ライフサイエンスコーパス: BRCA

1 BRCA genetic testing has substantial public health impac

2 BRCA mutation carriers are at increased risk of developi

3 BRCA mutation status has a major influence on survival i

4 BRCA mutation status was known for 107 patients (either

5 BRCA mutations are associated with poor survival outcome

6 BRCA mutations were prevalent in the largest study of Hi

7 BRCA status was known for 131 (96%) patients in the olap

8 BRCA testing is recommended for young women diagnosed as

9 BRCA(1/2) deficiency, defined as BRCA(1/2) mutations or

10 BRCA(1/2) mutations were associated with improved progre

11 BRCA(1/2) mutations were particularly common (23%) in hi

12 BRCA(1/2) somatic and germline mutations and expression

13 BRCA(1/2) transcript levels were assessed by quantitativ

14 BRCA-deficient status predisposing to RAD52-dependent sy

15 3%) of 23 BRCA2 carriers and 53 (22%) of 237 BRCA noncarriers (P < .001).

16 mutations or expression loss (in 24 [13.3%] BRCA(1/2)-wild-type cancers), was present in 67 ovarian

17 ng women who test positive vs negative for a BRCA mutation.

18 ined retrospectively): 41 (38%) of 107 had a BRCA mutation (20 in the olaparib plus chemotherapy grou

19 33 (16%) had a BRCA mutation.

20 in recurrent ovarian carcinoma harbouring a BRCA mutation or high percentage of genome-wide loss of

21 ata, these results point to a breakdown in a BRCA/FA-mSWI/SNF-DeltaNP63-mediated DNA repair and diffe

22 (n = 66), exploratory analyses showed that a BRCA-like genomic instability signature (n = 32) discrim

23 One patient was a BRCA mutation carrier and was excluded.

24 -oophorectomy is recommended to women with a BRCA mutation at age 35 years or thereafter to prevent b

25 itive recurrent serous ovarian cancer with a BRCA mutation have the greatest likelihood of benefiting

26 Of patients with a BRCA mutation, median PFS was significantly longer in th

27 ion in PFS, particularly, in patients with a BRCA mutation.

28 ib is most likely to benefit patients with a BRCA mutation.

29 progression-free survival in patients with a BRCA-mutant carcinoma was 16.6 months (95% CI 13.4-22.9;

30 ived it demonstrated greater knowledge about BRCA (mean score difference adjusted for demographics an

31 x stabilizer, with specific toxicity against BRCA deficiencies in cancer cells and polyclonal patient

32 The American BRCA Outcomes and Utilization of Testing (ABOUT) Study a

33 on the basis of tumour mutational analysis: BRCA mutant (deleterious germline or somatic), BRCA wild

34 cer cohort, and one-to-one matching (age and BRCA status) of each woman with breast cancer to a contr

35 a pivotal protein in the Fanconi anemia and BRCA pathway/network, is monoubiquitylated in the nucleu

36 Group 1-2), preoperative disease burden, and BRCA status.

37 score, family history of breast cancer, and BRCA mutations.

38 NA-PK-deficient quiescent leukemia cells and BRCA/DNA-PK-deficient proliferating leukemia cells were

39 oard-approved registry and received GCRA and BRCA testing within a consortium of 14 clinics.

40 ses, in vivo in unfavorable AML subtypes and BRCA wild-type breast cancer cells.

41 y commonly referred to as the Fanconi anemia-BRCA pathway.

42 The Fanconi anemia/BRCA (FA/BRCA) pathway is a DNA repair pathway that is r

43 VB, UVA does not activate the Fanconi anemia/BRCA DNA damage response pathway or the "recombinase" RA

44 ndent regulatory point in the Fanconi anemia/BRCA DSB/ICL repair pathway, illuminate the role of BRCA

45 es the genomic instability of Fanconi Anemia/BRCA pathway-deficient cells.

