ライフサイエンスコーパス: HRD

1 HRD also activates the cyclic GMP-AMP synthase (cGAS)-st

2 HRD classifiers were applied to the dataset and included

3 HRD genomic tumor classifiers suggested that 7% to 10% o

4 HRD in these models and patient samples was evaluated by

5 HRD is always expressed in D2, but in B6, it is expresse

6 HRD patients with germline or somatic alterations in any

7 HRD prevalence ranged between 14.5%-16.5% through target

8 HRD responses to previously-encoded ("old") negative ima

9 HRD scores and mutational signatures associated with HRD

10 HRD status was not prognostic in resected PDAC; however

11 HRD was associated with higher ex vivo PARPi sensitivity

12 eived anthracycline and no radiotherapy or a HRD <0.1Gy, by 60.4 (95% CI, 22.4-163.0) in those who ha

13 ver, a small subset of alterations affecting HRD, DDR and MMR genes may not be detected optimally.

14 An HRD enriched cohort (n = 71; 52 primary and 19 metastati

15 ose who had received no anthracycline and an HRD>/=30Gy, and 61.5 (95% CI, 19.6-192.8) in those who h

16 e who had received both anthracycline and an HRD>/=30Gy.

17 BRCA1 hypermethylation confers an HRD, immune cell type, genome-wide DNA methylation, and

18 thracycline and either no radiotherapy or an HRD<0.1Gy, the risk was multiplied by 18.4 (95% CI, 7.1-

19 dual-lumen cannula which was connected to an HRD via extracorporeal circulation.

20 Identification of EOC patients with an HRD phenotype may help tailor specific therapies.

21 mprove identification of MSI, CDK12(-/-) and HRD patients.

22 Chemotherapy information was collected and HRD was estimated.

23 nd 7.3% of germline variants in MMR, DDR and HRD genes, respectively.

24 known functional motifs, such as the DFG and HRD motifs.

25 tive correlation between PLK1 expression and HRD score, indicating that increased PLK1 expression sup

26 e residues, such as DFG-Asp, alphaC-Glu, and HRD-Asp, change protonation states dependent on the DFG,

27 i of kinases: the alphaB-alphaC helices, and HRD-motif loop, and DFG-motif.

28 Both the HIP and HRD/DER pathways contribute to the degradation of CPY*,

29 on-deficient HRD-Dup (BRCA1 mutant-like) and HRD-Del (BRCA2 mutant-like) tumours harboured inflammato

30 an HRP-RBL (52.0 mo), HRD-RBL (57.1 mo), and HRD-RBH subgroups (53.3 mo; all p < 0.0001).

31 e rare autosomal recessive syndrome known as HRD, a devastating disorder characterized by congenital

32 c breast cancer cohort, samples predicted as HRD had higher complete CR (AUC, 0.76 [95% CI, 0.54 to 0

33 mon in BRCA1- compared with BRCA2-associated HRD-PDAC.

34 P status partially correlated with DNA-based HRD test outcomes (70% concordance for both RECAP-CHORD

35 RECAP-HRD; 37%), was subjected to DNA-based HRD tests (i.e., Classifier of HOmologous Recombination

36 we describe DirectHRD, a genomic scar-based HRD classifier based on WGS.

37 to the FDA approval of the first scar-based HRD test.

38 Associations between HRD status and tumor subtype, age at diagnosis, and gene

39 The concordance between HRD biomarkers was 91%.

40 as associated with increased three-biomarker HRD score (22.2 for HBV RNA+ vs. 16.0 for HBV RNA-).

41 ations, gene set expression, three-biomarker HRD score and mutation-specific survival.

42 unction of the complex was observed for both HRD and DOA pathway substrates.

43 Regardless of the BRCA/HRD-status, the induction of ssGAPs in preclinical model

44 The underlying genes are called HRD (pronounced "herd"), for HMG-CoA reductase degradati

45 topic HMGR, required the function of certain HRD (HMGR degradation) and UBC genes.

