159
11400119-0	2001	Decreased expression of BRCA2 mRNA predicts favorable response to docetaxel in breast cancer.	Docetaxel	66-75	BRCA2 DNA repair associated	Homo sapiens	24-29
11906441-5	2001	It is not yet clear whether tamoxifen can reduce breast cancer incidence in women with BRCA1 and BRCA2 mutations, although preliminary evidence favors benefit for at least those with a BRCA2 mutation.	Tamoxifen	28-37	BRCA2 DNA repair associated	Homo sapiens	97-102
11400119-4	2001	BRCA2 mRNA levels (0.547 +/- 0.200, mean +/- SE) of responders to DOC treatment were significantly (p < 0.05) lower than those of non-responders (1.538 +/- 0.358), but there was no significant difference in BRCA1 mRNA levels between responders (0.389 +/- 0.081) and non-responders (0.779 +/- 0.172).	Docetaxel	66-69	BRCA2 DNA repair associated	Homo sapiens	0-5
11196174-6	2001	Importantly, inactivation of DNA-dependent protein kinase (DNA-PK) by wortmannin generates similar shifts from the fast to the slow component of rejoining in BRCA2-proficient and BRCA2-deficient cells.	Wortmannin	70-80	BRCA2 DNA repair associated	Homo sapiens	158-163
11295099-0	2001	Regulation of BRCA1 and BRCA2 transcript in response to cisplatin, adriamycin, taxol and ionising radiation is correlated to p53 functional status in ovarian cancer cell lines.	Cisplatin	56-65	BRCA2 DNA repair associated	Homo sapiens	24-29
11295099-0	2001	Regulation of BRCA1 and BRCA2 transcript in response to cisplatin, adriamycin, taxol and ionising radiation is correlated to p53 functional status in ovarian cancer cell lines.	Doxorubicin	67-77	BRCA2 DNA repair associated	Homo sapiens	24-29
11295099-0	2001	Regulation of BRCA1 and BRCA2 transcript in response to cisplatin, adriamycin, taxol and ionising radiation is correlated to p53 functional status in ovarian cancer cell lines.	Paclitaxel	79-84	BRCA2 DNA repair associated	Homo sapiens	24-29
11196174-6	2001	Importantly, inactivation of DNA-dependent protein kinase (DNA-PK) by wortmannin generates similar shifts from the fast to the slow component of rejoining in BRCA2-proficient and BRCA2-deficient cells.	Wortmannin	70-80	BRCA2 DNA repair associated	Homo sapiens	179-184
11130383-0	2000	Tamoxifen and risk of contralateral breast cancer in BRCA1 and BRCA2 mutation carriers: a case-control study.	Tamoxifen	0-9	BRCA2 DNA repair associated	Homo sapiens	63-68
11524552-8	2001	In an unpublicized presentation, Mary-Claire King presented very interesting results from the National Surgical Adjuvant Breast and Bowel Project Breast Cancer Prevention Trial suggesting that tamoxifen may be an effective chemopreventive drug for women with BRCA2, but not BRCA1, mutations.	Tamoxifen	193-202	BRCA2 DNA repair associated	Homo sapiens	259-264
11130383-8	2000	Tamoxifen protected against contralateral breast cancer for carriers of BRCA1 mutations (odds ratio 0.38, 95% CI 0.19-0.74) and for those with BRCA2 mutations (0.63, 0.20-1.50).	Tamoxifen	0-9	BRCA2 DNA repair associated	Homo sapiens	143-148
11130383-11	2000	INTERPRETATION: Tamoxifen use reduces the risk of contralateral breast cancer in women with pathogenic mutations in the BRCA1 or BRCA2 gene.	Tamoxifen	16-25	BRCA2 DNA repair associated	Homo sapiens	129-134
10609497-2	1999	The presence of the predominant Jewish BRCA1 and BRCA2 mutations in archival paraffin-embedded tumor tissue of four Jewish women with ovarian carcinoma who previously underwent ovulation induction with clomiphene citrate, was determined.	Paraffin	77-85	BRCA2 DNA repair associated	Homo sapiens	49-54
11034101-0	2000	BRCA1 and BRCA2 are necessary for the transcription-coupled repair of the oxidative 8-oxoguanine lesion in human cells.	8-hydroxyguanine	84-96	BRCA2 DNA repair associated	Homo sapiens	10-15
11034101-3	2000	We show that deficiency for either BRCA1 or BRCA2 in human cancer cells leads to a block of the RNA polymerase II transcription machinery at the 8-oxoguanine site and impairs the transcription-coupled repair of the lesion, leading to a high mutation rate.	8-hydroxyguanine	145-157	BRCA2 DNA repair associated	Homo sapiens	44-49
11034101-5	2000	These results represent the first demonstration of the essential contribution of BRCA1 and BRCA2 gene products in the repair of the 8-oxoguanine oxidative damage specifically located on the transcribed strand in human cells.	8-hydroxyguanine	132-144	BRCA2 DNA repair associated	Homo sapiens	91-96
10665701-1	2000	CONTEXT: Women with BRCA1- or BRCA2-associated breast cancer are at increased risk for contralateral breast cancer and ovarian cancer and therefore may consider secondary cancer prevention strategies, such as prophylactic surgery and tamoxifen therapy.	Tamoxifen	234-243	BRCA2 DNA repair associated	Homo sapiens	30-35
10594372-1	1999	The neuronal NO synthase (nNOS) flavin domain, which has similar redox properties to those of NADPH-cytochrome P450 reductase (P450R), contains binding sites for calmodulin, FAD, FMN, and NADPH.	4,6-dinitro-o-cresol	32-38	BRCA2 DNA repair associated	Homo sapiens	174-177
10594372-1	1999	The neuronal NO synthase (nNOS) flavin domain, which has similar redox properties to those of NADPH-cytochrome P450 reductase (P450R), contains binding sites for calmodulin, FAD, FMN, and NADPH.	NADP	94-99	BRCA2 DNA repair associated	Homo sapiens	174-177
10594372-4	1999	The air-stable semiquinone of the nNOS flavin domains showed similar redox properties to the corresponding FAD-FMNH(&z.ccirf;) of P450R.	4,6-dinitro-o-cresol	39-45	BRCA2 DNA repair associated	Homo sapiens	107-110
10594372-4	1999	The air-stable semiquinone of the nNOS flavin domains showed similar redox properties to the corresponding FAD-FMNH(&z.ccirf;) of P450R.	Adenosine Monophosphate	117-120	BRCA2 DNA repair associated	Homo sapiens	107-110
10551859-3	1999	In support of the biological significance of this interaction, we found that the complex of BRCA2 and Rad51 in breast cancer MCF-7 cells was diminished upon conditional expression of a wild-type, but not a mutated, BRC4 repeat using the tetracycline-inducible system.	Tetracycline	237-249	BRCA2 DNA repair associated	Homo sapiens	92-97
10550133-9	1999	With respect to steroid receptor status, BRCA2-associated tumors were more likely to be steroid receptor-positive, especially regarding progesterone receptor status (100% v 76.7% positive, respectively; P =.06).	Steroids	16-23	BRCA2 DNA repair associated	Homo sapiens	41-46
10550133-9	1999	With respect to steroid receptor status, BRCA2-associated tumors were more likely to be steroid receptor-positive, especially regarding progesterone receptor status (100% v 76.7% positive, respectively; P =.06).	Steroids	88-95	BRCA2 DNA repair associated	Homo sapiens	41-46
10446958-7	1999	Moreover, forced expression of a fusion protein containing green fluorescent protein and the first Rad51-binding BRC repeat of BRCA2 in cells with wild-type BRCA2 rendered them hypersensitive to IR and cisplatin and compromised IR-induced Rad51 foci formation.	Cisplatin	202-211	BRCA2 DNA repair associated	Homo sapiens	127-132
10446958-7	1999	Moreover, forced expression of a fusion protein containing green fluorescent protein and the first Rad51-binding BRC repeat of BRCA2 in cells with wild-type BRCA2 rendered them hypersensitive to IR and cisplatin and compromised IR-induced Rad51 foci formation.	Cisplatin	202-211	BRCA2 DNA repair associated	Homo sapiens	157-162