46 BRCA(1/2) deficiency, defined as BRCA(1/2) mutations or expression loss (in 24 [13.3%] BR

47 Tumours from 12 patients were established as BRCA wild-type, but could not be classified for LOH, bec

48 herapies for repair-deficient tumors such as BRCA mutated breast cancers.

49 known to be associated with outcome, such as BRCA mutation, PROVAR may provide clinically useful pred

50 e [IQR], 3.0-8.4) years after ascertainment, BRCA testing, or RRSO (whichever occurred last).

51 TNBC and suggests that functional RNA-based BRCA deficiency needs to be further examined in TNBC.

52 pose To investigate the associations between BRCA mutation status and computed tomography (CT) phenot

53 re fit to determine the associations between BRCA status, pCR, and survival.

54 repair in cells that lack crosstalk between BRCA-FA and MMR pathways.

55 rlies the importance of interactions between BRCA-FA and MMR pathways.

56 Importance: The link between BRCA mutations and uterine cancer is unclear.

57 P inhibitors in the treatment setting beyond BRCA mutant tumours.

58 Along with BRCA1 and BRCA2 (BRCA) mutations genomic loss of heterozygosity (LOH) mig

59 ts, our finding has implications for broader BRCA genetic testing for patients with pancreatic ductal

60 , analysed for the overall population and by BRCA status.

61 etrospective, preplanned analysis of data by BRCA mutation status from our randomised, double-blind,

62 ed exploratory analyses included efficacy by BRCA mutation status, assessed retrospectively.

63 f miRNA isoforms (isomiRs) in breast cancer (BRCA) and normal breast data sets from the Cancer Genome

64 family or personal history of breast cancer, BRCA mutation status, history of high-risk lesion or man

65 In 235 unselected ovarian cancers, BRCA(1/2) was sequenced in 235, assessed by copy number

66 nome Atlas (TCGA) Breast Invasive Carcinoma (BRCA) cohort.

67 5 single-agent activity in patients carrying BRCA mutations.

68 onses were observed in two patients carrying BRCA mutations: one with head and neck cancer and one wi

69 realized with the approval of first-in-class BRCA-targeted therapies for ovarian cancer and identific

70 dents whose clinicians ordered comprehensive BRCA testing, most were white non-Hispanic (2502 [69.0%]

71 unseling and, if indicated after counseling, BRCA testing.

72 with noninherited tumors that have decreased BRCA activity.

73 with homologous recombination deficiencies (BRCA mutant or BRCA wild-type and high loss of heterozyg

74 ntified tumors of a distinct BRCA-deficient (BRCA-D) TNBC subtype characterized by low levels of wild

75 hemotherapeutics that cause fork degradation.BRCA proteins have emerged as key stabilizing factors fo

76 Deleterious BRCA mutations were detected in 189 (25%) of 746 familia

77 A sequencing identified tumors of a distinct BRCA-deficient (BRCA-D) TNBC subtype characterized by lo

78 1), and not having a malignant neoplasm (eg, BRCA carriers) (OR, 3.13; 95% CI, 1.25-7.85; P = .01) we

79 their risk for ovarian cancer (for example, BRCA mutations).

80 itin recognition and the Fanconi anemia (FA)-BRCA ICL repair network.

81 The Fanconi anemia (FA)-BRCA pathway is critical for the repair of DNA interstra

82 omes: (1) defects in the Fanconi anemia (FA)/BRCA DNA repair pathway, (2) defects in telomere mainten

83 A key step in FA-BRCA pathway activation is the covalent attachment of mo

84 n the regulation of the activation of the FA-BRCA pathway and suggest a broader role for p21 in the o

85 Components of the FA-BRCA pathway are thought to function in the repair of DN

86 Activation of the FA-BRCA pathway occurs via the monoubiquitination of the FA

87 s reveal critical roles for FAAP20 in the FA-BRCA pathway of DNA damage repair and genome maintenance

88 uired for the functional integrity of the FA-BRCA pathway regulating DNA repair.