46 rmline mutations in the better characterized HRD genes (BRCA1, BRCA2, PALB2, ATM, ATR, CHEK2, RAD51,

47 ) in the ITT population, BRCA-mutant cohort, HRD cohort, and BRCA wild-type/LOH low patient subgroup,

48 umors with the same PV displayed contrasting HRD status, and age at diagnosis did not correlate with

49 ge, grade, and age and hazard rate of death (HRD).

50 eutral images while heart rate deceleration (HRD) and skin conductance responses (SCRs) were monitore

51 Here we identify an HR defect (HRD) gene signature that can be used to functionally ass

52 Evaluation of HR deficiency (HRD) and mutational signatures efficiently stratified re

53 Therefore, inducing HR deficiency (HRD) is a viable strategy to sensitize HR proficient can

54 Genomic features of HR deficiency (HRD) were detected in 7 of 12 PACCs undergoing WGS, incl

55 inducing agents through their HR deficiency (HRD), BRCA1-associated tumors display heterogeneous resp

56 rmance of this test to other HRR deficiency (HRD) detection methods.

57 rs with homologous recombination deficiency (HRD) (hazard ratio, 0.38; 95% CI, 0.24 to 0.59) and 9.3

58 redicts homologous recombination deficiency (HRD) and clinical outcomes directly from digital histopa

59 ures of homologous recombination deficiency (HRD) and mismatch repair deficiency (MMRD).

60 rboring homologous recombination deficiency (HRD) are sensitive to PARP inhibitors and platinum chemo

61 rs with homologous recombination deficiency (HRD) can benefit from platinum salts and poly(ADP-ribose

62 Homologous recombination deficiency (HRD) contributes to genomic instability and leads to sen

63 (MSI), homologous recombination deficiency (HRD) enriched with genomic deletions and BRCA2 aberratio

64 target homologous recombination deficiency (HRD) in breast cancer limits their overall effectiveness

65 Homologous recombination deficiency (HRD) in pancreatic ductal adenocarcinoma (PDAC), remains

66 ivalent homologous recombination deficiency (HRD) induced by these genetic and epigenetic BRCA pertur

67 Homologous recombination deficiency (HRD) is a defining characteristic in BRCA-deficient brea

68 Homologous recombination deficiency (HRD) is a predictive biomarker for efficacy of PARP (pol

69 Homologous recombination deficiency (HRD) is prevalent in cancer, sensitizing tumor cells to

70 er with homologous recombination deficiency (HRD) pathogenic germline variants (PGVs).

71 ons and homologous recombination deficiency (HRD) respectively.

72 ith the Homologous Recombination Deficiency (HRD) score, we found a positive correlation between PLK1

73 (PGA); homologous recombination deficiency (HRD) scores] and two novel [Shannon diversity index (SI)

74 less of homologous recombination deficiency (HRD) status.

75 nstrate homologous recombination deficiency (HRD) with characteristic genomic rearrangements.

76 (UPD), homologous recombination deficiency (HRD), epithelial-mesenchymal transition and inflammation

77 r shows homologous recombination deficiency (HRD), resulting in a BRCA-like phenotype that might rend

78 rs with homologous recombination deficiency (HRD), such as cancer patients with germline or somatic B

79 rboring homologous recombination deficiency (HRD), their clinical benefit remains limited, highlighti

80 Seven homologous recombination deficiency (HRD), two DNA damage response (DDR) and four mismatch re

81 al with homologous recombination deficiency (HRD), which we attribute to chromosome instability cause

82 -tBRCAm homologous recombination deficiency (HRD)-positive and non-tBRCAm intention-to-treat (ITT) po

83 ts with homologous recombination deficiency (HRD)-positive tumours (including patients with BRCA and

84 such as homologous recombination deficiency (HRD).

85 beyond homologous recombination deficiency (HRD).

