ライフサイエンスコーパス: PRS

1 PRS enrichment analyses revealed a significant interacti

2 PRS for increased education and diastolic blood pressure

3 PRS for MS were calculated based on a large genome-wide

4 PRS was derived from a genome-wide association study of

5 PRS were then combined using regression to assess which

6 PRS(metaGRS), the best performing PRS, was associated wi

7 PRSs for ASD and those for ADHD both were associated wit

8 PRSs for bipolar disorder and schizophrenia are associat

9 PRSs for coronary artery disease and years of education

10 PRSs have the highest performance in their corresponding

11 PRSs improved model discrimination over age and sex in t

12 PRSs were not correlated with tumor mutation burden, PD-

13 A PRS based on a GWAS of neuroticism (n = 390,278) was pos

14 A PRS based on the 10 established PTC SNPs showed a strong

15 A PRS developed for European-ancestry women is also predic

16 A PRS using 63 BMI-related variants predicted BMI (beta [S

17 ns with PD, to demonstrate the validity of a PRS and to demonstrate a novel gene-environment interact

18 The addition of a PRS does not significantly improve discrimination but re

19 Inhibition of EPRS using a PRS (prolyl-tRNA synthetase)-specific inhibitor, halofug

20 In contrast with a PRS for CAD, the lipid PRSs point to known and directly

21 xpect this integrated platform to accelerate PRS-related cancer research.

22 sure the impact of both (i) APOE and (ii) AD-PRS on a vulnerable cortico-limbic scene-processing netw

23 Despite this breakthrough, the effect of AD-PRS on brain function in young individuals remains unkno

24 re, estimated via polygenic risk scoring (AD-PRS).

25 We show that AD-PRS, not APOE, selectively influences activity within th

26 ADHD PRS explained ~ 1% (p value < 0.0001) of the variance in

27 We estimated associations between ADHD PRS, a general psychopathology factor, and several dimen

28 We derived ADHD PRS for 13,457 children aged 9 or 12 from the Child and

29 Higher ADHD PRS were statistically significantly associated with ele

30 nificant association with both diagnosis and PRS but also significant overlap with 36 PGC2 loci genes

31 nct polygenic risk scores (PRS(cis-eQTL) and PRS(GWAS)), and tested for predicting brain disorders or

32 ) and two genome-wide PRSs (PRS(metaGRS) and PRS(LDPred); 1.7 M and 6.6 M variants, respectively) der

33 sociated with suicide thoughts and NSSH, and PRS for self-harm behaviour predicted suicide thoughts a

34 essed two restricted PRSs (PRS(Tikkanen) and PRS(Tada); 28 and 50 variants, respectively) and two gen

35 he association of low-frequency variants and PRS with SUA levels in 3,194 individuals.

36 As GWAS sample sizes increase and PRSs become more powerful, PRSs are set to play a key ro

37 Among a range of applications, PRSs are exploited to assess shared etiology between phe

38 Even as PRSs are being introduced into clinical practice, there

39 We assessed PRS(313) interaction with age at first diagnosis, family

40 ent in Finland, 336 carriers) and an average PRS (10-90(th) percentile) have a lifetime risk of breas

41 Compared to having an average PRS, having a high PRS contributed 21% to 38% higher lif

42 ted nominal significant interactions between PRS and dietary quality and physical activity on 1-year

43 ment style may moderate the relation between PRS and PTSD.

44 riants associated with ADHD, and captured by PRS, also influence a general genetic liability towards

45 o was 1.36 (95% CI, 1.24-1.49) for the LDL-C PRS and 1.31 (95% CI, 1.19-1.43) for the TG PRS.

46 tween the lowest and highest 5% of the LDL-C PRS distribution.

47 slightly attenuated when adjusting for a CAD PRS (odds ratio, 1.26 [95% CI, 1.16-1.38] for LDL-C and

48 08), we evaluated associations between a CAD PRS and incident cardiovascular and fatal outcomes.

49 levels and partially overlapping with a CAD PRS.

50 e recommended for statin therapy if high CAD PRS were considered a guideline-based risk-enhancing fac

51 ce of an inverse association between the CAD PRS and risk of all-cause death (OR 0.91; 95% CI 0.85, 0

52 The CAD PRS strongly associated with prevalent CAD (odds ratio:

53 A genome-wide CAD PRS was applied to 47,108 individuals across 3 U.S. heal

54 In conclusion, PRS(313) is an independent factor associated with CBC ri

55 In conclusion, PRSs based on a small number of common germline variants

56 Depression PRSs significantly predicted depression, PTSD, and suici

57 are significantly associated with depression-PRS, in both discovery and replication analyses.