89 ANCD1/BRCA2 function cooperatively in the FA-BRCA pathway to repair damaged DNA.

90 n the regulation of the activation of the FA-BRCA pathway.

91 inks (ICLs) comprise what is known as the FA-BRCA pathway.

92 n the regulation of the activation of the FA-BRCA pathway: p21 promotes S-phase and DNA damage-induci

93 The Fanconi anemia/BRCA (FA/BRCA) pathway is a DNA repair pathway that is required f

94 nation with tumor-associated mutations in FA/BRCA pathway components.

95 teract independently of Chk1 and that the FA/BRCA pathway may also be involved in the response to pol

96 h the other genes encoding members of the FA/BRCA pathway.

97 ancers resulting from inactivation of the FA/BRCA pathway.

98 red for the functional integrity of the FANC-BRCA pathway of DNA damage response and repair.

99 mors with an inherent deficiency in the FANC/BRCA pathway of DNA repair.

100 on BRCA1 and BRCA2, components of the FANCD2/BRCA supercomplex.

101 Associations between CT features, BRCA mutation status, cytoreductive outcome, and progres

102 For BRCA-positive patients, CPM is clearly cost-effective, p

103 tated vs 82% [P = .02] and 80% [P = .05] for BRCA wild-type and BRCA1-mutated cases, respectively) an

104 3-year PFS, 44% for BRCA2-mutated vs 16% for BRCA wild-type cases), whereas neither BRCA1 mutations (

105 5-year OS, 61% for BRCA2-mutated vs 25% for BRCA wild-type cases) and PFS (adjusted HR, 0.40; 95% CI

106 r per sample, 84 for BRCA2-mutated vs 52 for BRCA wild-type cases, false discovery rate <0.1).

107 ependent cohort (n = 87): (i) enrichment for BRCA signature with prevalent defects in the homologous

108 ng therapeutic target of high importance for BRCA-deficient tumors.

109 11.7 [P = .02] and 12.5 [P = .04] months for BRCA wild-type and BRCA1-mutated cases, respectively).

110 ) are clinically effective predominantly for BRCA-mutant tumors.

111 We discuss the biological rationale for BRCA-PARP synthetic lethality, how the synthetic lethal

112 interventions aimed at reducing the risk for BRCA-related cancer in women with potentially harmful BR

113 Family Registry, negative by sequencing for BRCA mutations, were analyzed for the presence of the BR

114 ZH2 inhibition as a therapeutic strategy for BRCA-mutated breast and ovarian cancers.

115 o the development of selective therapies for BRCA-deficient cancers.

116 ancer drugs in phase III clinical trials for BRCA-deficient tumors.

117 integrative analysis of mRNA expression from BRCA data sets of the TCGA repository demonstrated that

118 us recombination (HR), which can result from BRCA reversion mutations.

119 ontumorigenic breast epithelial tissues from BRCA mutation carriers, FISH revealed elevated genomic i

120 ith tumors displaying encoded and functional BRCA deficiency.

121 Patients with functionally BRCA-D tumors had significantly better survival with sta

122 ing to the presence or absence of a germline BRCA mutation (gBRCA cohort and non-gBRCA cohort) and th

123 g to permuted blocks, stratified by germline BRCA status and previous anti-angiogenic therapy, to rec

124 Pathogenic germline BRCA mutations were identified in 14 patients (4.6%; 95%

125 ntitumor responses in patients with germline BRCA gene mutations.

126 in health disparities in women with germline BRCA mutations.

127 s +/- 10 [standard deviation]; six women had BRCA mutations) with no history of breast cancer underwe

128 and genetic testing for potentially harmful BRCA mutations in asymptomatic women with a family histo

129 story of cancer or known potentially harmful BRCA mutations in the family.