86 ing and homologous recombination deficiency (HRD).

87 on with homologous recombination deficiency (HRD).

88 al with homologous recombination deficiency (HRD).

89 OH) and homologous recombination deficiency (HRD).

90 rs were homologous recombination deficiency (HRD; BRCA mutation and loss of heterozygosity status) cl

91 homologous recombination repair deficiency (HRD) while the other is dominated by whole genome duplic

92 homologous recombination repair deficiency (HRD), mismatch repair deficiency, and tumour mutational

93 revealed that homologous repair deficiency (HRD)-related SBS3 increases at each time point in patien

94 n (HR) status (BRCA mutation, HR deficiency [HRD], or HR proficiency [HRP]).

95 Homologous recombination-deficient HRD-Dup (BRCA1 mutant-like) and HRD-Del (BRCA2 mutant-li

96 powerful strategy to eliminate HR-deficient (HRD) cancers, this is limited by an incomplete understan

97 onths]); homologous recombination deficient (HRD) cohort (236 rucaparib v 118 placebo; 7.93 months [9

98 odels of homologous recombination deficient (HRD) ovarian carcinoma.

99 valuated homologous recombination deficient (HRD) phenotypes in epithelial ovarian cancer (EOC) consi

100 s of the homologous recombination-deficient (HRD) status on the clinicopathologic features, chemother

101 Homologous recombination-deficient (HRD) tumours, including those harbouring mutations in th

102 d homologous recombination repair deficient (HRD) tumors are likely also PARP-inhibitor sensitive.

103 mologous recombination DNA repair deficient (HRD) tumors.

104 ly annotated by Takaya et al. (HR-deficient, HRD; HR-proficient, HRP), and (2) 226 clinical HGSOC cas

105 embrane-bound HMG-CoA reductase degradation (HRD) ubiquitin-ligase complex is a key player of the ER-

106 were analyzed: height of retinal detachment (HRD) at the fovea, central macular thickness (CMT), disr

107 signatures alone did not consistently detect HRD or predict clinical response across datasets.

108 0.87 and demonstrated the ability to detect HRD at tumor fractions as low as 1%, making it 10 times

109 Conventionally, detecting HRD involves screening for defects in BRCA1, BRCA2, and

110 e machine learning tools exist for detecting HRD based on mutational patterns.

111 Standard diagnostic tests for detecting HRD require molecular profiling, which is not universall

112 lack the sensitivity required for detecting HRD scars in low tumor purity samples, especially in liq

113 er), a machine learning method for detecting HRD using six mutational features.

114 Human remains detection (HRD) canines utilize this odor signature to locate human

115 hic pathogens that cause hairy root disease (HRD) on hydroponically grown Solanaceae and Cucurbitacea

116 HRD, and half of those that did not display HRD were explained by retention of the wild-type allele,

117 that the conserved UBN1 Hpc2-related domain (HRD) is a novel H3.3-specific-binding domain.

118 reported that the UBN1 Hpc2-related domain (HRD) specifically binds to H3.3/H4 over H3.1/H4.

119 lationship between the heart radiation dose (HRD) received during childhood and the risk of CD.

120 ad the lowest cost (-24.7%), followed by EAT-HRD and Milpa (~-20%).

121 , the EAT-Lancet Healthy Reference Diet (EAT-HRD) and its Mexican adaptation, the Milpa diet, and 3 p

122 n and proposed a healthy reference diet (EAT-HRD) that can be adapted to the culture, geography, and

123 Mexican adults consume higher than the EAT-HRD for grains (mostly refined), dairy, added sugars, an

124 and processed meats); and lower than the EAT-HRD for vegetables, fruits, legumes, nuts, tubers and st

125 The adaptation of the EAT-HRD to the Mexican context is a timely input for current

126 11 in S. cerevisiae is independent of either HRD or UBC gene function, but it is largely dependent on

127 ing a BRCA1/2 mutation, but with an elevated HRD-LOH score, who achieved a favorable pathologic respo

128 ane protein Hrd3, which is also required for HRD-dependent degradation.