10375022-8	1999	c-Myc protooncogene expression was strongly inhibited by treatment with estradiol as was expression of BRCA1 and BRCA2 genes, which is in agreement with their mitogenic-dependent expression, while expression of beta-actin, a housekeeping gene, was not affected by hormone treatment.	Estradiol	72-81	BRCA2 DNA repair associated	Homo sapiens	113-118
10662541-6	2000	In this report, we describe a fast and simple capillary electrophoresis (CE)-based method using a polymer network for screening the three common mutations in BRCA1 and BRCA2.	Polymers	98-105	BRCA2 DNA repair associated	Homo sapiens	168-173
10344722-5	1999	RESULTS: Of 26 agents screened, BRCA1 and BRCA2 mRNA reductions were observed in both cell lines after exposure to adriamycin (ADR), camptothecin (CPT), sodium selenite (SLN), and ultraviolet radiation (UV), while nitrogen mustard (HN2) caused mRNA reduction in DU-145 but not in Tsu-Prl.	Doxorubicin	115-125	BRCA2 DNA repair associated	Homo sapiens	42-47
10344722-5	1999	RESULTS: Of 26 agents screened, BRCA1 and BRCA2 mRNA reductions were observed in both cell lines after exposure to adriamycin (ADR), camptothecin (CPT), sodium selenite (SLN), and ultraviolet radiation (UV), while nitrogen mustard (HN2) caused mRNA reduction in DU-145 but not in Tsu-Prl.	Camptothecin	133-145	BRCA2 DNA repair associated	Homo sapiens	42-47
10344722-5	1999	RESULTS: Of 26 agents screened, BRCA1 and BRCA2 mRNA reductions were observed in both cell lines after exposure to adriamycin (ADR), camptothecin (CPT), sodium selenite (SLN), and ultraviolet radiation (UV), while nitrogen mustard (HN2) caused mRNA reduction in DU-145 but not in Tsu-Prl.	Camptothecin	147-150	BRCA2 DNA repair associated	Homo sapiens	42-47
10344722-5	1999	RESULTS: Of 26 agents screened, BRCA1 and BRCA2 mRNA reductions were observed in both cell lines after exposure to adriamycin (ADR), camptothecin (CPT), sodium selenite (SLN), and ultraviolet radiation (UV), while nitrogen mustard (HN2) caused mRNA reduction in DU-145 but not in Tsu-Prl.	Sodium Selenite	153-168	BRCA2 DNA repair associated	Homo sapiens	42-47
10344722-5	1999	RESULTS: Of 26 agents screened, BRCA1 and BRCA2 mRNA reductions were observed in both cell lines after exposure to adriamycin (ADR), camptothecin (CPT), sodium selenite (SLN), and ultraviolet radiation (UV), while nitrogen mustard (HN2) caused mRNA reduction in DU-145 but not in Tsu-Prl.	Nitrogen	214-222	BRCA2 DNA repair associated	Homo sapiens	42-47
19658353-3	1998	Recent studies suggest a role for BRCA 1 and BRCA 2 in transcriptional regulation, as it possesses a conserved NH2 terminal ring finger domain and an COOH domain.	Carbonic Acid	150-154	BRCA2 DNA repair associated	Homo sapiens	45-51
9774399-0	1998	Mutation at histidine 338 of gp91(phox) depletes FAD and affects expression of cytochrome b558 of the human NADPH oxidase.	Histidine	12-21	BRCA2 DNA repair associated	Homo sapiens	49-52
9774399-9	1998	These results indicate that His-338 is a very critical residue for FAD incorporation into the NADPH oxidase system.	Histidine	28-31	BRCA2 DNA repair associated	Homo sapiens	67-70
9834905-2	1998	Semiempirical quantum chemical calculations were used to investigate the role of the enzyme and FAD co-enzyme in the catalytic oxidation of glucose.	Glucose	140-147	BRCA2 DNA repair associated	Homo sapiens	96-99
9619832-4	1998	We found that several agents, including adriamycin (a DNA intercalator and inhibitor of topoisomerase II), camptothecin (a topoisomerase I inhibitor), and ultraviolet radiation induced significant decreases in BRCA1 and BRCA2 mRNA levels.	Doxorubicin	40-50	BRCA2 DNA repair associated	Homo sapiens	220-225
9679765-0	1998	Down-regulation of BRCA1 and BRCA2 in human ovarian cancer cells exposed to adriamycin and ultraviolet radiation.	Doxorubicin	76-86	BRCA2 DNA repair associated	Homo sapiens	29-34
9679765-4	1998	We found that Adriamycin (ADR) and ultraviolet (UV)radiation significantly down-regulated BRCA1 and BRCA2 mRNA expression in SK-OV-3 cells.	Doxorubicin	14-24	BRCA2 DNA repair associated	Homo sapiens	100-105
9679765-9	1998	The ADR doses required for significant decreases of BRCA1 and BRCA2 were about 10-15, 5-10 and 2 microM, respectively, for SK-OV-3, CAOV-3 and PA-1; the IC50 doses for loss of cell viability (determined by Trypan blue dye exclusion) were 23, 14 and 0.4 microM, respectively.	Trypan Blue	206-217	BRCA2 DNA repair associated	Homo sapiens	62-67
9665145-7	1998	Introduction of antisense BRCA2 deoxyribonucleotides into cells possessing normal BRCA2 function led to increased sensitivity to mitoxantrone (two-sided P = .008).	Deoxyribonucleotides	32-52	BRCA2 DNA repair associated	Homo sapiens	26-31
9665145-7	1998	Introduction of antisense BRCA2 deoxyribonucleotides into cells possessing normal BRCA2 function led to increased sensitivity to mitoxantrone (two-sided P = .008).	Deoxyribonucleotides	32-52	BRCA2 DNA repair associated	Homo sapiens	82-87
9665145-7	1998	Introduction of antisense BRCA2 deoxyribonucleotides into cells possessing normal BRCA2 function led to increased sensitivity to mitoxantrone (two-sided P = .008).	Mitoxantrone	129-141	BRCA2 DNA repair associated	Homo sapiens	26-31
9665145-7	1998	Introduction of antisense BRCA2 deoxyribonucleotides into cells possessing normal BRCA2 function led to increased sensitivity to mitoxantrone (two-sided P = .008).	Mitoxantrone	129-141	BRCA2 DNA repair associated	Homo sapiens	82-87
9560268-0	1998	The BRC repeats in BRCA2 are critical for RAD51 binding and resistance to methyl methanesulfonate treatment.	Methyl Methanesulfonate	74-97	BRCA2 DNA repair associated	Homo sapiens	19-24
9560268-6	1998	Inferring from the function of RAD51 in DNA repair, human pancreatic cancer cells, Capan-1, expressing truncated BRCA2 were shown to be hypersensitive to methyl methanesulfonate (MMS) treatment.	Methyl Methanesulfonate	154-177	BRCA2 DNA repair associated	Homo sapiens	113-118
9560268-6	1998	Inferring from the function of RAD51 in DNA repair, human pancreatic cancer cells, Capan-1, expressing truncated BRCA2 were shown to be hypersensitive to methyl methanesulfonate (MMS) treatment.	Methyl Methanesulfonate	179-182	BRCA2 DNA repair associated	Homo sapiens	113-118
9560268-7	1998	Exogenous expression of wild-type BRCA2, but not BRC-deleted mutants, in Capan-1 cells confers resistance to MMS treatment.	Methyl Methanesulfonate	109-112	BRCA2 DNA repair associated	Homo sapiens	34-39
9619832-4	1998	We found that several agents, including adriamycin (a DNA intercalator and inhibitor of topoisomerase II), camptothecin (a topoisomerase I inhibitor), and ultraviolet radiation induced significant decreases in BRCA1 and BRCA2 mRNA levels.	Camptothecin	107-119	BRCA2 DNA repair associated	Homo sapiens	220-225
9619832-5	1998	Decreased levels of BRCA1 and BRCA2 mRNAs were observed within 6-12 h after treatment with adriamycin and persisted for at least 72 h. Adriamycin also induced decreases in BRCA1 protein levels; but these decreases required several days.	Doxorubicin	91-101	BRCA2 DNA repair associated	Homo sapiens	30-35