130 ted cancer in women with potentially harmful BRCA mutations, including intensive cancer screening, me

131 at induces synthetic lethality in homozygous BRCA-deficient cells.

132 However, BRCA-deficient tumors represent only a small fraction of

133 ion and mutation analysis (GEMA) to identify BRCA- and DNA-PK-deficient leukemias either directly, us

134 ith elevated familial/genetic risk (FGR, ie, BRCA carrier status and/or family history of breast canc

135 More importantly, BRCA score provides significant prognostic value in both

136 In BRCA-mutant/sporadic TNBC patients, amplification of the

137 inhibitors have shown promising activity in BRCA-related cancers, its value in the treatment of trip

138 alone, with the greatest clinical benefit in BRCA-mutated patients, and had an acceptable and managea

139 the impact of immune checkpoint blockade in BRCA-mutated tumors.

140 Overall prognosis of breast cancer in BRCA carriers is similar to sporadic breast cancers.

141 sures: Incidence of uterine corpus cancer in BRCA+ women who underwent RRSO without hysterectomy comp

142 h higher odds of incomplete cytoreduction in BRCA wild-type HGSOC (multiple regression: P < .001 each

143 can increase chemotherapy-induced damage in BRCA-competent cells.

144 ism is involved in its sensitizing effect in BRCA-competent models of ovarian and colon cancer.

145 rated dose and initial signal of efficacy in BRCA-deficient ovarian cancers have been reported.

146 CA1/2-deficient cells, but their efficacy in BRCA-deficient patients is limited by drug resistance.

147 Although established in BRCA mutations, indications and interpretations of genet

148 reast cancer risk, but the role of folate in BRCA-associated breast cancer is not clear.

149 lopian tube segments are threefold higher in BRCA mutation carriers than in controls, correlating wit

150 tive proof of concept for PARP inhibition in BRCA-deficient breast cancers and shows a favourable the

151 P) inhibitor, induced synthetic lethality in BRCA-deficient cells.

152 ersed forks are the entry point for MRE11 in BRCA-deficient cells.

153 DA to treat ovarian cancer with mutations in BRCA genes.

154 etically targeted treatment with olaparib in BRCA-mutated advanced ovarian cancer.

155 Combined inhibition of Cdk1 and PARP in BRCA-wild-type cancer cells resulted in reduced colony f

156 ilar interactions with metabolic pathways in BRCA mutant cells.

157 and breast/ovarian cancer predisposition in BRCA mutant cells.

158 ion induced a similar metabolic responses in BRCA-mutant HCC1937 cells, but not in MCF7 and MDAMB231

159 tribution of specific histologic subtypes in BRCA+ women after RRSO without hysterectomy.

160 cal trials for other cancer types, including BRCA-mutant breast cancer.

161 ncreased activity in patients with inherited BRCA mutations and may also have a role in patients with

162 ge response, whereas PARP-1 inhibition kills BRCA-deficient tumor cells selectively, providing the fi

163 red an important management option for known BRCA gene mutation carriers.

164 was separately analyzed for women with known BRCA mutations (n=79).

165 breast cancer is low in patients with known BRCA mutations and EOC.

166 PI3K/mTOR pathway, altered in 60% of lines; BRCA DNA repair, 44%; and SYNE1-SYNE2, 60%.

167 lysis presented in this study directly links BRCA deficiency with increased clonal mutation burden an

168 nib inhibited 2 major DSB repair mechanisms, BRCA-mediated homologous recombination and DNA-dependent

169 aks that are repaired by 2 major mechanisms: BRCA-dependent homologous recombination and DNA-dependen

170 Extraction of 10 mg BRCA-/-, p53-/- breast tumor tissue or normal mammary gl

171 indings were noted for patients with mutated BRCA (HR 0.73 [0.45-1.17]; p=0.19) and wild-type BRCA (H

172 ability was similar in patients with mutated BRCA and the overall population.