58 ve (AUC), was highest for the LDpred-derived PRS (AUC = 0.654) including nearly 1.2 M genetic variant

59 Based on the LDpred-derived PRS, we are able to identify 30% of individuals without

60 We developed PRSs for 6 psychiatric disorders (schizophrenia, bipolar

61 rning the cause-and-effect can be difficult, PRSs could help to identify the driver biomarkers affect

62 In all diseases, PRSs improved reclassification over clinical thresholds,

63 Moreover, dopaminergic PRS appeared to interact with childhood life events in r

64 For each PRS construct, we provide measures on predictive perform

65 LDpred that makes use of LD information, EB-PRS also achieved 37.9%, 33.6%, 8.6%, 36.2%, 40.6% and 1

66 In this paper, we introduce EB-PRS, a novel method that leverages information for effec

67 cancer diagnosis, individuals with elevated PRS have an elevated risk of developing contralateral br

68 n hepatocytes from individuals with elevated PRS, supporting mechanistic links and suggesting a novel

69 cohorts to generate ancestry- and ethnicity PRSs.

70 rman population (DE) to develop and evaluate PRS in the same and different populations.

71 positive association between re-experiencing PRS and PTSD symptoms observed only among veterans with

72 Higher re-experiencing PRS and secure attachment style were independently assoc

73 Adding an extended PRS based on 592,475 common variants did not significant

74 res (PRSs) research, we created an extensive PRS online repository for 35 common cancer traits integr

75 -nucleotide polymorphisms were available for PRS-analyses.

76 After adjusting for PRSs, parental history still strongly predicted progress

77 Standard procedures for PRSs and GWAS were used along with extra steps to rule o

78 s; all general population samples), we found PRS to be associated with AVSD with odds ratios ranging

79 All four PRSs were strongly associated with their corresponding t

80 which increases to 84% (71-97%) with a high PRS ( > 90(th) percentile), and decreases to 49% (30-68%

81 a 1.7-m-tall person) than those with a high PRS (top quartile).

82 ared to having an average PRS, having a high PRS contributed 21% to 38% higher lifetime risk, and 4 t

83 A high PRS for CAD is associated with elevated risk for recurre

84 tment) between individuals with low and high PRS values.

85 p was related to PRS for CAD: 17.0% for high PRS patients (>90th percentile) and 11.4% for lower PRS

86 k reduction by alirocumab of 37% in the high PRS group (hazard ratio, 0.63 [95% CI, 0.46-0.86]; P=0.0

87 post hoc analyses to determine whether high PRS for CAD identifies higher-risk individuals, independ

88 ercentile, < + 1 SD) and 1 sibling with high PRS score (top few percentiles, i.e. > + 2 SD), the pred

89 Heart Association (46.2% for those with high PRS vs. 46.8% for all others, p = 0.54) or U.S. Preventi

90 Higher PRS(313) was associated with increased CBC risk: hazard

91 A higher PRS was associated with earlier age at PD diagnosis and

92 55-65% of the time the higher PRS sibling is the case.

93 Higher PRSs for ADHD were associated with less optimal senses.

94 Higher PRSs for ASD were associated with less optimal overall i

95 Eyes in the highest PRS quintile were 5.4-fold more likely to show early mor

96 urther studies are necessary to determine if PRSs can inform MINS surveillance.

97 Differences in PRS between the deconvoluted subpopulations are not alwa

98 There is no evidence of heterogeneity in PRS performance in Chinese, Malay and Indian women.

99 .2 to 1.3 per standard deviation increase in PRS and corresponding liability r(2) values of approxima

100 1.36]; P(PRS)=2.7x10(-11) per SD increase in PRS), independent of family history and smoking risk fac

101 lent CAD (odds ratio: 1.4 per SD increase in PRS; p < 0.0001).

102 tio for a one-standard-deviation increase in PRS=1.11, 95% CI=1.03, 1.21), and only the PRS for schiz

103 We show that incorporating PRS measurably improves prediction accuracy for most can

104 d guidelines for performing and interpreting PRS analyses.

