ライフサイエンスコーパス: Jewish

1 onia, chorea, and Creutzfeldt-Jakob with and Jewish.

2 Forty-seven percent were Catholic; 19% were Jewish; 16% were Protestant; and 6% were atheist or agno

3 try from North African (10.6%) and Sephardic Jewish (19.8%) sources.

4 D (N=31) and without PTSD (N=16) and healthy Jewish adults not exposed to the Holocaust (N=35).

5 ten the cause of FA in patients of Ashkenazi Jewish (AJ) ancestry, and we identified 2 novel FANCC mu

6 h Alzheimer's disease (AD), all of Ashkenazi Jewish (AJ) ancestry.

7 renia (SZ) susceptibility locus in Ashkenazi Jewish (AJ) and Han Chinese from Taiwan populations.

8 initis pigmentosa (RP) patients of Ashkenazi Jewish (AJ) descent, aiming to identify genotype-phenoty

9 y 80% of patients with MLIV are of Ashkenazi Jewish (AJ) descent, and two mutations, IVS3-2A-->G and

10 ere followed in our clinic were of Ashkenazi Jewish (AJ) descent, leading us to search for a common m

11 s more prevalent in individuals of Ashkenazi Jewish (AJ) descent.

12 ed better than the other models in Ashkenazi Jewish (AJ) families, BRCAPRO performed slightly better

13 o two densely typed data sets: 500 Ashkenazi Jewish (AJ) individuals and 56 Kenyan Maasai (MKK) indiv

14 rait with the highest frequency in Ashkenazi Jewish (AJ) individuals of Central European origin.

15 The Ashkenazi Jewish (AJ) population has long been viewed as a genetic

16 The Ashkenazi Jewish (AJ) population is a genetic isolate close to Eur

17 In the Ashkenazi Jewish (AJ) population of Israel, 11% of breast cancer a

18 IPD of a prevalent mutation in the Ashkenazi Jewish (AJ) population.

19 s and 1640 controls drawn from the Ashkenazi Jewish (AJ) population.

20 se locus in a French family and an Ashkenazi Jewish American family was also mapped to this region.

21 of pancreatitis (OR = 19, 95% CI: 3.1, 120), Jewish ancestry (OR = 1.8, 95% CI: 1.1, 3.1), and ABO bl

22 Whereas young age (P < .01), Ashkenazi Jewish ancestry (P < .01), triple-negative breast cancer

23 in unrelated affected persons, 3 of Georgian Jewish ancestry and 14 of Turkish ancestry.

24 with type 1 Gaucher disease (64 of Ashkenazi Jewish ancestry and 64 of non-Jewish extraction) and 24

25 658 controls; both groups were of Ashkenazi Jewish ancestry and from New York, New York.

26 ics may reflect the presence of unrecognized Jewish ancestry in this population.

27 requency hearing loss in 2 families of Iraqi Jewish ancestry was due to homozygosity for the protein

28 Three siblings of Moroccan Jewish ancestry were compound heterozygotes for p.A33D a

29 0/172) of patients specifically of Ashkenazi Jewish ancestry were heterozygous for a nonsense, frames

30 Two families of Ashkenazi Jewish ancestry were homozygous for an 18 base pair in-f

31 atients belonging to 4 families of Ashkenazi Jewish ancestry were homozygous for either p.D104A or p.

32 founder alleles among patients of Ashkenazi Jewish ancestry with breast cancer.

33 entrosomal protein 78, in six individuals of Jewish ancestry with CRD and SNHL.

34 re much more common in patients of Ashkenazi Jewish ancestry with sporadic and familial PD than in th

35 ular disease, benign breast conditions, age, Jewish ancestry, family history, and the Klinefelter syn

36 almost exclusively individuals of Ashkenazi Jewish ancestry, is characterized by high levels of the

37 All 21 affected probands are of Jewish ancestry.

38 ic white patients with and without Ashkenazi Jewish ancestry.

39 und almost exclusively in those of Ashkenazi Jewish ancestry.

40 mutations in patients with PD who are of non-Jewish ancestry.