129 augment existing therapeutic strategies for HRD cancers.

130 Genomic and functional HRD biomarkers were assessed in untreated breast and ova

131 less than 70% of tumors displayed functional HRD, and half of those that did not display HRD were exp

132 RD by genomic instability scores, functional HRD by RAD51, and gene-specific loss of heterozygosity w

133 s (STING), to unexpectedly directly generate HRD.

134 eprogram the DNA damage response to generate HRD, sensitizing BRCA-proficient cancers to PARPi.

135 Genomic HRD by genomic instability scores, functional HRD by RAD

136 accuracy than HRR gene mutations and genomic HRD analysis for predicting PARPi response (95%, 67%, an

137 er, the prevalence of functional and genomic HRD was 55.2% (16 of 29) and 61.1% (11 of 18) for RAD51C

138 ated by DNA sequencing of HRR genes, genomic HRD tests, and RAD51 foci detection.

139 A greater HRD was weakly associated with postoperative VA (Pearson

140 spite the low quality of evidence, a greater HRD, disruption of the EZ and/or ELM, presence of ICCs,

141 There is a clear need to harmonize HRD definitions and to validate the optimal biomarker fo

142 ency was assessed by loss of heterozygosity (HRD-LOH) in pretreatment core breast biopsies.

143 nce of RAD51 foci in tumor cells, and a high HRD score suggest a deleterious effect of this mutation

144 apeutic option for BRCA2-mutated and/or high HRD score patients with GEA, including patients with fam

145 e only approach that consistently identified HRD in whole-exome-sequenced breast and ovarian cancers,

146 nt in 43 of 49 germline carriers identifying HRD-PDAC.

147 rforms germline testing alone in identifying HRD-PDAC.

148 bone geometry of the catalytically important HRD motif deviates from ideality in high-resolution stru

149 for clinical management and trial design in HRD breast cancers.

150 No between-group difference in HRD was observed for novel negative images at recognitio

151 inomas were defined mainly by differences in HRD-related and APOBEC-related mutational signatures and

152 ygosis, and yet is significantly enriched in HRD patients (frequency = 2.1%, i.e., a 3.5-fold enrichm

153 Depleting eTregs in HRD mouse models, with or without PARP inhibition, signi

154 igated Usa1p to understand its importance in HRD complex action.

155 sessed progression-free survival (invPFS) in HRD and intent-to-treat (ITT) populations.

156 c insights into this renowned oncoprotein in HRD.

157 (n = 6) or gCHEK2 (n = 2) did not result in HRD-PDAC by any of the classifiers.

158 ciated with higher benefit from veliparib in HRD cancer, as were decreasing KELIM values in HRP cance

159 Individual HRD-associated mutational signatures alone did not consi

160 omising strategy to pharmacologically induce HRD and enhance the efficacy of PARPi therapies in TNBC.

161 e were estrogen receptor positive and lacked HRD.

162 ed the Hmg-CoA reductase degradation ligase (HRD-ligase), and degraded by cytosolic 26S proteasomes.

163 and two of them had increased tumor HRD-LOH/HRD-LST scores.

164 iency-large-scale state transitions [HRD-LOH/HRD-LST] scores were 12.68 and 5.11, respectively), wher

165 Mean HRD-LOH scores were higher in responders compared with n

166 observed diets, optimal diets showed a mean HRD score increase of 13.91 (95% confidence interval: 13

167 was 35.9 mo, shorter than HRP-RBL (52.0 mo), HRD-RBL (57.1 mo), and HRD-RBH subgroups (53.3 mo; all p

168 Despite high response rates, most HRD cancers ultimately develop resistance to PARPi treat

169 as a unique mechanism that rescues a mutant HRD allele by producing a functional TBCE protein.

