ライフサイエンスコーパス: BRCA

1 BRCA carriers with cT1-3 (>= 1.5 cm), cN0-3 HER2-negativ

2 BRCA proteins protect reversed forks from nucleolytic de

3 BRCA testing is recommended for young women diagnosed as

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

5 33 (16%) had a BRCA mutation.

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

7 women (N = 124) who were unlikely to have a BRCA mutation and at average population risk for breast

8 urbed forks undergoing degradation, but in a BRCA wild-type condition.

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

10 not have a first-degree family history of a BRCA-related cancer and, in the absence of a personal hi

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

12 s from patients with mCRPC associated with a BRCA alteration treated with rucaparib 600 mg twice dail

13 ety populations included 115 patients with a BRCA alteration with or without measurable disease.

14 ase, which includes not only patients with a BRCA mutation but also a population with BRCA wild-type

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

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

17 ceptor (ER)-positive (+) breast cancer among BRCA carriers.

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

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

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

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

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

23 ulation, BRCA-mutant cohort, HRD cohort, and BRCA wild-type/LOH low patient subgroup, respectively.

24 red therapy resistance in tissue culture and BRCA patient tumors.

25 ive profiles against both BRCA-deficient and BRCA-proficient cancer cells in cellular assays.

26 ADP-ribose) polymerase (PARP) inhibition and BRCA deficiency is exploited to treat breast and ovarian

27 3 months [95% CI, 5.93 to 9.53 months]); and BRCA wild-type/loss of heterozygosity (LOH) low patient

28 tumor activities in both BRCA-proficient and BRCA-deficient tumors.

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

30 IRC) from The Cancer Genome Atlas (TCGA) and BRCA from Gene Expression Omnibus (GEO) suggest that the

31 RPi in patients with both BRCA-wild-type and BRCA-mutant tumors and provides a rationale for combinin

32 itional pathways, such as the Fanconi anemia-BRCA pathway, became perturbed only after long-term cult

33 BRCA2, or other genes in the Fanconi anemia/BRCA pathway, and these tumors have been shown to be par

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

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

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

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

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

39 e biomarker assays of responsiveness (beyond BRCA mutations), assessment of the mechanisms underlying

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

41 rior antiproliferative profiles against both BRCA-deficient and BRCA-proficient cancer cells in cellu

42 ted synergistic antitumor activities in both BRCA-proficient and BRCA-deficient tumors.

43 ical efficacy of PARPi in patients with both BRCA-wild-type and BRCA-mutant tumors and provides a rat

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

45 editary breast cancer genes BRCA1 and BRCA2 (BRCA).

46 BRCA1 or BRCA2 (BRCA) alterations are common in men with metastatic cast

47 In subgroup analyses by BRCA mutation status, the ratio of expected to observed

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

49 gemogenovatucel-T in patients stratified by BRCA mutation status is warranted.

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

51 ponding pathways, we divided breast cancers (BRCAs) into five subgroups and glioblastoma multiformes

52 thylation data of breast invasive carcinoma (BRCA) and kidney renal clear cell carcinoma (KIRC) from

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

54 d heritable cancer risk in BRCA1/2 carriers (BRCA-associated cancer types).

55 r (TNBC) in germline BRCA mutation carriers (BRCA carriers).

56 hree inherited autosomal dominant conditions-BRCA-related hereditary breast and ovarian cancer (HBOC)

57 assigned patients with a centrally confirmed BRCA mutation, and safety analyses included all patients

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

59 instability high/mismatch repair deficiency, BRCA mutations, and TRK alterations are provided for all

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

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

62 lations included patients with a deleterious BRCA alteration who received >= 1 dose of rucaparib.

63 ity in patients with mCRPC and a deleterious BRCA alteration, but with a manageable safety profile co

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

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

66 treatable molecular alterations (like ERBB2, BRCA and MSI) in small bowel carcinomas.

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

68 ation with the canonical Fanconi anemia (FA)/BRCA pathway remain unclear.

69 t FANCD2, and knockdown of TRAIP promotes FA/BRCA pathway activation.

70 thway for repairing psoralen-ICL, and the FA/BRCA pathway is only activated when NEIL3 is not present

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

72 g double-strand breaks (DSBs), unlike the FA/BRCA pathway.