41 Sixty-four Ashkenazi Jewish and 147 non-Jewish white families were studied.

42 pound haplotype frequencies for an Ashkenazi Jewish and a British sample.

43 pe 1 was present in 19 families of Ashkenazi Jewish and European ancestry, whereas haplotype 2 occurr

44 basis of studies in individuals of Ashkenazi Jewish and European ancestry.

45 Christian faith as well as Buddhist, Hindu, Jewish and Islamic perspectives.

46 yopathy has been obtained through studies of Jewish and Japanese patient cohorts carrying founder mut

47 All participants were Ashekanzi Jewish and most patients (98.1%) with GD carried at leas

48 erban, and Libyan) and comparison with other Jewish and non-Jewish groups demonstrated distinctive No

49 ish paternal lineages, as well as non-Levite Jewish and non-Jewish R1a samples.

50 this gene have been demonstrated in Tunisian Jewish and Palestinian kindreds with BCS.

51 emselves and all 4 grandparents as Ashkenazi Jewish and participated in the New York Breast Cancer St

52 Unlinked autosomal microsatellites in six Jewish and two non-Jewish populations were genotyped, an

53 our previous linkage results from Ashkenazi Jewish (ASHK) and African American (AFRAM) families.

54 nes in Old Order Amish (AMISH) and Ashkenazi Jewish (ASHK) families was investigated.

55 1,371 males from 29 populations, including 7 Jewish (Ashkenazi, Roman, North African, Kurdish, Near E

56 ore 1914 show the greatest increases in anti-Jewish attitudes.

57 These Jewish authorities reject the notion that generosity and

58 found to be more common among individuals of Jewish background.

59 yndrome trial, we genotyped 3,258 SNPs in 10 Jewish Bloom syndrome cases and 31 non-Bloom syndrome Je

60 ients were genotyped for the three Ashkenazi Jewish BRCA founder mutations (185delAG and 5382insC in

61 The findings in Ashkenazi Jewish BRCA1 mutation carriers should be confirmed.

62 Ninety-one percent of Jewish BRCA1/2-positive women carried a CJM.

63 ains another founder effect in all Ashkenazi-Jewish cases.

64 Here, in a cohort of Ashkenazi Jewish centenarians, their offspring, and offspring-matc

65 genetic variations in a cohort of Ashkenazi Jewish centenarians, their offspring, and offspring-matc

66 93%) for PCV7/13 serotypes among Bedouin and Jewish children <12 months old, respectively, and 32% (-

67 itored in prospective studies of Bedouin and Jewish children <3 years old in southern Israel between

68 ypes, rates of progression among Bedouin and Jewish children aged <12m declined 74% (55-85%) and 43%

69 dinal data from 369 Bedouin children and 400 Jewish children in Israel who were enrolled in a 7-valen

70 the first 4 Bedouin children and the first 4 Jewish children who were younger than 5 years old and at

71 raeli individuals with CRC self-described as Jewish, Christian and Muslim.

72 e-wide scan in the largest to date Ashkenazi Jewish cohort of 1130 Parkinson patients and 2611 pooled

73 In the National Jewish cohort, the C allele at E375A was associated with

74 In the primary (National Jewish) cohort, these polymorphisms were also compared w

75 ts of studying complex diseases in Ashkenazi Jewish cohorts.

76 in this report occurred among U.S. Orthodox Jewish communities during 2009 and 2010.

77 The results suggest that most Jewish communities were founded by relatively few women,

78 , its incidence is high within the Ashkenazi Jewish community.

79 e of international support from the Diaspora Jewish community; and a strong desire for acceptance by

80 ific haplogroups suggests that the Sephardic Jewish component is the more ancient.

81 s from the 235 IBD pedigrees than in 149 non-Jewish controls (P=0.015).

82 elated, non-Jewish UC cases and 653 new, non-Jewish controls (P=0.021).

83 e two mutant DCXR alleles in 1,067 Ashkenazi Jewish controls was 0.0173, suggesting a pentosuria freq

84 trating possible applications in Islamic and Jewish countries.