170 bility score (GIS) used by Myriad's MyChoice HRD assay; (2) substitution base signature 3 (SBS3); (3)

171 typically as important as Hrd1 in the native HRD complex.

172 les distinctly separated HRD tumors from non-HRD tumors.

173 Hmg2p degradation occurs by the action of HRD genes that direct Hmg2p to the ubiquitin-proteasome

174 tational signatures due to the activities of HRD-associated mutational processes.

175 opsies, DirectHRD achieved 100% detection of HRD with high specificity (>90%).

176 pathogenic variants and genomic features of HRD, suggesting that PACC should be considered as part o

177 t do not harbor gBRCA/PALB2 have features of HRD.

178 However, the impact of HRD and related therapies on the tumor microenvironment

179 However, the impact of HRD on centromeres and transposable elements remains lar

180 The incidence of HRD-negative was 16% (21/129) and was more common for BR

181 lostery occurred prior to and independent of HRD-dependent ubiquitination.

182 iated with genomic "scarring," indicative of HRD history, but exhibited no clear correlations with cl

183 s but exhibiting genomic scars indicative of HRD led to the FDA approval of the first scar-based HRD

184 Notably, induction of HRD in both TP53 mutant and WT AMLs follows the pattern

185 itumor activity was observed irrespective of HRD score.

186 s and other signatures (surrogate markers of HRD).

187 Clearly, DNA methylation of HRD precedes chromatin compaction and loss of expression

188 sis did not correlate with the occurrence of HRD.

189 in Ashkenazi Jewish (AJ); and prevalence of HRD based on other definitions (ie, alterations in other

190 Surrogate readouts of HRD identify a greater proportion of patients with HRD t

191 Regulation of HRD-dependent Hmg2p degradation appears to occur by the

192 Our data indicated that the role of HRD genes in protein degradation, even in this highly de

193 higher frequencies of features suggestive of HRD (27% versus 21%) and a higher proportion of PIK3CA m

194 Genomic features suggestive of HRD, PIK3CA mutations with CNAs, and CNAs were associate

195 an be targeted to improve PARPi treatment of HRD cancers and may provide a means to overcome PARPi re

196 tential strategy to improve the treatment of HRD cancers.

197 clusively utilizes a highly specific type of HRD scar-small deletions with microhomology-and its asso

198 tions affecting HR-/DDR-related genes and/or HRD.

199 he presence or absence of gBRCA mutations or HRD status, with moderate bone marrow toxicity.

200 ivity was seen regardless of gsLOH status or HRD score.

201 reg-focused therapeutics for HGSOC and other HRD-related tumors.

202 ib (HRD, n = 185; ITT, n = 427) and placebo (HRD, n = 49; ITT, n = 111).

203 DeepHRD can predict HRD in breast and ovarian cancers directly from routine

204 n nonplatinum treatment outcome by predicted HRD status in three breast cancer cohorts, including CR

205 DeepHRD predicted HRD from held-out H&E-stained breast cancer slides in TC

206 ade serous ovarian cancer, DeepHRD-predicted HRD samples had better OS after first-line (HR, 0.46; P

207 ould serve as a valuable tool for predicting HRD and clinical response in breast and ovarian cancers.

208 er as a routine predictive and/or prognostic HRD biomarker to guide clinical decision-making.

209 ) selected based on the RECAP test (26 RECAP-HRD; 37%), was subjected to DNA-based HRD tests (i.e., C

210 appears that the physiologically regulated, HRD-dependent degradation of HMGR is effected by a progr

211 Here, we demonstrate a functionally relevant HRD evident at genomic and transcriptomic levels pointin

212 in 656 (26.8%), including features reporting HRD (298 [12.2%] total cases and 76 [6.3%] ER-positive,

213 follow-up was ~59 months for both rucaparib (HRD, n = 185; ITT, n = 427) and placebo (HRD, n = 49; IT

214 The signatures S3 (HRD, P = 0.006) and S4 (tobacco, P = 0.011) were prognos

215 lyses for HR-positive tumors signatures, S3 (HRD, P < 0.001) and S13 (APOBEC, P = 0.001) as well as e

216 RECAP) test is a functional method to select HRD tumors based on their inability to form RAD51 foci.

217 tly examined the association of the separate HRD complex components with various ERAD substrates.