105 work condenses these summary statistics into PRSs using various approaches such as linkage disequilib

106 suming no caffeine, those in the highest IOP PRS quartile consuming >= 321 mg/day showed a 3.90-fold

107 association: among those in the highest IOP PRS quartile, consuming > 480 mg/day versus < 80 mg/day

108 Eyes in the highest IOP PRS quintile showed an early morning IOP increase of 4.3

109 nship: compared with those in the lowest IOP PRS quartile consuming no caffeine, those in the highest

110 However, the IOP PRS also modified this relationship: compared with those

111 However, the IOP PRS modified this association: among those in the highes

112 The IOP PRS was correlated positively with maximum IOP, disease

113 We used a validated IOP PRS derived from 146 IOP-associated variants in a linear

114 A validated IOP PRS was associated with higher early morning IOP and mea

115 In contrast with a PRS for CAD, the lipid PRSs point to known and directly modifiable risk factors

116 e), and decreases to 49% (30-68%) with a low PRS ( < 10(th) percentile).

117 ; P=0.004) versus a 13% reduction in the low PRS group (hazard ratio, 0.87 [95% CI, 0.78-0.98]; P=0.0

118 e reduction by alirocumab in high versus low PRS groups of 6.0% and 1.5%, respectively, and a relativ

119 with placebo was greater in high versus low PRS patients.

120 ients (>90th percentile) and 11.4% for lower PRS patients (<=90th percentile; P<0.001); this PRS rela

121 epression under stress than at baseline (MDD-PRS x stress interaction beta = 0.036, P = 0.005).

122 antially less of the association between MDD-PRS and depression when under stress than at baseline, s

123 Finally, we found that low MDD-PRS may have particular use in identifying individuals w

124 epressive disorder polygenic risk score (MDD-PRS) derived from the most recent Psychiatric Genomics C

125 stress than at baseline, suggesting that MDD-PRS adds unique predictive power in depression predictio

126 Together, these findings suggest that MDD-PRS holds promise in furthering our ability to predict v

127 5,227 training physicians, we found that MDD-PRS predicted depression under training stress (beta = 0

128 eta = 0.095, P = 4.7 x 10(-16)) and that MDD-PRS was more strongly associated with depression under s

129 his association was mediated across multiple PRS thresholds by white matter microstructure, specifica

130 aminergic, glutamatergic, and neuroendocrine PRS showed evidence of association with unemotional scor

131 The obesity PRS showed distinct effects on lifespan in Japanese and

132 ~2.7-fold risk and women in the lowest 1% of PRS distribution has ~0.4-fold risk of developing breast

133 isk distribution, women in the highest 1% of PRS distribution have a ~2.7-fold risk and women in the

134 High polygenic risk (top 20% of PRS) conferred 1.9-fold odds of developing CAD (p < 0.00

135 ntial pitfall in the clinical application of PRS.

136 o UK Biobank may distort the associations of PRS derived from case-control studies or populations ini

137 (N = 1,027) according to the distribution of PRS(313) was quantified using Cox regression analyses.

138 We evaluated main and interactive effects of PRS and attachment style on PTSD symptoms in a nationall

139 Furthermore, we studied interactions of PRS with smoking during pregnancy and childhood life eve

140 so demonstrate that stratifying on levels of PRS identifies significantly divergent 5-year risk traje

141 entile and 20.5% at the 90(th) percentile of PRS(313).

142 a direct impact on the clinical usability of PRS for risk prediction models using PRS: a population e

143 bility-has led to the routine application of PRSs across biomedical research.

144 te the importance and growing application of PRSs, there are limited guidelines for performing PRS an

145 inear regressions to examine associations of PRSs with neuromotor scores and autistic traits.

146 uss different methods for the calculation of PRSs, provide an introductory online tutorial, highlight

147 The validation and evaluation of PRSs will also be discussed, including the recognition t

148 PRS, individuals in the top decile group of PRSs have a close to sevenfold greater risk (95% CI, 5.4

149 highlight the potential clinical utility of PRSs for CHD as well as the need to assemble diverse coh

150 g evidence regarding the clinical utility of PRSs is considered across four different domains: inform

151 rovides evidence for the additional value of PRSs in clinical disease prediction.

152 ur trans-biobank study offers a new value of PRSs in prioritization of risk factors that could be pot

153 and 59 in modules unrelated to diagnosis or PRS.

154 After mutual adjustment for the other PRSs, only the PRS for bipolar disorder predicted progre

155 istory+smoking), 1.24 [95% CI, 1.14-1.35]; P(PRS)=1.27x10(-6)).