85 % CI, 366.3-420.2 per 100,000) for Ashkenazi Jewish couples.

86 986A > C found in APBD patients of Ashkenazi Jewish decent.

87 benefited from the influx of several stellar Jewish dermatologists who were major contributors to the

88 likely to be women (53.1%) and of Ashkenazi Jewish descent (76.8%) in comparison with individuals wh

89 participants, four of whom were of Ashkenazi Jewish descent and three of whom did not meet family-his

90 0% of patients with familial PD of Ashkenazi Jewish descent likely carry the G2019S mutation in the L

91 A total of 896 individuals of Ashkenazi Jewish descent were ascertained in Israel from 267 multi

92 d on 44 large American families of Ashkenazi Jewish descent, each with at least two affected siblings

93 We focused on families of Ashkenazi Jewish descent, to reduce genetic heterogeneity, and, as

94 pulation of both non-Ashkenazi and Ashkenazi Jewish descent, using a sample set representative of the

95 Here, we report a family of Ashkenazi Jewish descent, with 2 out of 3 children affected by CDD

96 SZ cases and 490 controls, all of Ashkenazi Jewish descent.

97 ns, using 29 multiplex families of Ashkenazi Jewish descent.

98 bjects and 150 control subjects of Ashkenazi Jewish descent.

99 h African Jews constitute the second largest Jewish Diaspora group.

100 ther; to European, Middle Eastern, and other Jewish Diaspora groups; and to their former North Africa

101 as a common Middle Eastern origin with other Jewish Diaspora populations, but also suggest that the A

102 ed at about the time of the beginning of the Jewish diaspora, explaining its presence in non-Ashkenaz

103 ttleneck in a.d. 75, at the beginning of the Jewish Diaspora.

104 understand its origin in the context of the Jewish diasporas and subsequent founder events.

105 beginning at a time that coincides with the Jewish Diasporas.

106 enome-wide association study on an Ashkenazi Jewish discovery group (n=428) was performed using Affym

107 The complete 14-marker haplotypes of non-Jewish disease chromosomes, which are crucial for the ge

108 known as "Riley-Day syndrome"), an Ashkenazi Jewish disorder, is the best known and most frequent of

109 Of 235 anonymous Ashkenazi Jewish DNA samples, one was heterozygous for the 1303+1G

110 ly ethical, ultimately its ethical status in Jewish ethics and law is inextricably connected to solvi

111 asians, African Americans, and the Ashkenazi Jewish ethnic group.

112 trol chromosomes were of confirmed Ashkenazi Jewish ethnicity.

113 s when the data were stratified by Ashkenazi Jewish ethnicity; however, there was some evidence of he

114 4 of Ashkenazi Jewish ancestry and 64 of non-Jewish extraction) and 24 patients with type 3 Gaucher d

115 etic Research Study dataset and 19 Ashkenazi Jewish families collected at Johns Hopkins University.

116 families represent a combined dataset of 17 Jewish families from the Fred Hutchinson Cancer Research

117 The 36 Jewish families represent a combined dataset of 17 Jewis

118 We studied 2 large Ashkenazi Jewish families with a high prevalence of CD in an attem

119 prostate cancer susceptibility genes with 36 Jewish families, which represent a stratification of her

120 I was born into a Jewish family in Breslau, Germany, right before the rise

121 h autosomal recessive inheritance in a large Jewish family originating from Morocco.

122 mutation c.1034G>T p.G345V in the Ashkenazi Jewish family.

123 nd a genetically more homogeneous (Ashkenazi Jewish) family collection to perform a 9-cM autosomal ge

124 ) known to cause PCD, including an Ashkenazi Jewish founder mutation in DNAI2.

125 61 analyses) or for three specific Ashkenazi Jewish founder mutations (2,539 analyses) were correlate

126 The Ashkenazi Jewish founder mutations 185delAG and 5382insC (BRCA1) w

127 solve the issues of within and between-group Jewish genetic identity.