218 ir methylation profiles distinctly separated HRD tumors from non-HRD tumors.

219 DeepHRD was compared with four standard HRD molecular tests using breast (n = 349) and ovarian (

220 ency and nature of tBRCAm, HRD score status [HRD-positive (score 42) versus HRD-negative (score <42)

221 n the F-helix hydrogen bonds to the strained HRD backbone in diverse eukaryotic and eukaryotic-like p

222 S 37.3 versus 23.0 months] in the non-tBRCAm HRD-positive and 0.63 (95% CI 0.52-0.76, P < 0.0001; mPF

223 ab followed by bevacizumab in the non-tBRCAm HRD-positive and non-tBRCAm ITT populations.

224 The frequency and nature of tBRCAm, HRD score status [HRD-positive (score 42) versus HRD-neg

225 amples from 161/302 patients yielded tBRCAm, HRD and gsLOH data for 143 (47%), 129 (43%) and 125 (41%

226 Recent analyses have shown that HRD cancers exhibit characteristic mutational signatures

227 We therefore suggest that HRD as predicted by a functional RAD51 assay correlates

228 ents with recurrent disease, suggesting that HRD continues to be an active mutagenic process after di

229 The HRD (HMG-CoA reductase degradation) pathway is a conserv

230 The HRD complex engages in lumen to cytosol communication re

231 The HRD in C2 also decreased compared with C1, although to a

232 The HRD is capable of reversal of anticoagulation following

233 The HRD pathway is a conserved route of ubiquitin-dependent,

234 The HRD phenotype was most common in high grade serous EOC.

235 The HRD run time averaged 27.4 +/-1.5 mins targeted to remov

236 The HRD run time was determined by a previously established

237 The HRD, therefore, can serve as an alternative to achieve h

238 The HRD-LOH assay was able to identify patients with sporadi

239 Because the HRD genes were required for the degradation of both regu

240 binations of compounds are recognized by the HRD canines.

241 east HMG-CoA reductase (Hmg2p) occurs by the HRD endoplasmic reticulum quality control pathway, imply

242 ted endoplasmic reticulum degradation by the HRD pathway.

243 lding of Hmg2, leading to degradation by the HRD pathway; we call this process mallostery.

244 tested this model by directly comparing the HRD dependency of the ER-associated degradation for vari

245 nregulated substrates of ER degradation, the HRD genes are the agents of HMG-R degradation but not th

246 erevisiae that functions separately from the HRD/DER pathway comprised of Hrd1p, Hrd3p, Der1p, and Ub

247 the strain because of a peptide flip in the HRD backbone.

248 w-up duration was 14 months; patients in the HRD group had lower tumor progression rates at 6 months,

249 dual-specificity depends on residues in the HRD+2 and APE-4 positions that are uncommon in either se

250 ation of HIP substrates does not involve the HRD/DER pathway ubiquitin ligase Hrd1p, but instead uses

251 erized quality control ubiquitin ligase, the HRD complex, which is responsible for the endoplasmic re

252 Moreover, the HRD gene signature serves as an effective drug discovery

253 through the plasma separation chamber of the HRD (where heparin was bound to PLL), and reinfused into

254 support the model of a dimeric state of the HRD complex and provide first-time evidence of self-asso

255 er binding to Hrd3, another component of the HRD complex.

256 ino acid residues and on the function of the HRD genes.

257 volved in the function and regulation of the HRD pathway of ERAD.