173 d treatment among women with BRCA mutations (BRCA+ women), the role of concomitant hysterectomy is co

174 of which are upregulated in triple negative BRCA in white but not black women.

175 P = .006) compared with patients with a non-BRCA-like (NBL) profile, respectively.

176 hat allows for the detection of BRCA and non-BRCA germline mutations in individuals with high risks o

177 Less common non-BRCA mutations have also been identified and contribute

178 nd interpretations of genetic testing in non-BRCA mutations are not well defined.

179 In non-BRCA patients, cost-effectiveness of CPM is highly depen

180 g the synthetic lethal concept to target non-BRCA-mutant cancers also has clear potential, and we dis

181 otherapy than patients whose tumors were not BRCA-D (log-rank test, p = 0.021), and they had signific

182 ic effect on cell survival in the absence of BRCA genes, suggesting that the inhibition of this mutag

183 a evolution and result in the acquisition of BRCA-like traits, which could be therapeutically exploit

184 ver, we observed significant correlations of BRCA score with genome instability and neoadjuvant chemo

185 NA double-strand breaks, and a deficiency of BRCA proteins sensitizes cancer cells to PARP inhibition

186 werful tool that allows for the detection of BRCA and non-BRCA germline mutations in individuals with

187 in most countries, routine implementation of BRCA testing for ovarian cancer patients has been incons

188 his review will focus on the implications of BRCA status in the patient with high-grade serous ovaria

189 ty in preclinical tumour models with loss of BRCA and PTEN function.

190 ering the implications for family members of BRCA carriers, and possibly tailored chemotherapeutic tr

191 This review examines the prevalence of BRCA mutations in women with breast cancer, as well as c

192 The prevalence of BRCA(1/2) mutations in germline DNA from unselected ovar

193 s (DSB) involves the targeted recruitment of BRCA tumor suppressors to damage foci through binding of

194 strategy to overcome the PARPi resistance of BRCA-deficient cancers.

195 BRCA(1/2) changes, given the sensitivity of BRCA-mutated cancers to poly (ADP ribose) polymerase-1 (

196 A transcriptional signature of BRCA-D TNBC tumors was independently validated to be sig

197 vidence that post-transcriptional studies of BRCA will benefit from transcending the one-locus-one-mi

198 ides foundations for the rational therapy of BRCA-deficient cancers, and offers general insights into

199 r therapeutic opportunities for treatment of BRCA-deficient tumors.

200 Frequency and trends in the use of BRCA testing and how genetic information is used to make

201 mmends against routine genetic counseling or BRCA testing for women whose family history is not assoc

202 nts with EOC with either sporadic disease or BRCA(1/2) germline mutations was used for development of

203 wild-type and LOH high (LOH high group), or BRCA wild-type and LOH low (LOH low group).

204 s recombination deficiencies (BRCA mutant or BRCA wild-type and high loss of heterozygosity), and the

205 ERPRETATION: In patients with BRCA mutant or BRCA wild-type and LOH high platinum-sensitive ovarian c

206 In patients with BRCA mutant or BRCA wild-type and LOH high platinum-sensitive ovarian c

207 ies of 11 159 women whose clinicians ordered BRCA testing between December 2011 and December 2012.

208 th plan members whose clinicians had ordered BRCA testing.

209 Pathogenic BRCA mutations were identified in 4.6% of a large cohort

210 A total of 780 (87.0%) of 897 women reported BRCA testing by 1 year after breast cancer diagnosis (me

211 er in 2012 and 2013, respectively, reporting BRCA testing (P < .001).

212 In doing so, this ligand sensitizes BRCA-deficient tumor cells to genotoxic therapy.

213 ortant to determine the frequency of somatic BRCA(1/2) changes, given the sensitivity of BRCA-mutated

214 ociated with deleterious germline or somatic BRCA mutations), patients with homologous recombination

215 CA mutant (deleterious germline or somatic), BRCA wild-type and LOH high (LOH high group), or BRCA wi

216 le, our framework calculates sample-specific BRCA scores, which indicates homologous recombination (H

217 prospective, nonrandomized comparison study, BRCA mutation carriers and women with a high familial ri

218 mologous recombination deficiency subgroups: BRCA mutant (n=40), LOH high (n=82), or LOH low (n=70).