9619832-5	1998	Decreased levels of BRCA1 and BRCA2 mRNAs were observed within 6-12 h after treatment with adriamycin and persisted for at least 72 h. Adriamycin also induced decreases in BRCA1 protein levels; but these decreases required several days.	Doxorubicin	135-145	BRCA2 DNA repair associated	Homo sapiens	30-35
9619832-8	1998	Adriamycin-induced down-regulation of BRCA1 and BRCA2 mRNAs was first observed at doses that yielded relatively little cytotoxicity and little or no apoptotic DNA fragmentation.	Doxorubicin	0-10	BRCA2 DNA repair associated	Homo sapiens	48-53
9619832-11	1998	However, the adriamycin-induced reduction in BRCA1 and BRCA2 mRNA levels was correlated with p53 functional status.	Doxorubicin	13-23	BRCA2 DNA repair associated	Homo sapiens	55-60
9619832-12	1998	MCF-7 cells transfected with a dominant negative mutant p53 (143 val-->ala) required at least tenfold higher doses of adriamycin to down-regulate BRCA1 and BRCA2 mRNAs than did parental MCF-7 cells or control-transfected MCF-7 clones.	Doxorubicin	121-131	BRCA2 DNA repair associated	Homo sapiens	159-164
7686905-2	1993	Brain NO (nitric oxide) synthase contains FAD, FMN, heme, and tetrahydrobiopterin as prosthetic groups and represents a multi-functional oxidoreductase catalyzing oxidation of L-arginine to NO and L-citrulline, formation of H2O2, and reduction of cytochrome c.	Nitric Oxide	10-22	BRCA2 DNA repair associated	Homo sapiens	42-45
8895509-1	1996	The steady state levels of BRCA1 and BRCA2 mRNAs were shown to be coordinately elevated by the steroid hormone estrogen but not progesterone in the human breast cancer cell lines BT-483 and MCF-7.	Steroids	95-110	BRCA2 DNA repair associated	Homo sapiens	37-42
8895509-2	1996	Two different antiestrogens, trans 4"-hydroxytamoxifen and ICI 182,780, blocked the elevation of BRCA1 and BRCA2 mRNA levels, confirming that the effect was mediated through the estrogen receptor.	trans 4"-hydroxytamoxifen	29-54	BRCA2 DNA repair associated	Homo sapiens	107-112
8895509-4	1996	Cycloheximide blocked the estrogen effect implying that estrogen induces synthesis of an unidentified estrogen-responsive protein(s) that then result in the elevation of BRCA1 and BRCA2 mRNAs.	Cycloheximide	0-13	BRCA2 DNA repair associated	Homo sapiens	180-185
9168997-5	1997	For MCF-7 cells, the level of BRCA2 transcript decreased as cells were released from nocodazole-mediated metaphase arrest.	Nocodazole	85-95	BRCA2 DNA repair associated	Homo sapiens	30-35
9365162-0	1997	Absence of methylation of CpG dinucleotides within the promoter of the breast cancer susceptibility gene BRCA2 in normal tissues and in breast and ovarian cancers.	cytidylyl-3'-5'-guanosine	26-43	BRCA2 DNA repair associated	Homo sapiens	105-110
9365162-4	1997	We have examined the hypothesis that expression of the BRCA2 gene may be suppressed in sporadic breast cancers by a mechanism that is associated with increased methylation of cytosine residues in the promoter region.	Cytosine	175-183	BRCA2 DNA repair associated	Homo sapiens	55-60
9365162-5	1997	Using a HpaII/MspI digestion-polymerase chain reaction based assay, the presence of 5-methylcytosine in three CpG dinucleotides within the BRCA2 promoter was assessed in 18 breast or ovarian cancer cell lines, in an SV40 large T antigen immortalized cell line derived from normal breast epithelial cells, in 64 primary sporadic breast cancers and peripheral blood leucocytes from these cases and in a number of other normal human tissues.	5-Methylcytosine	84-100	BRCA2 DNA repair associated	Homo sapiens	139-144
8954538-1	1996	NADPH cytochrome P450 reductase binds two flavin cofactors, FMN and FAD, per molecule of reductase.	4,6-dinitro-o-cresol	42-48	BRCA2 DNA repair associated	Homo sapiens	68-71
8954538-7	1996	The 8-NH2-FAD and 8-OH-FAD analog-reconstituted FMN-bound reductase catalyzes the reduction of ferricyanide at rates of 0.43 and 0.28 mumol/min/ nmol reductase, respectively.	hexacyanoferrate III	95-107	BRCA2 DNA repair associated	Homo sapiens	10-13
8954538-7	1996	The 8-NH2-FAD and 8-OH-FAD analog-reconstituted FMN-bound reductase catalyzes the reduction of ferricyanide at rates of 0.43 and 0.28 mumol/min/ nmol reductase, respectively.	hexacyanoferrate III	95-107	BRCA2 DNA repair associated	Homo sapiens	23-26
8954538-10	1996	The free flavins, i.e., FMN, 8-OH-FAD, 8-NH2-FAD, and riboflavin, are able to support ferricyanide reduction at a rate of 0.40, 0.52, 0.87, and 0.16 mumol/min/nmol flavin, respectively.	Flavins	9-16	BRCA2 DNA repair associated	Homo sapiens	34-37
8954538-10	1996	The free flavins, i.e., FMN, 8-OH-FAD, 8-NH2-FAD, and riboflavin, are able to support ferricyanide reduction at a rate of 0.40, 0.52, 0.87, and 0.16 mumol/min/nmol flavin, respectively.	Flavins	9-16	BRCA2 DNA repair associated	Homo sapiens	45-48
8954538-10	1996	The free flavins, i.e., FMN, 8-OH-FAD, 8-NH2-FAD, and riboflavin, are able to support ferricyanide reduction at a rate of 0.40, 0.52, 0.87, and 0.16 mumol/min/nmol flavin, respectively.	hexacyanoferrate III	86-98	BRCA2 DNA repair associated	Homo sapiens	34-37
8954538-10	1996	The free flavins, i.e., FMN, 8-OH-FAD, 8-NH2-FAD, and riboflavin, are able to support ferricyanide reduction at a rate of 0.40, 0.52, 0.87, and 0.16 mumol/min/nmol flavin, respectively.	hexacyanoferrate III	86-98	BRCA2 DNA repair associated	Homo sapiens	45-48
8954538-10	1996	The free flavins, i.e., FMN, 8-OH-FAD, 8-NH2-FAD, and riboflavin, are able to support ferricyanide reduction at a rate of 0.40, 0.52, 0.87, and 0.16 mumol/min/nmol flavin, respectively.	4,6-dinitro-o-cresol	9-15	BRCA2 DNA repair associated	Homo sapiens	34-37
8954538-10	1996	The free flavins, i.e., FMN, 8-OH-FAD, 8-NH2-FAD, and riboflavin, are able to support ferricyanide reduction at a rate of 0.40, 0.52, 0.87, and 0.16 mumol/min/nmol flavin, respectively.	4,6-dinitro-o-cresol	9-15	BRCA2 DNA repair associated	Homo sapiens	45-48
1320407-1	1992	A sensitive and specific chemiluminescence (CL) method with bacterial luciferase was adapted for accurate measurement of the flavins FAD and FMN in the membrane and cytosolic fractions of neutrophils prepared from pig and human blood.	Flavins	125-132	BRCA2 DNA repair associated	Homo sapiens	133-136
33941784-2	2021	In this post hoc exploratory biomarker analysis of pre- and post-platinum ARIEL2 samples, RAD51C and RAD51D mutations and high-level BRCA1 promoter methylation predict response to rucaparib, similar to BRCA1/BRCA2 mutations.	rucaparib	180-189	BRCA2 DNA repair associated	Homo sapiens	208-213
33970687-0	2021	Phase II Study of Maintenance Rucaparib in Patients With Platinum-Sensitive Advanced Pancreatic Cancer and a Pathogenic Germline or Somatic Variant in BRCA1, BRCA2, or PALB2.	rucaparib	30-39	BRCA2 DNA repair associated	Homo sapiens	158-163
33970687-1	2021	PURPOSE: Olaparib, a poly (ADP-ribose) polymerase (PARP) inhibitor (PARPi), is approved as maintenance therapy for patients with advanced pancreatic cancer (PC) and a germline BRCA1 or BRCA2 pathogenic variant (PV).	olaparib	9-17	BRCA2 DNA repair associated	Homo sapiens	185-190