258 At the end of the HRD run, heparin concentration decreased to 0.51+/-0.09

259 Usa1p is a recently discovered member of the HRD ubiquitin ligase complex.

260 Use of the HRD was not associated with any adverse hemodynamic reac

261 rane protein Der1, which is a subunit of the HRD-ligase, is involved in the export of aberrant polype

262 ned before, during, and after the use of the HRD.

263 Compared with HR-competent patients, the HRD group was predominantly serous with a higher median

264 CPY* overexpression likely saturates the HRD/DER pathway and activates the HIP pathway, so the sl

265 uch as the hydrophobic regulatory spine, the HRD motif, and the electrostatic switch.

266 as led to the reasonable hypothesis that the HRD (Hmg CoA reductase degradation) gene-encoded protein

267 nzyme A reductase (HMGR), indicated that the HRD complex discerns between a degradation-competent "mi

268 We have discovered that the HRD ubiquitin ligase complex associates with both ERAD s

269 om those of Der1p, which is recruited to the HRD complex by Usa1p.

270 These data favor models in which the HRD gene-encoded proteins function as specificity factor

271 Direct comparison of these HRD tests in clinical trials will be required to evaluat

272 More importantly, this HRD gene signature is able to predict clinical outcomes

273 By using this HRD gene signature as a functional network analysis tool

274 In addition to HRD, CRISPR screening revealed a spectrum of synthetic l

275 In addition to HRD/BRCA status, the tumor primary chemosensitivity obse

276 s) BRCA1 protein that mediated resistance to HRD-targeted therapies.

277 RNASEH2B loss is unrelated to HRD and preclinically sensitizes to PARP inhibition.

278 a1185stop tumors responded markedly worse to HRD-targeted therapy than did Brca15382stop tumors.

279 in-specific DNA methylation of the transgene HRD.

280 on deficiency-large-scale state transitions [HRD-LOH/HRD-LST] scores were 12.68 and 5.11, respectivel

281 ceipt of neoadjuvant chemotherapy, and tumor HRD status.

282 tations, and two of them had increased tumor HRD-LOH/HRD-LST scores.

283 .28; 95% CI, 0.13 to 0.61) or BRCA wild-type HRD cancer (hazard ratio, 0.43; 95% CI, 0.26 to 0.70), c

284 ing domain in UBN1, located between the UBN1 HRD and middle domain, which binds DNA through electrost

285 veal that conserved residues within the UBN1-HRD and H3.3 G90 as key determinants of UBN1-H3.3-bindin

286 emical and biophysical studies show the UBN1-HRD preferentially binds H3.3/H4 over H3.1/H4.

287 LRS uncovered HRD-related genomic and epigenomic alterations in previo

288 tion, but was inversely correlated with UPD, HRD and tumour infiltration by CD68(+) monocytes.

289 Clinical validity and utility of various HRD biomarkers are under investigation.

290 score status [HRD-positive (score 42) versus HRD-negative (score <42) using the Myriad myChoice(R) CD

291 ompared prospectively in HR-competent versus HRD patients.

292 ts completed an image recognition task where HRD, SCRs and affective ratings were recorded again.

293 We now define the mechanisms through which HRD is induced in BRCA-proficient TNBC and OC.

294 es and mutational signatures associated with HRD were elevated in the BRCA1-mutated tumors.

295 sponses to chemotherapy were correlated with HRD status.

296 PARPi sensitivity correlated with HRD, increased genomic instability, and activation of th

297 entify a greater proportion of patients with HRD than analyses limited to gene-level approaches.

298 lymerase inhibitors to include patients with HRD-positive ovarian cancer beyond those with BRCA mutat

299 ovarian cancer, especially in patients with HRD-positive platinum-sensitive disease, which includes

300 - or PALB2-mutant breast cancer treated with HRD-targeted therapy who developed progressive disease-1

301 ith advanced ovarian cancer with and without HRD.