128 bly, gene ontology analysis of the Ashkenazi Jewish genetic signature revealed an enrichment of genes

129 Rapid decay of IBD in Ashkenazi Jewish genomes was consistent with a severe bottleneck f

130 d genetic distance, we found that the Libyan Jewish group retains genetic signatures distinguishable

131 ere part of a larger Ashkenazi and Sephardic Jewish group.

132 PMs at the IBD1 locus exist in the high-risk Jewish group.

133 Here, genome-wide analysis of seven Jewish groups (Iranian, Iraqi, Syrian, Italian, Turkish,

134 , genome-wide analysis of five North African Jewish groups (Moroccan, Algerian, Tunisian, Djerban, an

135 reek, and Ashkenazi) and comparison with non-Jewish groups demonstrated distinctive Jewish population

136 an) and comparison with other Jewish and non-Jewish groups demonstrated distinctive North African Jew

137 Eastern, Yemenite, and Ethiopian) and 16 non-Jewish groups from similar geographic locations.

138 blood group and serum markers suggested that Jewish groups had Middle Eastern origin with greater gen

139 A from each of nine geographically separated Jewish groups, eight non-Jewish host populations, and an

140 n, Donna Bratton, and colleagues at National Jewish Health demonstrated that phagocytosis of apoptoti

141 In response, the National Jewish Health Institutional Animal Care and Use Committe

142 g disease in the Adult Care Unit at National Jewish Health, Denver, Colorado, in the January 2006 to

143 We genotyped more than 1,300 Ashkenazi Jewish healthy volunteers from the Hebrew University Gen

144 Jewish heritage was overrepresented, and five multiplex

145 We identified a patient of Ashkenazi Jewish heritage with germ-line heterozygous mutations in

146 ncating mutation in exon 9 and had Ashkenazi Jewish heritage.

147 e HNPCC trial, we genotyped 8,549 SNPS in 13 Jewish HNPCC cases whose colon cancers exhibited microsa

148 men diagnosed with PPCM delivering at Barnes-Jewish Hospital between 2004 to 2014.

149 nducted a prospective cohort study in Barnes Jewish Hospital between June 2011 and May 2012 of hospit

150 ed in the heart transplant program at Barnes Jewish Hospital from 1994 to 2008.

151 The sepsis alert developed at Barnes-Jewish Hospital was shown to increase early therapeutic

152 Patients admitted to Barnes-Jewish Hospital without diarrhea were enrolled from June

153 for Candida species was conducted at Barnes-Jewish Hospital, a 1250-bed urban teaching hospital (Jan

154 Barnes-Jewish Hospital, Saint Louis, MO (January 15, 2015, to D

155 rogram for the Department of Surgery, Barnes Jewish Hospital, St. Louis, Missouri.

156 B admitted between 2008 and 2015 from Barnes-Jewish Hospital.

157 (2)) during gastric bypass surgery at Barnes-Jewish Hospital.

158 aphically separated Jewish groups, eight non-Jewish host populations, and an Israeli Arab/Palestinian

159 The cohort included all Jewish individuals born in Israel over 5 consecutive yea

160 n, Asian, Caucasian, Hispanic, and Ashkenazi Jewish individuals from the greater New York metropolita

161 ay-based genotype analyses of 1477 Ashkenazi Jewish individuals with CD and 2614 Ashkenazi Jewish ind

162 ewish individuals with CD and 2614 Ashkenazi Jewish individuals without CD (controls).

163 o be present in a random sample of Ashkenazi Jewish individuals, at approximately the predicted carri

164 In a genetic analysis of Ashkenazi Jewish individuals, we associated CD with a frameshift m

165 ith CD in an independent cohort of Ashkenazi Jewish individuals.

166 done on NOD2/CARD15-translated regions in 12 Jewish individuals.

167 ith CD in an independent cohort of Ashkenazi Jewish individuals.

168 orse saving Palestinian children than saving Jewish Israeli children, this proportion decreased when

169 e the lives of five children who were either Jewish Israeli or Palestinian.