33970687-14	2021	CONCLUSION: Maintenance rucaparib is a safe and effective therapy for platinum-sensitive, advanced PC with a PV in BRCA1, BRCA2, or PALB2.	rucaparib	24-33	BRCA2 DNA repair associated	Homo sapiens	122-127
33771885-5	2021	Men who had progression-free survival of <=3 months despite enzalutamide/abiraterone treatment were more likely to have baseline CTC genomic loss of CHD1, PTEN, PHLPP1, and ZFHX3 and gains of BRCA2, KDM5D, MYCN, and SPARC.	abiraterone	73-84	BRCA2 DNA repair associated	Homo sapiens	192-197
33236159-11	2021	In HCT116 TP53-/- cells carrying BRCA2 pathogenic mutations, TP53 inactivating mutations were associated with lower sensitivity to olaparib in vitro.	olaparib	131-139	BRCA2 DNA repair associated	Homo sapiens	33-38
34906479-8	2022	BRCA1 p.(Cys64Arg) and BRCA2 p.(Trp2626Cys) were associated with particularly low risks of breast cancer compared with other PVs.	trp2626cys	32-42	BRCA2 DNA repair associated	Homo sapiens	23-28
32795228-11	2020	CONCLUSION: Rucaparib has antitumor activity in patients with mCRPC and a deleterious BRCA alteration, but with a manageable safety profile consistent with that reported in other solid tumor types.	rucaparib	12-21	BRCA2 DNA repair associated	Homo sapiens	86-90
34968781-3	2022	BRCA2 degradation reportedly requires ubiquitination of the C-terminal region; thus, fragments of amino acid (aa) residues 2241-2940 were produced and assayed for their degradation following cycloheximide (CHX) treatment.	Cycloheximide	191-204	BRCA2 DNA repair associated	Homo sapiens	0-5
34968781-3	2022	BRCA2 degradation reportedly requires ubiquitination of the C-terminal region; thus, fragments of amino acid (aa) residues 2241-2940 were produced and assayed for their degradation following cycloheximide (CHX) treatment.	Cycloheximide	206-209	BRCA2 DNA repair associated	Homo sapiens	0-5
34968781-4	2022	The results showed that aa 2491-2580 affected the degradation of BRCA2, especially lysine (Lys) 2497.	Lysine	83-89	BRCA2 DNA repair associated	Homo sapiens	65-70
34968781-4	2022	The results showed that aa 2491-2580 affected the degradation of BRCA2, especially lysine (Lys) 2497.	Lysine	91-94	BRCA2 DNA repair associated	Homo sapiens	65-70
32795228-0	2020	Rucaparib in Men With Metastatic Castration-Resistant Prostate Cancer Harboring a BRCA1 or BRCA2 Gene Alteration.	rucaparib	0-9	BRCA2 DNA repair associated	Homo sapiens	91-96
32795228-2	2020	We present results from patients with mCRPC associated with a BRCA alteration treated with rucaparib 600 mg twice daily in the phase II TRITON2 study.	rucaparib	91-100	BRCA2 DNA repair associated	Homo sapiens	62-66
32790492-7	2020	For patients with germline or somatic pathogenic or likely pathogenic variants in BRCA1 (g/sBRCA1) or BRCA2 (g/sBRCA2) genes should be treated with olaparib.	olaparib	148-156	BRCA2 DNA repair associated	Homo sapiens	102-107
34952473-4	2022	An expression plasmid was created to induce BRCA2 activation upon the addition of estradiol by introducing mutations to the binding sequences for the transcription factors USF1, E2F1, and NF-kappaB within the promoter region of BRCA2.	Estradiol	82-91	BRCA2 DNA repair associated	Homo sapiens	44-49
34952473-4	2022	An expression plasmid was created to induce BRCA2 activation upon the addition of estradiol by introducing mutations to the binding sequences for the transcription factors USF1, E2F1, and NF-kappaB within the promoter region of BRCA2.	Estradiol	82-91	BRCA2 DNA repair associated	Homo sapiens	228-233
34952473-5	2022	Then, the estrogen receptor (ER) sites of the proteins that interact with BRCA2 upon the addition of estradiol were identified.	Estradiol	101-110	BRCA2 DNA repair associated	Homo sapiens	74-79
34952473-6	2022	Both proteins were bound by the helical domain of BRCA2 and activation function-2 of the ER, suggesting that this binding may regulate the transcriptional activity of pS2, a target gene of the estradiol-ER, by suppressing the binding of SRC-1, a coactivator required for activation of the transcription factor.	Estradiol	193-202	BRCA2 DNA repair associated	Homo sapiens	50-55
34873471-5	2021	Interestingly, BR101801 inhibited not only phosphorylation of DNA-PK catalytic subunit in NHEJ factors but also BRCA2 protein level in homologous recombination (HR) factors.	br101801	15-23	BRCA2 DNA repair associated	Homo sapiens	112-117
34598946-1	2021	PURPOSE: The poly(ADP-ribose) polymerase (PARP) inhibitor rucaparib is approved in the US for patients with metastatic castration-resistant prostate cancer (mCRPC) and a deleterious germline and/or somatic BRCA1 or BRCA2 (BRCA) alteration.	rucaparib	58-67	BRCA2 DNA repair associated	Homo sapiens	215-220
34598946-1	2021	PURPOSE: The poly(ADP-ribose) polymerase (PARP) inhibitor rucaparib is approved in the US for patients with metastatic castration-resistant prostate cancer (mCRPC) and a deleterious germline and/or somatic BRCA1 or BRCA2 (BRCA) alteration.	rucaparib	58-67	BRCA2 DNA repair associated	Homo sapiens	222-226
34598946-10	2021	CONCLUSION: Plasma, tissue, and local testing of mCRPC patients can be used to identify men with BRCA+ mCRPC who can benefit from treatment with the PARP inhibitor rucaparib.	rucaparib	164-173	BRCA2 DNA repair associated	Homo sapiens	97-101
34812730-1	2022	Olaparib is the first Health Canadaapproved agent in metastatic prostate cancer to use a companion diagnostic to identify alterations in BRCA1, BRCA2, or ATM.	olaparib	0-8	BRCA2 DNA repair associated	Homo sapiens	144-149
34871431-3	2021	We found that loss of MED12 confers resistance to cisplatin and PARP inhibitors in both BRCA1- and BRCA2-deficient cells, which is associated with restoration of both homologous recombination and replication fork stability.	Cisplatin	50-59	BRCA2 DNA repair associated	Homo sapiens	99-104
34598946-0	2021	Response to rucaparib in BRCA-mutant metastatic castration-resistant prostate cancer identified by genomic testing in the TRITON2 study.	rucaparib	12-21	BRCA2 DNA repair associated	Homo sapiens	25-29
34900718-7	2021	Recently, a new class of molecules has emerged as a standard of care for patients with triple negative breast cancer and germline BRCA1 or BRCA2 mutation: poly (ADP-ribose) (PARP) inhibitors.	Poly Adenosine Diphosphate Ribose	155-172	BRCA2 DNA repair associated	Homo sapiens	139-144
34750509-3	2021	In order to assess whether other genes implicated in NAD+ metabolism were synthetic lethal with BRCA1 or BRCA2 gene defects, we carried out a genetic screen, which identified a synthetic lethality between BRCA1 and genetic inhibition of either of two sirtuin (SIRT) enzymes, SIRT1 or SIRT6.	NAD	53-57	BRCA2 DNA repair associated	Homo sapiens	105-110
34767113-7	2021	PBM&PBSO were found to be most cost-effective and dominated all other strategies in women with a BRCA1 or BRCA2 mutation.	pbm	0-3	BRCA2 DNA repair associated	Homo sapiens	106-111
34309473-3	2021	Based on the results of the EMBRACA trial, talazoparib was approved for the treatment of patients with advanced germline BRCA1/2 mutant breast cancer.	talazoparib	43-54	BRCA2 DNA repair associated	Homo sapiens	121-128