156 odds ratio(PRS), 1.26 [95% CI, 1.18-1.36]; P(PRS)=2.7x10(-11) per SD increase in PRS), independent of

157 PRS(metaGRS), the best performing PRS, was associated with CHD in all three cohorts; hazar

158 there are limited guidelines for performing PRS analyses, which can lead to inconsistency between st

159 Here we evaluate the best performing PRSs for European-ancestry women using data from 17,262

160 izes increase and PRSs become more powerful, PRSs are set to play a key role in research and stratifi

161 While present PRSs typically explain only a small fraction of trait va

162 A high systolic blood pressure PRS was trans-ethnically associated with a shorter lifes

163 We assessed two restricted PRSs (PRS(Tikkanen) and PRS(Tada); 28 and 50 variants, respect

164 nts, respectively) and two genome-wide PRSs (PRS(metaGRS) and PRS(LDPred); 1.7 M and 6.6 M variants,

165 Psychiatric PRSs are moderately associated with psychiatric diagnose

166 Four of the 6 psychiatric PRSs were associated with their primary phenotypes (odds

167 The average QTc-PRS in LQTS was 88.0+/-7.2 and explained only ~2.0% of t

168 80 ms (n=120) had a significantly higher QTc-PRS (89.3+/-6.7) than patients with a QTc<480 ms (n=303,

169 There was no difference in QTc-PRS between symptomatic (n=156, 88.6+/-7.3) and asymptom

170 There was no difference in QTc-PRS or QTc between genotypes.

171 in a prototype QTc-polygenic risk score (QTc-PRS).

172 The QTc-PRS explained <2% of the QTc variability in our LQT1, LQ

173 The QTc-PRS in LQTS probands (n=137; 89.3+/-6.8) was significant

174 A weighted QTc-PRS (range, 0-154.8 ms) was calculated for each patient,

175 e results: Given 1 sibling with normal-range PRS score (< 84 percentile, < + 1 SD) and 1 sibling with

176 was strongly associated with AAA (odds ratio(PRS), 1.26 [95% CI, 1.18-1.36]; P(PRS)=2.7x10(-11) per S

177 history and smoking risk factors (odds ratio(PRS+family history+smoking), 1.24 [95% CI, 1.14-1.35]; P

178 After years of research, PRSs are increasingly used in clinical settings.

179 ature on how both genome-wide and restricted PRSs are developed and the relative merit of each.

180 strongly associated with CHD than restricted PRSs were.

181 We assessed two restricted PRSs (PRS(Tikkanen) and PRS(Tada); 28 and 50 variants, r

182 Furthermore, in the target sample, PRS for self-harm ideation were significantly associated

183 The schizophrenia PRS shows promise in enhancing risk prediction in person

184 e perform phenome-wide polygenic risk score (PRS) analyses on 67 complex traits.

185 We performed polygenic risk score (PRS) analyses to investigate shared genetic etiology bet

186 an established 77-SNP polygenic risk score (PRS) and non-genetic risk factors for YOBC.

187 A polygenic risk score (PRS) based on a GWAS of risk-tolerance (n = 466,571) was

188 A polygenic risk score (PRS) derived from genome-wide association studies of pos

189 We built a 201-variant polygenic risk score (PRS) for CAD and tested for interaction with diabetes pr

190 e incremental value of polygenic risk score (PRS) for coronary artery disease, we added the score to

191 study, we developed a polygenic risk score (PRS) for DILI by aggregating effects of numerous genome-

192 lygenic score (PGS) or polygenic risk score (PRS) is an estimate of an individual's genetic liability

193 ssociation testing and polygenic risk score (PRS) methods to examine rare and common variants.

194 GWAS results to build polygenic risk score (PRS) models in three PTC study groups from Ohio (1,544 p

195 In addition, a polygenic risk score (PRS) of 188 prostate cancer variants was strongly associ

196 thors sought to assess polygenic risk score (PRS) prediction of subsequent psychosis in persons at hi

197 t interactions using a polygenic risk score (PRS) that combined the effects of 111 genetic variants a

198 derived a genome-wide polygenic risk score (PRS) to identify a subset of the population at greater r

199 A polygenic risk score (PRS) was strongly associated with increased risk of T2D-

200 cer (N = 49,674) and a polygenic risk score (PRS, N = 9,365).