170 We assessed Jewish-Israeli and Arab-Palestinian adolescents for brai

171 Furthermore, higher oxytocin levels in the Jewish-Israeli majority and tighter brain-to-brain synch

172 randomized field experiment, conducted among Jewish Israelis during widespread violence.

173 igious belief, changes the relative value of Jewish Israelis' lives (compared with Palestinian lives)

174 ritings of major contemporary authorities of Jewish law and ethics whose halakhic positions on bioeth

175 In addition, Israeli Ashkenazi Jewish LRRK2 p.G2019S carriers (mean age at onset, 57.9

176 , as well as in 33.8% of other R1a Ashkenazi Jewish males and 5.9% of 303 R1a Near Eastern males, whe

177 Orthodox Jewish married women (N=380) ages 19 to 58 responded to

178 r seen between 1992 and 2004 at the National Jewish Medical and Research Center (n = 55).

179 7R ZnT-2 mutation in two unrelated Ashkenazi Jewish mothers with infants displaying TNZD.

180 We evaluated how these common Jewish mutations (CJMs) affect cancer risks and risk red

181 erved on both the AJ chromosomes and the non-Jewish N370S chromosomes, suggesting the occurrence of a

182 roups; and to their former North African non-Jewish neighbors has not been well defined.

183 est number of exposures occurring around the Jewish New Year.

184 rouped as Caucasian, Asian, Arabic, Turkish, Jewish or Afro-American.

185 from multiply affected families of Georgian Jewish or German ancestry.

186 diculoneuropathy in infants of North-African Jewish origin from 4 unrelated families.

187 in a separate study population of Ashkenazi Jewish origin suggests that variant(s) located near or w

188 ported in approximately 40 patients of Iraqi Jewish origin, allowing the mapping of the disease to ch

189 le sources for lineages ascribed a Sephardic Jewish origin, these proportions attest to a high level

190 of 85 anonymous Israeli individuals of Iraqi Jewish origin.

191 Ten of 11 families had Ashkenazi Jewish origins and the N48K CLRN1 mutation.

192 ries study design, 179 consecutive Ashkenazi Jewish ovarian cancer patients were genotyped for AR rep

193 -Ashkenazi Levite R1a clade, other Ashkenazi Jewish paternal lineages, as well as non-Levite Jewish a

194 This is the largest study to date on a non-Jewish patient sample with a detailed genotype/phenotype

195 with 8.3% (95% CI, 3.1%-20.1%) in Ashkenazi Jewish patients (n = 41) and 2.2% (95% CI, 0.7%-6.9%) in

196 haplotype carrying only the 268S variant in Jewish patients (OR = 3.13, P=.0023) but not in non-Jews

197 of BRCA1 and BRCA2 in an unselected group of Jewish patients and to compare the clinical characterist

198 utation-specific) A636P testing in Ashkenazi Jewish patients at risk for Hereditary Nonpolyposis Colo

199 ight patients have mild symptoms of HPS; two Jewish patients had received the diagnosis of ocular, ra

200 All the Georgian Jewish patients were homozygous for a mutation encoding

201 Of the 187 Jewish patients who underwent resection for PAC, tissue

202 was identified in 22 (14%) of 161 Ashkenazi Jewish patients with a history of adenomatous polyps and

203 Overall, 14.1% (142 of 1007) of Ashkenazi Jewish patients with breast cancer in the NYBCS carried

204 However, among Ashkenazi Jewish patients with breast cancer who do not carry one

205 e relevant genetic information for Ashkenazi Jewish patients with breast cancer.

206 Ashkenazi Jewish patients with CD and a positive family history we

207 incidence of BRCA mutations among Ashkenazi Jewish patients with fallopian tube carcinoma (FTC) or p

208 Substantial proportions of Ashkenazi Jewish patients with FTC or PPC are BRCA mutation carrie

209 omatous polyps and in 1 (5%) of 20 Ashkenazi Jewish patients with hyperplastic polyps.