73 Here we show that the NEIL3 and the FA/BRCA pathways are non-epistatic in psoralen-ICL repair.

74 Furthermore, we introduce Famdenovo.BRCA for hereditary breast and ovarian cancer syndrome a

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

76 We evaluated the performance of five BRCA mutation risk predictive models in a Chinese cohort

77 Indications for screening were as follows: BRCA mutation carrier or history of chest radiation (BRC

78 For BRCA-positive participants, BOADICEA and IBIS were well

79 the ratio of expected to observed cases for BRCA-negative women was 1.02 (95% CI 0.93-1.12) for BOAD

80 patients that met the clinical criteria for BRCA testing but had received a negative BRCA1/2 result

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

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

83 typically used to recommend individuals for BRCA testing: self-reported Jewish ancestry and family h

84 , poly(ADP-ribose) polymerase inhibitors for BRCA mutation carriers and, quite recently, immunotherap

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

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

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

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

89 minority of cancers have breast cancer gene (BRCA) mutations that confer sensitivity to poly (ADP-rib

90 m age-matched cancer-free women from the GEO BRCA data and confirmed their enrichment in the progress

91 A germline BRCA mutation (BRCAm) in ovarian cancer patients provide

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

93 Of 203 patients with a germline BRCA mutation (gBRCAmut), 99 had a PR and 104 had a CR t

94 ing to the presence or absence of a germline BRCA mutation-gBRCAmut and non-gBRCAmut cohorts.

95 -mutated, metastatic breast cancer; germline BRCA-mutated, metastatic ovarian cancer; metastatic gast

96 enrolled into four initial cohorts: germline BRCA-mutated, metastatic breast cancer; germline BRCA-mu

97 = 40 years and harbored deleterious germline BRCA mutations.

98 d Drug Administration, olaparib for germline BRCA-mutated pancreatic ductal adenocarcinoma is expecte

99 le-negative breast cancer (TNBC) in germline BRCA mutation carriers (BRCA carriers).

100 cancer of any histology with known germline BRCA mutations.

101 cancer of any histology with known germline BRCA mutations; confirmed diagnosis of recurrent breast

102 r 6 months in patients with a known germline BRCA pathogenic variant (gBRCA-positive) and operable br

103 med, oncologist-led 'mainstreaming' germline BRCA testing pathway in 255 ovarian cancer patients at I

104 ng' approach led to a 95% uptake of germline BRCA testing and a mean turnaround time of 20.6 days.

105 hment of 'mainstreaming', uptake of germline BRCA testing was 14% with a mean turnaround time of 148.

106 sion-free survival in patients with germline BRCA mutation-associated advanced breast cancer.

107 Of 1,252 patients with germline BRCA mutations (BRCA1, 811 patients; BRCA2, 430 patients

108 Young women with germline BRCA mutations have unique reproductive challenges.

109 fter breast cancer in patients with germline BRCA mutations is safe without apparent worsening of mat

110 st cancer outcomes in patients with germline BRCA mutations.

111 in health disparities in women with germline BRCA mutations.

112 ever, only 15%-20% of ovarian cancers harbor BRCA mutations, therefore additional therapies are requi

113 t (TNBC) and ovarian cancers (OCs) harboring BRCA mutations, generating homologous recombination defi

114 f MAD2L1 in breast cancer patients with high BRCA-pathway activity.

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

116 ars in BRCA1 or BRCA2 mutation carriers (ie, BRCA-positive women), tested non-carriers and untested p

117 non-carriers and untested participants (ie, BRCA-negative women), and participants younger than 50 y

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

119 In BRCA-deficient cells, ssDNA gaps developed because repli

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

121 gnificantly higher with CDDP than with AC in BRCA carriers with stage I-III HER2-negative breast canc

122 versus doxorubicin-cyclophosphamide (AC) in BRCA carriers with stage I-III human epidermal growth fa

123 ended versus taxanes to treat advanced BC in BRCA carriers.

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

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

126 ciency (HRD) is a defining characteristic in BRCA-deficient breast tumors caused by genetic or epigen

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

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

129 52 NTD forms nuclear foci upon DNA damage in BRCA-deficient human cells and promotes DNA double-stran

130 ed protein that promotes fork degradation in BRCA-deficient cells by acetylating H4K8 at stalled repl

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

132 nhibitors (PARPis) have clinical efficacy in BRCA-deficient cancers, but not BRCA-intact tumors, incl

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

134 NMTis) plus PARPis enhance PARPi efficacy in BRCA-proficient AML subtypes, breast, and ovarian cancer

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

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

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

138 e mechanisms through which HRD is induced in BRCA-proficient TNBC and OC.