34904808-2	2021	Rucaparib was approved for tumors that harbor alterations in BRCA1 and BRCA2 following progression on chemotherapy and androgen receptor-directed therapy, whereas olaparib was approved for tumors that harbor alterations in a broader range of DNA damage repair genes following progression on androgen receptor-directed therapy.	rucaparib	0-9	BRCA2 DNA repair associated	Homo sapiens	71-76
34419699-4	2021	In particular, sensitivity characterized cells harboring mutations in the hereditary breast/ovarian cancer genes, BRCA1 or BRCA2, that function in the repair of DSBs by homologous recombination (HR).	1,2-di-(4-sulfamidophenyl)-4-butylpyrazolidine-3,5-dione	161-165	BRCA2 DNA repair associated	Homo sapiens	123-128
34778033-1	2021	Background: BRCA2 mutation has a more substantial impact on the homologous recombination and superior therapeutic response to platinum-based chemotherapy than BRCA1 mutation.	Platinum	126-134	BRCA2 DNA repair associated	Homo sapiens	12-17
34309133-0	2021	Rapid progression of metastatic pancreatic adenocarcinoma during platinum-based therapy in a patient harboring a pathogenic BRCA2 germline variant.	Platinum	65-73	BRCA2 DNA repair associated	Homo sapiens	124-129
34309133-5	2021	(3, 4) In contrast, platinum-based therapies would be predicted to be significantly less effective for PDACs in patients with pathogenic BRCA germline variants who have cancers which lack BRCA LOH.	Platinum	20-28	BRCA2 DNA repair associated	Homo sapiens	137-141
34309133-5	2021	(3, 4) In contrast, platinum-based therapies would be predicted to be significantly less effective for PDACs in patients with pathogenic BRCA germline variants who have cancers which lack BRCA LOH.	Platinum	20-28	BRCA2 DNA repair associated	Homo sapiens	188-192
34309133-9	2021	Here, we present a patient harboring a pathogenic BRCA germline variant whose PDAC grew rapidly during platinum-based therapy and lacked BRCA LOH and therefore was not likely BRCA-related.	Platinum	103-111	BRCA2 DNA repair associated	Homo sapiens	50-54
34309133-10	2021	Given the molecular fingerprint of BRCA-related PDAC in patients with pathogenic BRCA germline variants and the mechanism of action of platinum-based therapies and PARP inhibitors, this case underscores the importance of future studies aimed at determining whether the lack of BRCA LOH in PDACs in pathogenic BRCA germline variant carriers is a biomarker of less responsiveness to platinum-based chemotherapy and PARP inhibitors.	Platinum	381-389	BRCA2 DNA repair associated	Homo sapiens	35-39
34697207-6	2021	The use of platinum-based chemotherapy, to which heterozygous BRCA2 carriers are known to respond, may have had a beneficial anticancer effect, but caution is advised given its extreme immediate toxicity at standard dosing.	Platinum	11-19	BRCA2 DNA repair associated	Homo sapiens	62-67
34658299-0	2021	Prognostic Prediction of BRCA Mutations by 18F-FDG PET/CT SUVmax in Breast Cancer Objectives: This study aimed to investigate the prognostic prediction of germline BRCA1 and BRCA2 mutations by comparing the maximum standardized uptake value (SUVmax) obtained from 18fluoride-fluorodeoxyglucose positron emission tomography/computed tomography (18F-FDG PET/CT), which is considered a prognostic factor in breast cancer (BC).	Fluorodeoxyglucose F18	43-50	BRCA2 DNA repair associated	Homo sapiens	174-179
34658299-0	2021	Prognostic Prediction of BRCA Mutations by 18F-FDG PET/CT SUVmax in Breast Cancer Objectives: This study aimed to investigate the prognostic prediction of germline BRCA1 and BRCA2 mutations by comparing the maximum standardized uptake value (SUVmax) obtained from 18fluoride-fluorodeoxyglucose positron emission tomography/computed tomography (18F-FDG PET/CT), which is considered a prognostic factor in breast cancer (BC).	18fluoride-fluorodeoxyglucose	264-293	BRCA2 DNA repair associated	Homo sapiens	174-179
34658299-0	2021	Prognostic Prediction of BRCA Mutations by 18F-FDG PET/CT SUVmax in Breast Cancer Objectives: This study aimed to investigate the prognostic prediction of germline BRCA1 and BRCA2 mutations by comparing the maximum standardized uptake value (SUVmax) obtained from 18fluoride-fluorodeoxyglucose positron emission tomography/computed tomography (18F-FDG PET/CT), which is considered a prognostic factor in breast cancer (BC).	Fluorodeoxyglucose F18	344-351	BRCA2 DNA repair associated	Homo sapiens	174-179
34309473-0	2021	Development of the PARP inhibitor talazoparib for the treatment of advanced BRCA1 and BRCA2 mutated breast cancer.	talazoparib	34-45	BRCA2 DNA repair associated	Homo sapiens	86-91
34309473-6	2021	EXPERT OPINION: Talazoparib has been a major advance in the treatment of germline BRCA1/2 mutation breast cancer with both clinical efficacy and improvement in quality of life compared to standard cytotoxic chemotherapy.	talazoparib	16-27	BRCA2 DNA repair associated	Homo sapiens	82-89
34572083-3	2021	The aim of this study is to assess the effects of the PARPi rucaparib in vitro using cell lines with BRCA2 mutations in comparison to those with BRCA2 wild type.	rucaparib	60-69	BRCA2 DNA repair associated	Homo sapiens	101-106
34616022-3	2021	We show that DNA polymerase theta (POLtheta)-mediated end joining (TMEJ) repairs DSBs arising during the S phase in BRCA2-deficient cells only after the onset of the ensuing mitosis.	dsbs	81-85	BRCA2 DNA repair associated	Homo sapiens	116-121
34593815-4	2021	Here, we delineate a pathway where ATM and ATR kinases phosphorylate a highly conserved region in BRCA2 in response to DSBs.	dsbs	119-123	BRCA2 DNA repair associated	Homo sapiens	98-103
34657048-5	2021	Alterations in different DNA damage repair genes, including BRCA2, ATM, CDK12, or mismatch repair genes, are linked to favorable response to targeted therapies such as poly(adenosine diphosphate-ribose)polymerase(PARP)inhibitors or immune checkpoint inhibitors.	Adenosine	173-182	BRCA2 DNA repair associated	Homo sapiens	60-65
34572083-5	2021	RESULTS: The BRCA2 mutant ovarian cancer cell line PEO1 exhibited higher PARP1 activity when treated with H2O2 compared to wild type cell lines.	Hydrogen Peroxide	106-110	BRCA2 DNA repair associated	Homo sapiens	13-18
34302857-2	2021	We aimed to clarify whether BRCA2 BRC domain-associated mutation correlates with sensibility of platinum-based chemotherapy and survival in high-grade serous ovarian cancer(HGSOC).	Platinum	96-104	BRCA2 DNA repair associated	Homo sapiens	28-33
34616818-0	2021	Successful treatment of refractory lung adenocarcinoma harboring a germline BRCA2 mutation with olaparib: A case report.	olaparib	96-104	BRCA2 DNA repair associated	Homo sapiens	76-81
34616818-10	2021	CONCLUSION: This is a rare case of lung adenocarcinoma in a patient with a BRCA2 germline mutation who had long-term benefit from olaparib combination treatment, suggesting that NGS-based genetic testing may render the possibility of long-term survival in NSCLC patients after disease progression.	olaparib	130-138	BRCA2 DNA repair associated	Homo sapiens	75-80
34734039-0	2021	Olaparib effectively treats local recurrence of extrahepatic cholangiocarcinoma in a patient harboring a BRCA2-inactivating mutation: a case report.	olaparib	0-8	BRCA2 DNA repair associated	Homo sapiens	105-110