219 atients at diagnosis, followed by subsequent BRCA recovery upon progression by copy number gain and/o

220 containing significantly more mutations than BRCA wild-type cases across the whole exome (median muta

221 cation fork processing, direct evidence that BRCA gene products regulate homologous recombination at

222 Here we report that BRCA proteins prevent nucleolytic degradation by protect

223 Herein we report that BRCA-1-defective human breast cancer cells are more sens

224 from our detailed mRNA analysis suggest that BRCA-associated cancer risk is likely not markedly incre

225 The BRCA and NHEJ pathways are required for the repair of CX

226 mbination (HR)-deficient tumors, such as the BRCA-associated breast and ovarian cancers.

227 at ablates phosphoprotein recognition by the BRCA C terminus (BRCT) domains of BRCA1 elicits tumors i

228 A tumor-suppressive role for the BRCA proteins as "chromosome custodians" helps to explai

229 Mutations in the BRCA C-terminal (BRCT) domain of BRCA1 frequently create

230 rtly due to the presence of mutations in the BRCA genes.

231 ree survival was significantly longer in the BRCA mutant (hazard ratio 0.27, 95% CI 0.16-0.44, p<0.00

232 ent 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 hi

233 24 patients in the BRCA mutant subgroup, 56 patients in the LOH high subgro

234 Several proteins in the BRCA-Fanconi anemia (FA) pathway, such as FANCJ, BRCA1,

235 lticenter trial enrolled 296 carriers of the BRCA mutation (153 BRCA1 and 128 BRCA2 carriers, and 15

236 Study results suggest that carriers of the BRCA mutation younger than 40 years may not benefit from

237 However, the majority of the BRCA mutation-positive patients did not actually meet th

238 E MR imaging surveillance of carriers of the BRCA mutation.

239 addition of an EZH2 inhibitor sensitizes the BRCA-mutant breast cells to PARPi.

240 Unlike the BRCA-FA pathway, the MMR pathway is not essential for ce

241 nts with sporadic disease, patients with the BRCA-like (BL) profile had improved disease-free surviva

242 Thus, BRCA-associated cancers are sensitive to DNA-damaging ag

243 of cytoreductive outcome varied according to BRCA mutation status.

244 expanding the utility of PARP inhibitors to BRCA-proficient cancers.

245 e noted in survival outcomes with respect to BRCA status and type of NST received.

246 Results are sensitive to BRCA-positive status and assumptions of QOL differences

247 sing targeted agents currently used to treat BRCA-mutant ovarian cancer and are in clinical trials fo

248 or suspected deleterious germline or tumour BRCA mutation.

249 The two BRCA proteins are linked by a third tumor suppressor, PA

250 (HR 0.73 [0.45-1.17]; p=0.19) and wild-type BRCA (HR 0.99 [0.63-1.55]; p=0.96).

251 mors were analyzed for loss of the wild-type BRCA gene and/or protein expression.

252 dings were noted for patients with wild-type BRCA, although the difference between groups was lower (

253 ncer cells are more sensitive than wild-type BRCA-1 counterparts to COH29 in vitro and in vivo.

254 genetic counseling, most US women undergoing BRCA genetic testing do not receive this clinical servic

255 delineation of the basic science underlying BRCA network function holds promise to maximally exploit

256 atabase review of 364 patients who underwent BRCA mutation testing for EOC (stages I-IV) between 1998

257 pective study included 108 patients (33 with BRCA mutant and 75 with BRCA wild-type HGSOC) who underw

258 08 patients (33 with BRCA mutant and 75 with BRCA wild-type HGSOC) who underwent CT before primary de

259 azi Jewish was significantly associated with BRCA mutation carrier status (P=.02, P<.001, and P=.05,

260 c lymphadenopathy at CT were associated with BRCA mutation status (multiple regression: P < .001 for

261 genetics clinician and its association with BRCA knowledge, understanding, and satisfaction were ass

262 effective treatment for ovarian cancer with BRCA mutations.