201 ombined into distinct polygenic risk scores (PRS(cis-eQTL) and PRS(GWAS)), and tested for predicting

202 ciations between ADHD polygenic risk scores (PRS) and a broad range of childhood psychiatric symptoms

203 ssociation between MS polygenic risk scores (PRS) and brain imaging outcomes from a large, population

204 Polygenic risk scores (PRS) for breast cancer have potential to improve risk pr

205 Polygenic risk scores (PRS) for coronary artery disease (CAD) identify high-ris

206 studies indicate high polygenic risk scores (PRS) for coronary artery disease (CAD) identify individu

207 ally, we test whether polygenic risk scores (PRS) for self-harm ideation and self-harm behaviour pred

208 Polygenic risk scores (PRS) for the 22 risk factors were computed in 26,431 AD

209 generating predictive polygenic risk scores (PRS) from genome-wide association studies (GWASs) includ

210 Polygenic risk scores (PRS) may soon be used to predict inflammatory bowel dise

211 Polygenic risk scores (PRS) provide a personalized genetic susceptibility profi

212 centile of underlying polygenic risk scores (PRS), compared to average risk, ranges from 12 for testi

213 on with schizophrenia polygenic risk scores (PRSs) and with diagnosis, and also for enrichment in gen

214 approaches including polygenic risk scores (PRSs) are now widely used in medical research; however,

215 While polygenic risk scores (PRSs) are poised to be translated into clinical practice

216 native approach using polygenic risk scores (PRSs) based on genome-wide association studies (GWAS) fo

217 search has shown that polygenic risk scores (PRSs) can be used to stratify women according to their r

218 growing evidence that polygenic risk scores (PRSs) can identify individuals with elevated lifetime ri

219 -2006), we calculated polygenic risk scores (PRSs) for ASD and attention-deficit/hyperactivity disord

220 dividuals, calculated polygenic risk scores (PRSs) for common variants, and validated the association

221 Because polygenic risk scores (PRSs) for coronary heart disease (CHD) are derived from

222 Polygenic risk scores (PRSs) for major depression, bipolar disorder, and schizo

223 stigation or yielding polygenic risk scores (PRSs) for prognostication.

224 Polygenic risk scores (PRSs) have been consistently associated with elevated br

225 Polygenic risk scores (PRSs) have shown promise in predicting susceptibility to

226 ific collaboration on polygenic risk scores (PRSs) research, we created an extensive PRS online repos

227 based on genome-wide polygenic risk scores (PRSs) using millions of genetic variants has attracted m

228 low atopic dermatitis polygenic risk scores (PRSs) were associated with longer OS under anti-PD-L1 mo

229 Additionally, 3 polygenic risk scores (PRSs) were generated with 97 BMI variants previously ide

230 We derived polygenic risk scores (PRSs) with ~6M variants separately for LDL-C and TG with

231 and is governed by a proline-rich sequence (PRS) in CD3e that binds to the first Src homology 3 (SH3

232 acial disorder called Pierre Robin sequence (PRS).

233 te individual-level genome-wide and gene-set PRS in the NeuroIMAGE target-sample.

234 A significant PRS-by-attachment style interaction was also observed (b

235 Based on the 10-SNP PRS, individuals in the top decile group of PRSs have a

236 dictive value of integrating cancer-specific PRS with family history and modifiable risk factors for

237 thods have been proposed to improve standard PRS by utilizing external information, such as linkage d

238 d a higher rate of postreperfusion syndrome (PRS; 53.9% vs 26.2%; P = .002), postreperfusion cardiac

239 or LDL-C and 1.24 [95% CI, 1.13-1.36] for TG PRS).

240 PRS and 1.31 (95% CI, 1.19-1.43) for the TG PRS.

241 1.55 (95% CI, 1.48-1.61) mmol/L with the TG PRS.

242 tal malformations, directly demonstrate that PRS is an enhanceropathy, and illustrate how small chang

243 Using mouse models, we demonstrate that PRS phenotypic specificity arises from the convergence o

244 in disease cases, supporting the notion that PRS-associated analytes represent presymptomatic disease

245 be discussed, including the recognition that PRS validity is intrinsically linked to the methodologic

246 We show that PRS have potential for risk stratification for cancers o

247 s in independent clinical datasets show that PRSs were associated with SCZ and MDD diagnostics, and w

248 The PRS also refines the risk assessment of women with first

249 The PRS discriminates psychosis converters from nonconverter

250 The PRS predicted the susceptibility to DILI in patients tre

251 The PRS was based on the latest schizophrenia and bipolar ge

252 The PRS was used in a separate testing set (70%) to examine

253 sk and to determine the impact of adding the PRS to a previously validated psychosis risk calculator.