210 Jewish patients with PAC resected between January 1986 a

211 nce of germline BRCA1 and BRCA2 mutations in Jewish patients with pancreatic adenocarcinoma (PAC) is

212 uding 6.1% in BRCA1/2 (5.1% in non-Ashkenazi Jewish patients) and 4.6% in other breast/ovarian cancer

213 A was fully sequenced for 1883 non-Ashkenazi Jewish patients, and mutations were identified in 7%, sh

214 rmatics approach in a consanguineous Iranian-Jewish pedigree led to the identification of a homozygou

215 Interestingly, the small number of Ashkenazi Jewish pedigrees (n=11) analyzed in this study contribut

216 ed to define the relatedness of contemporary Jewish people.

217 Orthodox Jewish persons accounted for 97% of case patients.

218 oom syndrome cases and 31 non-Bloom syndrome Jewish persons as a comparison group.

219 of sporadic colon cancer; and, in Ashkenazi Jewish persons, a mutation that was previously thought t

220 d in German-speaking countries at that time, Jewish physicians were particularly vulnerable to persec

221 185delAG mutation is common in the Ashkenazi Jewish population and has been thought to result in loss

222 1307K allele is found in 6% of the Ashkenazi Jewish population and in 1%-2% of Sephardi Jews; it conf

223 roups demonstrated distinctive North African Jewish population clusters with proximity to other Jewis

224 h non-Jewish groups demonstrated distinctive Jewish population clusters, each with shared Middle East

225 aplotype in both and Caucasian and Ashkenazi Jewish population data sets, suggests that this haplotyp

226 SDs) at increased frequency in the Ashkenazi Jewish population has suggested to many the operation of

227 The Ashkenazi Jewish population is of potential utility in disease-map

228 The Ashkenazi Jewish population represents a unique population for stu

229 l clustering and increased prevalence in the Jewish population support a role for a major genetic sus

230 e pulse model and show that in the Ashkenazi Jewish population the admixture fraction is correlated w

231 for the genetic diagnosis of MLIV in the non-Jewish population, are presented here for the first time

232 urpose, we selected cases from the Ashkenazi Jewish population, in which the mutant alleles are expec

233 In the endogamous Georgian Jewish population, the Gly47Arg carrier frequency was 0.

234 factor XI deficiency, outside the Ashkenazi Jewish population, to be highly heterogeneous.

235 r diseases over-represented in the Ashkenazi Jewish population.

236 affects 1/3600 live births in the Ashkenazi Jewish population.

237 cell cycle regulator CHEK2 in the Ashkenazi Jewish population.

238 ars to be relatively common in the Ashkenazi Jewish population.

239 for rapid carrier screening in the Ashkenazi Jewish population.

240 that is particularly common in the Ashkenazi Jewish population.

241 ge disorder found primarily in the Ashkenazi Jewish population.

242 autosomal dominant mutation in the Ashkenazi Jewish population.

243 ith sporadic and familial PD than in the non-Jewish population.

244 ccurred and that segregates in the Ashkenazi Jewish population.

245 and 1,640 controls drawn from the Ashkenazi Jewish population.

246 population clusters with proximity to other Jewish populations and variable degrees of Middle Easter

247 al microsatellites in six Jewish and two non-Jewish populations were genotyped, and the relationships

248 untries and isolation from one another, most Jewish populations were not significantly different from

249 se in white populations, 13-30% in Ashkenazi Jewish populations, and 30-40% in North African Arab-Ber

250 mutation frequencies of white and Ashkenazi Jewish populations, and may not be applicable to other p

251 1L mutations in Middle Eastern and Ashkenazi Jewish populations, respectively.

252 th greater genetic similarity between paired Jewish populations.

253 (CD) has the highest prevalence in Ashkenazi Jewish populations.

254 o occurs at low frequencies in non-Ashkenazi Jewish populations.

255 i Levites, members of a paternally inherited Jewish priestly caste, display a distinctive founder eve

256 Forty-seven of the 115 (40%) Ashkenazi Jewish probands had point mutations; no genomic rearrang

257 In the 136 non-Ashkenazi Jewish probands, 36 (26%) BRCA point mutations and 8 (6%

258 In the non-Ashkenazi Jewish probands, genomic rearrangements constituted 18%

259 neages, as well as non-Levite Jewish and non-Jewish R1a samples.