34734039-3	2021	In this study, we report a case of a postoperative recurrence ECC patient harboring a breast cancer 2 (BRCA2)-inactivating rearrangement mutation that had an obvious reaction to olaparib therapy.	olaparib	178-186	BRCA2 DNA repair associated	Homo sapiens	86-101
34734039-3	2021	In this study, we report a case of a postoperative recurrence ECC patient harboring a breast cancer 2 (BRCA2)-inactivating rearrangement mutation that had an obvious reaction to olaparib therapy.	olaparib	178-186	BRCA2 DNA repair associated	Homo sapiens	103-108
34734039-11	2021	This is the first report demonstrating the clinical benefits of olaparib in a BRCA2 rearrangement-harboring patient with ECC.	olaparib	64-72	BRCA2 DNA repair associated	Homo sapiens	78-83
34302857-6	2021	CONCLUSIONS: Somatic mutations in BRCA2 BRC domain confer a higher sensitivity to platinum-based therapy and are associated with a favourable survival in HGSOC.	Platinum	82-90	BRCA2 DNA repair associated	Homo sapiens	34-39
34425813-0	2021	A novel germline BRCA2 mutation in a Chinese patient with prostate cancer sensitive to platinum chemotherapy: a case report.	Platinum	87-95	BRCA2 DNA repair associated	Homo sapiens	17-22
34761636-0	2021	Some subgroups might get less benefit from adjuvant olaparib trial in high-risk, HER2-negative and germline BRCA2 BRCA1- or BRCA2-mutated early breast cancer patients.	olaparib	52-60	BRCA2 DNA repair associated	Homo sapiens	108-113
34761636-0	2021	Some subgroups might get less benefit from adjuvant olaparib trial in high-risk, HER2-negative and germline BRCA2 BRCA1- or BRCA2-mutated early breast cancer patients.	olaparib	52-60	BRCA2 DNA repair associated	Homo sapiens	124-129
34425813-8	2021	CONCLUSIONS: This case demonstrated that the carboplatin could have a dramatic antitumor effect on patients with prostate cancer with germline BRCA2 mutations and family history will help to ensure that patients and their families can be provided with proper genetic counseling.	Carboplatin	45-56	BRCA2 DNA repair associated	Homo sapiens	143-148
34445211-1	2021	Several poly (adenosine diphosphate-ribose) polymerase (PARP) inhibitors are now in clinical use for tumours with defects in BReast CAncer genes BRCA1 or BRCA2 that result in deficient homologous recombination repair (HRR).	Adenosine	14-23	BRCA2 DNA repair associated	Homo sapiens	154-159
34081848-0	2021	Adjuvant Olaparib for Patients with BRCA1- or BRCA2-Mutated Breast Cancer.	olaparib	9-17	BRCA2 DNA repair associated	Homo sapiens	46-51
34602949-8	2021	In this rare case, more patient studies are needed to determine the contribution of DH in BRCA2 and ATM genes to the phenotype.	2-(3,5-dihydroxyphenyl)-6-hydroxybenzothiazole	84-86	BRCA2 DNA repair associated	Homo sapiens	90-95
34367977-1	2021	Poly-(ADP)-ribose polymerase inhibitors (PARPi) and platinum-based drugs are promising therapies for triple negative breast cancers (TNBC) with BRCA1 or BRCA2 loss.	Platinum	52-60	BRCA2 DNA repair associated	Homo sapiens	153-158
34234458-0	2021	Remarkable Response to Olaparib in a Patient with Combined Hepatocellular-Cholangiocarcinoma Harboring a Biallelic BRCA2 Mutation.	olaparib	23-31	BRCA2 DNA repair associated	Homo sapiens	115-120
34234458-7	2021	Our experience indicates that BRCA2 mutations could be a potential therapeutic target for patients with cHCC-CC.	chcc-cc	104-111	BRCA2 DNA repair associated	Homo sapiens	30-35
34348152-4	2021	In BRCA2-deficient cells, intracellular reactive oxygen species (ROS) are elevated, and ROS scavengers suppress the mtDNA defects.	Reactive Oxygen Species	40-63	BRCA2 DNA repair associated	Homo sapiens	3-8
34348152-4	2021	In BRCA2-deficient cells, intracellular reactive oxygen species (ROS) are elevated, and ROS scavengers suppress the mtDNA defects.	Reactive Oxygen Species	65-68	BRCA2 DNA repair associated	Homo sapiens	3-8
34348152-4	2021	In BRCA2-deficient cells, intracellular reactive oxygen species (ROS) are elevated, and ROS scavengers suppress the mtDNA defects.	Reactive Oxygen Species	88-91	BRCA2 DNA repair associated	Homo sapiens	3-8
34517749-1	2021	Aim: To compare the cost-effectiveness of olaparib versus control treatment in metastatic castration-resistant prostate cancer patients with at least one gene mutation in BRCA1, BRCA2 or ATM from the US payer perspective.	olaparib	42-50	BRCA2 DNA repair associated	Homo sapiens	178-183
34367927-4	2021	This platinum/PARPi cross-resistance mechanism applies both for BRCA1 and BRCA2 genes and has been repeatedly validated in various laboratory models and multiple clinical studies.	Platinum	5-13	BRCA2 DNA repair associated	Homo sapiens	74-79
34081848-11	2021	CONCLUSIONS: Among patients with high-risk, HER2-negative early breast cancer and germline BRCA1 or BRCA2 pathogenic or likely pathogenic variants, adjuvant olaparib after completion of local treatment and neoadjuvant or adjuvant chemotherapy was associated with significantly longer survival free of invasive or distant disease than was placebo.	olaparib	157-165	BRCA2 DNA repair associated	Homo sapiens	100-105
34206543-9	2021	KPT-8602 with or without olaparib was shown to reduce homologous recombination-regulated DNA damage response targets including BRCA1, BRCA2, CHEK1, EXO1, BLM, RAD51, LIG1, XRCC3 and RMI2.	olaparib	25-33	BRCA2 DNA repair associated	Homo sapiens	134-139
34071148-7	2021	A prospective cohort study showed that RRSO reduced all-cause mortality in both pre- and postmenopausal women; however, RRSO significantly reduced the risk of breast cancer for BRCA2 pathogenic variant carriers, but not for BRCA1 pathogenic variant carriers.	rrso	39-43	BRCA2 DNA repair associated	Homo sapiens	177-182
34148027-0	2021	Efficacy of carboplatin chemotherapy in a metastatic, castration-resistant BRCA2 mutation positive prostate cancer patient Osszefoglalo.	Carboplatin	12-23	BRCA2 DNA repair associated	Homo sapiens	75-80
34148027-12	2021	Here we present a case of BRCA2 mutant prostate cancer, which was diagnosed at a metastatic stage and showed no or only little response to androgen deprivation and docetaxel therapies.	Docetaxel	164-173	BRCA2 DNA repair associated	Homo sapiens	26-31
34086042-15	2021	Multiclonal BRCA2 reversion mutations associated with resistance to PARP inhibitors and platinum chemotherapy were detected in ctDNA from 2 patients.	Platinum	88-96	BRCA2 DNA repair associated	Homo sapiens	12-17
34091215-10	2021	However, PC arising in BRCA-2 carriers has a DNA repair defect, which is sensitive to platin based chemotherapy and mitomycin C.	Platinum	86-92	BRCA2 DNA repair associated	Homo sapiens	23-29
34091215-10	2021	However, PC arising in BRCA-2 carriers has a DNA repair defect, which is sensitive to platin based chemotherapy and mitomycin C.	Mitomycin	116-127	BRCA2 DNA repair associated	Homo sapiens	23-29
34140467-3	2021	In addition, ART558 elicits DNA damage and synthetic lethality in BRCA1- or BRCA2-mutant tumour cells and enhances the effects of a PARP inhibitor.	ART558	13-19	BRCA2 DNA repair associated	Homo sapiens	76-81
34071148-7	2021	A prospective cohort study showed that RRSO reduced all-cause mortality in both pre- and postmenopausal women; however, RRSO significantly reduced the risk of breast cancer for BRCA2 pathogenic variant carriers, but not for BRCA1 pathogenic variant carriers.	rrso	120-124	BRCA2 DNA repair associated	Homo sapiens	177-182