254 gression to analyze interactions between the PRS and 14 established risk factors.

255 found evidence of an interaction between the PRS and diabetes.

256 s showed a decreased association between the PRS and YOBC risk for women who had ever used hormonal b

257 3.89) and a stronger association between the PRS and YOBC risk in pre-menopausal women (OR = 2.46 ver

258 Gen study with 8401 breast cancer cases, the PRS modifies the breast cancer risk of two high-impact f

259 In conclusion, the PRS may interact with hormonal birth control use and wit

260 We constructed the PRS using a family-based study of 1,291 women diagnosed

261 For Europeans, the PRS was correlated with risk calculator variables of inf

262 The C-index for the PRS(313) alone was 0.563 (95%CI = 0.547-0.586).

263 reening recommendations that incorporate the PRS.

264 At the population level, the top 20% of the PRS distribution accounts for 4.0% to 30.3% of incident

265 ier age at PD diagnosis and inclusion of the PRS in the PREDICT-PD algorithm led to a modest improvem

266 In FinnGen, comparing the highest 5% of the PRS to the lowest 95%, CAD odds ratio was 1.36 (95% CI,

267 formation contributed by the addition of the PRS to the risk calculator was less than severity of dis

268 Finally, the value of the PRS will lie in considering it along with other clinical

269 tual adjustment for the other PRSs, only the PRS for bipolar disorder predicted progression to bipola

270 n PRS=1.11, 95% CI=1.03, 1.21), and only the PRS for schizophrenia predicted progression to psychotic

271 ng contralateral breast cancer, and that the PRS can considerably improve risk assessment among their

272 the observed phenotypes, suggesting that the PRS differences might reflect biases from the uncorrecte

273 se with a family history of CRC, whereas the PRS based on known GWAS variants identified only top 10%

274 ts for CRC assumed to be 0.003), whereas the PRS of the 140 known variants identified from GWASs had

275 dentify two clusters of enhancers within the PRS-associated region that regulate SOX9 expression duri

276 We evaluated the PRSs in two biobanks: the Michigan Genomics Initiative (

277 While one SD increase in the PRSs for total cholesterol (odds ratio [OR] = 0.92; 95%

278 These PRS and GWAS results from this large Peruvian cohort adv

279 Because these PRSs have been developed in women of European ancestry,

280 Cross-trait associations for these PRSs suggest a broader effect of genetic liability beyon

281 ith multiomic profiling and found that these PRSs were associated with 766 detectable alterations in

282 patients (<=90th percentile; P<0.001); this PRS relationship was not explained by baseline LDL-C or

283 of MACE in the placebo group was related to PRS for CAD: 17.0% for high PRS patients (>90th percenti

284 highlight common misconceptions relating to PRS results, offer recommendations for best practice and

285 glaucoma population, individuals in the top PRS decile reach an absolute risk for glaucoma 10 years

286 previously reported risk factors in AD using PRS and MR supports a causal role for education, blood p

287 netic predisposition to breast cancer (using PRS) and MD and microcalcifications was positive, while

288 lity of PRS for risk prediction models using PRS: a population effect must be kept in mind when apply

289 the association between a recently validated PRS of 313 germline variants (PRS(313)) and contralatera

290 A 29-variant PRS was strongly associated with AAA (odds ratio(PRS), 1

291 ntly validated PRS of 313 germline variants (PRS(313)) and contralateral breast cancer (CBC) risk.

292 When PRS was included with preoperative and preoperative plus

293 It is under debate whether PRS models can be applied-without loss of precision-to p

294 A genome-wide PRS for CAD comprising 6 579 025 genetic variants was ev

295 Genome-wide PRS showed evidence of association with uncaring scores

296 variants, respectively) and two genome-wide PRSs (PRS(metaGRS) and PRS(LDPred); 1.7 M and 6.6 M vari

297 th clinical risk factors to test genome-wide PRSs for coronary heart disease, type 2 diabetes, atrial

298 Genome-wide PRSs were more strongly associated with CHD than restric

299 associations of "restricted" and genome-wide PRSs with CHD in three major racial and ethnic groups in

300 r separate lifestyle behaviors interact with PRS and affect changes in CRFs in each intervention grou

301 We assessed performance without and with PRSs via area under the receiver operating characteristi