139 Inhibition of RAD52 leads to lethality in BRCA-deficient cells.

140 inhibitor (CHK1i) prexasertib monotherapy in BRCA wild-type (BRCAwt) HGSOC patients.

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

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

143 Inhibition of PARP1 in BRCA-mutated cancers has been observed to be clinically

144 s strategy aims to widen the use of PARPi in BRCA-competent and olaparib-resistant cancers, making fu

145 response rates to PARP inhibitors (PARPi) in BRCA-mutated epithelial ovarian cancers (EOC), PARPi res

146 ibitors (PARPis), but the role for PARPis in BRCA-proficient cancers is not well established.

147 upregulating the Wnt/beta-catenin pathway in BRCA-mutated EOC cells.

148 ilar interactions with metabolic pathways in BRCA mutant cells.

149 lled forks, resulting in PARPi resistance in BRCA-deficient cells.

150 hat m(6)A contributes to PARPi resistance in BRCA-deficient EOC cells by upregulating the Wnt/beta-ca

151 ZD10 mRNA contributes to PARPi resistance in BRCA-deficient EOC cells via upregulation of Wnt/beta-ca

152 Polymerase) inhibitor (PARPi) resistance in BRCA-deficient tumors.

153 ors of fork stability and PARPi responses in BRCA-deficient cells, which provides key insights into t

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

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

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

157 Replication analyses using two independent BRCA data sets suggest that DMRs detected based on DV ar

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

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

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

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

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

163 6.28 months [95% CI, 4.85 to 7.47 months]); BRCA-mutant cohort (130 rucaparib v 66 placebo; 9.37 mon

164 Overall, mutant BRCA is an indispensable founding event for some tumours

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

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

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

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

169 Conversely, among patients with non-BRCA-associated cancer types, most carriers of these BRC

170 efficacy in BRCA-deficient cancers, but not BRCA-intact tumors, including glioblastoma (GBM).

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

172 py, regardless of the presence or absence of BRCA mutations.

173 ks has been associated to chemoresistance of BRCA-deficient cancer cells.

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

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

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

177 cation gaps underlie the hypersensitivity of BRCA-deficient cancer and that defects in homologous rec

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

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

180 nded to platinum-based therapy regardless of BRCA mutation status.

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

182 ork integrity and promotes the resistance of BRCA-deficient cells to PARP-inhibitors.

183 The exquisite sensitivity of BRCA-deficient cells to 3' blocks indicates that they re

184 py enhances PARPi efficacy in the setting of BRCA-proficient cancer.

185 he cohort harbored a mutational signature of BRCA and APOBEC/AID.

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

187 inducing BRCAness in a much larger subset of BRCA-proficient tumors, with significant translational p

188 on pathway that is important for survival of BRCA-deficient cells.

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

190 laparib is FDA approved for the treatment of BRCA-mutated breast, ovarian and pancreatic cancers.

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

192 on is essential for maintaining viability of BRCA-deficient cells owing to its ability to promote DNA

193 ism of how RAD52 contributes to viability of BRCA-deficient cells remains unknown.

194 ese activities fail to maintain viability of BRCA-deficient cells.

195 n receptor and progesterone receptor) and/or BRCA mutations.

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

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

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

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

200 ciation was not modified by familial risk or BRCA mutation status (P interactions >0.05).

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

202 1.66 to 5.40 months) in the ITT population, BRCA-mutant cohort, HRD cohort, and BRCA wild-type/LOH l

203 n genes encoding DNA damage repair proteins (BRCA and FANC) were detected in 14% of PDACs.

204 pered by the challenge of obtaining purified BRCA complexes for mechanistic studies.

205 ation carrier or history of chest radiation (BRCA/RT group), family history of breast cancer (FH grou

206 Although guidelines recommend BRCA testing for all women with non-mucinous epithelial

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

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

209 y be a promising strategy to radio-sensitise BRCA-deficient cancers.

210 damage response to generate HRD, sensitizing BRCA-proficient cancers to PARPi.

211 ficacy in the clinical management of several BRCA-mutated tumors.