34258530-0	2021	Prominent response to platinum-based chemotherapy in a patient with BRCA2 mutant-neuroendocrine prostate cancer and MDM2 amplification.	Platinum	22-30	BRCA2 DNA repair associated	Homo sapiens	68-73
34123730-0	2021	Effect of cisplatin on metastatic castration-resistant prostate cancer with BRCA2 mutation: A case report.	Cisplatin	10-19	BRCA2 DNA repair associated	Homo sapiens	76-81
34123730-3	2021	We administered 80 mg/m2 cisplatin triweekly to a patient with metastatic castration-resistant PCa (mCRPC) with the BRCA2 mutation, and after ten cycles, the prostate-specific antigen was dramatically decreased.	Cisplatin	25-34	BRCA2 DNA repair associated	Homo sapiens	116-121
34123730-4	2021	We suggest that BRCA2 mutations may indicate the use of cisplatin for treating patients with mCRPC.	Cisplatin	56-65	BRCA2 DNA repair associated	Homo sapiens	16-21
35425960-4	2022	Laboratory models from BRCA1/BRCA2-associated breast cancer, HGSOC, and PaC were developed and evaluated for their response to PARPi and cisplatin.	Cisplatin	137-146	BRCA2 DNA repair associated	Homo sapiens	29-34
34258531-0	2021	Editorial Comment to Prominent response to platinum-based chemotherapy in a patient with BRCA2 mutant-neuroendocrine prostate cancer and MDM2 amplification.	Platinum	43-51	BRCA2 DNA repair associated	Homo sapiens	89-94
34700141-1	2021	Cancers with mutations in BRCA2 have defective DNA repair capacity which is potentially targetable with poly-ADP(ribose) polymera se (PARP) inhibitors such as olaparib and rucaparib.	Poly Adenosine Diphosphate Ribose	104-120	BRCA2 DNA repair associated	Homo sapiens	26-31
34700141-1	2021	Cancers with mutations in BRCA2 have defective DNA repair capacity which is potentially targetable with poly-ADP(ribose) polymera se (PARP) inhibitors such as olaparib and rucaparib.	olaparib	159-167	BRCA2 DNA repair associated	Homo sapiens	26-31
34700141-1	2021	Cancers with mutations in BRCA2 have defective DNA repair capacity which is potentially targetable with poly-ADP(ribose) polymera se (PARP) inhibitors such as olaparib and rucaparib.	rucaparib	172-181	BRCA2 DNA repair associated	Homo sapiens	26-31
35435472-0	2022	A phase 1 and pharmacodynamic study of chronically-dosed, single-agent veliparib (ABT-888) in patients with BRCA1- or BRCA2-mutated cancer or platinum-refractory ovarian or triple-negative breast cancer.	veliparib	71-80	BRCA2 DNA repair associated	Homo sapiens	118-123
35001340-13	2022	In xenograft mice model, tumor volume in Olaparib and Olaparib/shBRCA2 group was 376.12 and 84.95mm3 when tumor weight was 0.46 g and 0.12 g. In addition, the level of RAD51, RAD50, MRE11, and NBS was increased by Olaparib alone but decreased reversely after knockdown of BRCA2 in Daoy cells.	olaparib	41-49	BRCA2 DNA repair associated	Homo sapiens	272-277
35001340-13	2022	In xenograft mice model, tumor volume in Olaparib and Olaparib/shBRCA2 group was 376.12 and 84.95mm3 when tumor weight was 0.46 g and 0.12 g. In addition, the level of RAD51, RAD50, MRE11, and NBS was increased by Olaparib alone but decreased reversely after knockdown of BRCA2 in Daoy cells.	olaparib	54-62	BRCA2 DNA repair associated	Homo sapiens	272-277
35001340-14	2022	CONCLUSIONS: Knockdown of BRCA2 increases the sensitivity of medulloblastoma cells to Olaparib and strengthens the efficacy of Olaparib in vitro and in vivo.	olaparib	86-94	BRCA2 DNA repair associated	Homo sapiens	26-31
35001340-14	2022	CONCLUSIONS: Knockdown of BRCA2 increases the sensitivity of medulloblastoma cells to Olaparib and strengthens the efficacy of Olaparib in vitro and in vivo.	olaparib	127-135	BRCA2 DNA repair associated	Homo sapiens	26-31
35001340-0	2022	BRCA2 deficiency increases sensitivity of medulloblastoma to Olaparib by inhibiting RAD51-mediated DNA damage repair system.	olaparib	61-69	BRCA2 DNA repair associated	Homo sapiens	0-5
35001340-7	2022	RESULTS: Knockdown of BRCA2 enhanced the inhibitory effect of Olaparib on proliferation of Daoy and LN229 cells.	olaparib	62-70	BRCA2 DNA repair associated	Homo sapiens	22-27
35611209-9	2022	Two identified reverse missense mutations in partner and localizer of BRCA2 (PALB2) may have recovered the reading frame, restoring function of the primary germline PALB2 mutation and causing resistance to the PARP inhibitor olaparib.	olaparib	225-233	BRCA2 DNA repair associated	Homo sapiens	70-75
35495117-3	2022	Taking advantage of a library of rare tripeptides, which we first tested for their in vitro binding affinity to SMYD3 and then used as in silico probes, we recently identified BRCA2, ATM, and CHK2 as direct SMYD3 interactors.	tripeptides	38-49	BRCA2 DNA repair associated	Homo sapiens	176-181
35448200-7	2022	PFS of first exposure to taxanes was 8.1 months in mutated patients and 5.7 months in non-mutated patients (p = 0.32) and significantly longer among patients with ATM/BRCA1/BRCA2 mutations compared to the others (10.6 months vs. 5.5 months, p = 0.04).	Taxoids	25-32	BRCA2 DNA repair associated	Homo sapiens	173-178
35048954-9	2022	CONCLUSION: While COCP use in BRCA1 and BRCA2 mutation carriers initially increases breast/ovarian/endometrial cancer risk, it strongly decreases lifetime cancer risk.	cocp	18-22	BRCA2 DNA repair associated	Homo sapiens	40-45
35267488-8	2022	In preclinical studies and several case series, poly(adenosine diphosphate-ribose)polymerase inhibitors showed antitumor effects on uLMS cell lines with BRCA2 mutations or HRD and in recurrent or persistent cases of uLMS with BRCA2 mutations.	Adenosine	53-62	BRCA2 DNA repair associated	Homo sapiens	153-158
35385581-6	2022	We find that templated insertions (TINS) consistent with TMEJ repair are highly specific to tumors with pathogenic bi-allelic mutations in BRCA2 and that high TINS genomic signature content in advanced ovarian cancers associate with overall survival following treatment with platinum agents.	Platinum	275-283	BRCA2 DNA repair associated	Homo sapiens	139-144
35149083-5	2022	Furthermore, ethanol treatment was also found to promote HCC progression by markedly activating oncogenes (RAS, MYC, MET, and HER2), while remarkably suppressing tumor suppressor genes (BRCA2 and APC).	Ethanol	13-20	BRCA2 DNA repair associated	Homo sapiens	186-191
35399625-5	2022	After thioridazine treatment, levels of glutathione, and BRCA2, RAD51, and ERCC1 proteins were decreased.	Thioridazine	6-18	BRCA2 DNA repair associated	Homo sapiens	57-62
35324529-0	2022	Rapid and durable response to fifth-line lorlatinib plus olaparib in an ALK-rearranged, BRCA2-mutated metastatic lung adenocarcinoma patient with critical tracheal stenosis: a case report.	olaparib	57-65	BRCA2 DNA repair associated	Homo sapiens	88-93
35078817-10	2022	In a BRCA2-mutant patient-derived triple-negative breast cancer (TNBC) xenograft model, complete tumor regression was achieved with 3-5 days of daily AZD6738 per week concurrent with olaparib.	ceralasertib	150-157	BRCA2 DNA repair associated	Homo sapiens	5-10
35078817-10	2022	In a BRCA2-mutant patient-derived triple-negative breast cancer (TNBC) xenograft model, complete tumor regression was achieved with 3-5 days of daily AZD6738 per week concurrent with olaparib.	olaparib	183-191	BRCA2 DNA repair associated	Homo sapiens	5-10