260 Only five of the 394 patients were Ashkenazi Jewish, revealing that, unlike the type A form of NPD, t

261 effect for ADH2*2 against heavy drinking in Jewish samples but also suggest the importance of enviro

262 Transmission was focused within Jewish schools for boys, where students spend many hours

263 ies among 260 Ashkenazi (AJ) and 80 Sephardi Jewish (SJ) individuals, we genotyped six CYP2C9 and eig

264 50 AJ and 53 members of 10 Sephardi/Oriental Jewish (SOJ) multiplex families with CD, in 36 AJ patien

265 t in non-Jews, suggesting the existence of a Jewish-specific additional disease-predisposing factor o

266 and Asian populations enabled the Ashkenazi Jewish-specific component of the variance to be characte

267 rging approaches, we identified an Ashkenazi Jewish-specific genetic signature that differentiated th

268 horectomy (RRSO), by CJM and self-identified Jewish status.

269 Patients 2-8 are of Oriental Jewish stock of Iraqi or Iranian origin with facial malf

270 esent in approximately 7% of older Ashkenazi Jewish study subjects (OR, 1.7; 95% CI, 1.2-2.4; P < 0.0

271 amilies and had a carrier rate of 1:66 among Jewish subjects of North-African origin.

272 Seventeen Jewish subjects were familiarized with biographies of ei

273 Among Ashkenazi Jewish subjects, either mutation was found in 15% of pat

274 and 3% of controls, and among non-Ashkenazi Jewish subjects, either mutation was found in 3% of pati

275 ong the test individuals, 126 were Ashkenazi Jewish, three were male subjects, 243 had breast cancer,

276 h 93% of the mutant alleles in our Ashkenazi Jewish type 1 patients were N370S, c.84-85insG, IVS2+1G-

277 ed for only 49% of mutant alleles in the non-Jewish type 1 patients.

278 ated in an association analysis of Ashkenazi Jewish type 2 diabetic (n = 275) and control (n = 342) s

279 Previously, in a genome scan of Ashkenazi Jewish type 2 diabetic families, we observed linkage to

280 icated in a second set of 258 unrelated, non-Jewish UC cases and 653 new, non-Jewish controls (P=0.02

281 allele was also more frequent in the 156 non-Jewish UC probands from the 235 IBD pedigrees than in 14

282 adjusted for age, registry, race/ethnicity, Jewish upbringing, education, and childhood domicile.

283 re adjusted for age and ethnicity (Ashkenazi Jewish vs others) as fixed effects and study center as a

284 ong-Term Care or self-reporting as Ashkenazi Jewish was significantly associated with BRCA mutation c

285 Sixty-four Ashkenazi Jewish and 147 non-Jewish white families were studied.

286 nd lower carriage of R702W compared with non-Jewish whites with CD.

287 In a study of 2 large Ashkenazi Jewish with multiple cases of CD, we found the genetic b

288 An Ashkenazi Jewish woman with Gaucher disease has a huge spleen and

289 icantly more likely to undergo RRSO than non-Jewish women (54% v 41%, respectively; odds ratio, 1.87;

290 6%) had 29 separate mutations; there were 11 Jewish women carrying three founder mutations.

291 While observant Jewish women live in a culture defined by a high degree

292 Within BRCA1 mutation carriers, Ashkenazi Jewish women were about five times more likely to have T

293 Jewish women were significantly more likely to undergo R

294 t testing be considered in all non-Ashkenazi Jewish women with an estimated mutation prevalence >or=1

295 ovarian cancer were determined for Ashkenazi Jewish women with inherited mutations in the tumor suppr

296 Among Ashkenazi Jewish women, 3 mutations in BRCA1 and BRCA2 severely in

297 er risk approximately 2-fold among Ashkenazi Jewish women, whereas CHEK2.P85L is a neutral allele.

298 Of these women, 969 were self-identified Jewish women.

299 more likely to have TNBC than non-Ashkenazi Jewish women.

300 ports of a select group of married observant Jewish women.