263 inhibitors selectively kill tumor cells with BRCA mutations.

264 sponse, and genome instability compared with BRCA wild-type.

265 matic women who have not been diagnosed with BRCA-related cancer.

266 umor biopsy specimens from six patients with BRCA germline mutations.

267 INTERPRETATION: In patients with BRCA mutant or BRCA wild-type and LOH high platinum-sens

268 In patients with BRCA mutant or BRCA wild-type and LOH high platinum-sens

269 dure for three nested cohorts: patients with BRCA mutations (carcinoma associated with deleterious ge

270 .77]; p=0.0012), especially in patients with BRCA mutations (HR 0.21 [0.08-0.55]; p=0.0015).

271 In recent clinical trials, EOC patients with BRCA mutations exhibited favorable responses to the PARP

272 Patients with BRCA mutations or prior mantle radiation (n = 52) accoun

273 nts with BRCA-mutant HGSOC and patients with BRCA wild-type HGSOC.

274 ee survival was longer than in patients with BRCA wild-type LOH low carcinomas.

275 ee survival was longer than in patients with BRCA wild-type LOH low carcinomas.

276 ur LOH can be used to identify patients with BRCA wild-type platinum-sensitive ovarian cancers who mi

277 The overall survival data in patients with BRCA wild-type were HR 0.83 (95% CI 0.55-1.24, nominal p

278 breast cancer surveillance for patients with BRCA-associated EOC needs to be reevaluated given the lo

279 Patients with BRCA-associated epithelial ovarian cancer have improved

280 ificantly shorter PFS for both patients with BRCA-mutant HGSOC (multiple regression: hazard ratio [HR

281 e CT features differed between patients with BRCA-mutant HGSOC and patients with BRCA wild-type HGSOC

282 ificantly shorter PFS for both patients with BRCA-mutant HGSOC and those with BRCA wild-type HGSOC.

283 uctive outcome and survival in patients with BRCA-mutant HGSOC and those with BRCA wild-type HGSOC.

284 with cytoreductive outcome for patients with BRCA-mutant HGSOC, presence of PD in lesser sac (odds ra

285 Six patients with BRCA-mutant solid tumors were also enrolled at the MTD.

286 hing statistical significance, patients with BRCA-mutated platinum-sensitive recurrent serous ovarian

287 ity of maintenance olaparib in patients with BRCA-mutated platinum-sensitive recurrent serous ovarian

288 Model results are tested with BRCA and HIV data sets and with carefully constructed si

289 d ratio [HR] = 26.7 P < .001) and those with BRCA wild-type HGSOC (univariate analysis: reader 1, HR

290 tients with BRCA-mutant HGSOC and those with BRCA wild-type HGSOC.

291 tients with BRCA-mutant HGSOC and those with BRCA wild-type HGSOC.

292 iven for the treatment of advanced TNBC with BRCA gene dysfunction.

293 ays hallmark genomic features of tumors with BRCA mutations and HR defects, cementing the pathogenici

294 When available for tumors with BRCA(1/2) mutations, germline DNA was sequenced.

295 RRSO) is standard treatment among women with BRCA mutations (BRCA+ women), the role of concomitant hy

296 breast and gynecologic cancer in women with BRCA mutations.

297 ective risk-reduction strategy in women with BRCA mutations.

298 tomy has an impact on survival in women with BRCA-associated breast cancer.

299 Women with BRCA-associated epithelial ovarian cancer represent a un

300 itor olaparib compared with patients without BRCA mutations.