35107878-5	2022	Pyridostatin is a small molecule that binds G4s and is specifically toxic to BRCA1/2-deficient cells in vitro.	pyridostatin	0-12	BRCA2 DNA repair associated	Homo sapiens	77-84
35107878-7	2022	Here, we demonstrate that pyridostatin exhibits a high specific activity against BRCA1/2-deficient tumours, including patient-derived xenograft tumours that have acquired PARP inhibitor (PARPi) resistance.	pyridostatin	26-38	BRCA2 DNA repair associated	Homo sapiens	81-88
35107878-9	2022	Consistent with this, chemical inhibitors of DNA-PKcs, a core component of C-NHEJ kinase activity, act synergistically with pyridostatin in eliminating BRCA1/2-deficient cells and tumours.	pyridostatin	124-136	BRCA2 DNA repair associated	Homo sapiens	152-159
35107878-10	2022	Furthermore, we demonstrate that pyridostatin triggers cGAS/STING-dependent innate immune responses when BRCA1 or BRCA2 is abrogated.	pyridostatin	33-45	BRCA2 DNA repair associated	Homo sapiens	114-119
35107878-12	2022	Overall, our results demonstrate that pyridostatin is a compound suitable for further therapeutic development, alone or in combination with paclitaxel and DNA-PKcs inhibitors, for the benefit of cancer patients carrying BRCA1/2 mutations.	pyridostatin	38-50	BRCA2 DNA repair associated	Homo sapiens	220-227
35409418-4	2022	Surprisingly, BRCA2 CTRBD expression in HeLa cells increased their resistance to X-ray irradiation and mitomycin C.	Mitomycin	103-114	BRCA2 DNA repair associated	Homo sapiens	14-19
35409418-8	2022	To the best of our knowledge, our study is the first to report the ability of the BRCA2 functional domain to confer resistance to X-ray irradiation and mitomycin C treatment by increased homologous recombination efficiency.	Mitomycin	152-163	BRCA2 DNA repair associated	Homo sapiens	82-87
35442721-0	2022	Common Variant in ALDH2 Modifies the Risk of Breast Cancer Among Carriers of the p.K3326* Variant in BRCA2.	k3326	83-88	BRCA2 DNA repair associated	Homo sapiens	101-106
35442721-2	2022	Aldehydes that accumulate in cells under insufficient aldehyde oxidation were most recently shown to trigger carcinogenesis by promoting depletion of BRCA2 protein.	Aldehydes	0-9	BRCA2 DNA repair associated	Homo sapiens	150-155
35442721-2	2022	Aldehydes that accumulate in cells under insufficient aldehyde oxidation were most recently shown to trigger carcinogenesis by promoting depletion of BRCA2 protein.	Aldehydes	54-62	BRCA2 DNA repair associated	Homo sapiens	150-155
35442721-4	2022	We hypothesized that this allele could modify breast cancer risk in women with the BRCA2 p.K3326* low-penetrance variant through reduced function of ALDH2, increased accumulation of cellular aldehydes, and depletion of BRCA2 protein.	k3326	91-96	BRCA2 DNA repair associated	Homo sapiens	83-88
35442721-4	2022	We hypothesized that this allele could modify breast cancer risk in women with the BRCA2 p.K3326* low-penetrance variant through reduced function of ALDH2, increased accumulation of cellular aldehydes, and depletion of BRCA2 protein.	k3326	91-96	BRCA2 DNA repair associated	Homo sapiens	219-224
35442721-4	2022	We hypothesized that this allele could modify breast cancer risk in women with the BRCA2 p.K3326* low-penetrance variant through reduced function of ALDH2, increased accumulation of cellular aldehydes, and depletion of BRCA2 protein.	Aldehydes	191-200	BRCA2 DNA repair associated	Homo sapiens	83-88
35267488-8	2022	In preclinical studies and several case series, poly(adenosine diphosphate-ribose)polymerase inhibitors showed antitumor effects on uLMS cell lines with BRCA2 mutations or HRD and in recurrent or persistent cases of uLMS with BRCA2 mutations.	Adenosine	53-62	BRCA2 DNA repair associated	Homo sapiens	226-231
35200549-0	2022	An Unexpected Tumor Reduction: Treatment with Olaparib Monotherapy in Heavily Pretreated BRCA2 Mutated Metastatic Pancreatic Cancer.	olaparib	46-54	BRCA2 DNA repair associated	Homo sapiens	89-94
35210863-1	2022	Purpose: The US Food and Drug Administration has recently granted accelerated approval of the poly(ADP-ribose) polymerase (PARP) inhibitor rucaparib as treatment for men with metastatic castration-resistant prostate cancer (mCRPC) associated with a deleterious germline or somatic BRCA1 or BRCA2 (BRCA) alteration.	rucaparib	139-148	BRCA2 DNA repair associated	Homo sapiens	290-295
35051747-2	2022	Until now, PARP inhibitors like olaparib are the first successful case of utilizing synthetic lethality-based therapy to treat cancers with DNA-repairing deficiency (e.g. BRCA1 or BRCA2 mutation), which has fueled the search for more targetable components in the DDR signaling pathway by exploiting synthetic lethality, including but not limited to DNA-PK, ATR, ATM, CHK1, and WEE1.	olaparib	32-40	BRCA2 DNA repair associated	Homo sapiens	180-185
35169388-5	2022	When neoadjuvant therapy has failed to achieve the desired remission in BRCA1 and BRCA2 mutations, the administration of the PARP inhibitor olaparib has demonstrated an impressive response.	olaparib	140-148	BRCA2 DNA repair associated	Homo sapiens	82-87
35400012-0	2022	Complete Response of a Mutated BRCA2 Metastatic Clear Cell Endometrial Adenocarcinoma to the Poly (ADP ribose) Polymerase (PARP) Inhibitor Olaparib.	olaparib	139-147	BRCA2 DNA repair associated	Homo sapiens	31-36
35400012-7	2022	Case Report: We here present the case report of an 81-year-old woman with a mutated BRCA2 metastatic clear cell endometrial adenocarcinoma that showed an excellent clinical and radiological response to the PARP inhibitor olaparib.	olaparib	221-229	BRCA2 DNA repair associated	Homo sapiens	84-89
34387603-0	2022	Response to olaparib in metastatic lung adenocarcinoma with germline BRCA2 mutation: a case report.	olaparib	12-20	BRCA2 DNA repair associated	Homo sapiens	69-74
34387603-3	2022	Here, we report a case of a germline BRCA2-mutated metastatic lung adenocarcinoma, non-small-cell lung cancer, responded well to olaparib.	olaparib	129-137	BRCA2 DNA repair associated	Homo sapiens	37-42
34387603-6	2022	As disease progression was confirmed and the presence of germline BRCA2 mutation, the combinational treatment of olaparib/anlotinib was applied to achieve partial response 1 month later, and the progression-free survival was extended for another 5 months.	olaparib	113-121	BRCA2 DNA repair associated	Homo sapiens	66-71
34387603-7	2022	This study shows metastatic lung adenocarcinoma with BRCA2 mutation could also respond well to PARP inhibitor, broadening the spectrum of BRCA-mutated cancers suitable for olaparib therapy.	olaparib	172-180	BRCA2 DNA repair associated	Homo sapiens	53-58
35005470-0	2022	First successful case of platinum-based chemotherapy for neuroendocrine prostate cancer with BRCA2 and PTEN alterations.	Platinum	25-33	BRCA2 DNA repair associated	Homo sapiens	93-98
35005470-2	2022	Case presentation: We report the case of a Japanese patient with advanced castration-resistant prostate cancer who exhibited a prominent response to platinum therapy and had coexisting BRCA2 and PTEN mutations according to retrospective multigene panel analysis.	Platinum	149-157	BRCA2 DNA repair associated	Homo sapiens	185-190