212 ilar for patients with a germline or somatic BRCA alteration and for patients with a BRCA1 or BRCA2 a

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

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

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

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

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

218 Surprisingly, BRCA reversion mutations and an ability to form RAD51 fo

219 onale combination strategies that can target BRCA wild-type and homologous recombination (HR) DNA rep

220 , which provides key insights into targeting BRCA-deficient tumors and identifying epigenetic modulat

221 emically inhibiting Fen1 selectively targets BRCA-deficient cells.

222 e correlation for 1256 samples from the TCGA-BRCA project between TPM and FPKM reported by TPMCalcula

223 The discovery that BRCA-mutant cancer cells are exquisitely sensitive to in

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

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

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

227 The BRCA set (n=220) included 109 women with BRCA1 mutations

228 The BRCA set comprised women with a BRCA1 mutation but witho

229 The BRCA-encoded products form complexes with other tumor su

230 comitant loss of PCNA-ubiquitination and the BRCA pathway results in increased nascent DNA degradatio

231 alue for biopsies performed (PPV(3)) for the BRCA/RT group (41%; 95% CI: 26%, 56%) compared with the

232 Understanding how the BRCA tumor suppressor network executes its biological fu

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

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

235 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

236 24 patients in the BRCA mutant subgroup, 56 patients in the LOH high subgro

237 RCA1 mutation carriers aged <35 years in the BRCA set 4.40 [1.14-24.36], p=0.031).

238 In the BRCA set, women with BRCA1 mutations younger than 50 yea

239 ly longer with rucaparib than placebo in the BRCA-mutant and homologous recombination-deficient cohor

240 ncer detection rate (CDR) was highest in the BRCA/RT group (26 per 1000 examinations; 95% confidence

241 importance of the proper cooperation of the BRCA and PALB2 proteins in genome maintenance.

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

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

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

245 In this cohort, 12.5% of the BRCA-negative breast cancer patients were found to carry

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

247 The application of CBNA to the BRCA dataset demonstrates that it is more effective than

248 ate that ssDNA replication gaps underlie the BRCA cancer phenotype, "BRCAness," and we propose they a

249 oxicity of genotoxic agents and underlie the BRCA-cancer phenotype "BRCAness," yielding promising bio

250 was lower for the FH group compared with the BRCA/RT group (P = .02).

251 nt for the PH or HRL group compared with the BRCA/RT group (P = .14 and .18, respectively).

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

253 form the discussion around broader access to BRCA genetic testing.

254 of cytoreductive outcome varied according to BRCA mutation status.

255 motherapies, such as cisplatin used to treat BRCA-deficient tumors, do not initially cause DNA double

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

257 bitors (PARPis) are used clinically to treat BRCA-mutated breast tumors.

258 nd a potential therapy paradigm for treating BRCA-proficient cancers like NSCLC.

259 In turn, BRCA-deficient cells utilize error-prone DNA-repair path

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

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

262 nderlie their clinical activities in various BRCA-mutated tumors.

263 pair is poorly understood, it is unclear why BRCA-deficient cells require APE2 for viability.

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

265 08 patients (33 with BRCA mutant and 75 with BRCA wild-type HGSOC) who underwent CT before primary de

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

267 ection may represent a way to cooperate with BRCA-dependent fork stabilization.

268 tic women who have never been diagnosed with BRCA-related cancer, as well as those with a previous di

269 D)-positive tumours (including patients with BRCA and without BRCA mutations) sensitive to their last

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

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

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

273 mised to three nested cohorts: patients with BRCA mutations, patients with homologous recombination d

274 limited data are available in patients with BRCA mutations.

275 inhibitors (PARPi) in oncology patients with BRCA mutations.

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

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

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

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

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

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

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

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

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

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

286 results provide reassurance to patients with BRCA-mutated breast cancer interested in future fertilit

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

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

289 b has demonstrated efficacy in patients with BRCA-positive metastatic breast cancer.

290 h a BRCA mutation but also a population with BRCA wild-type disease.

291 RD-positive ovarian cancer beyond those with BRCA mutations.

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

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

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

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

296 ing breast MRI is recommended for women with BRCA mutation or a history of chest radiation, but guide

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

298 RP) have demonstrated efficacy in women with BRCA-mutant ovarian cancer.

299 rs (including patients with BRCA and without BRCA mutations) sensitive to their last platinum-based t

300 PARPi in breast and ovarian cancers without BRCA mutations, but the underlying mechanism is not clea