ライフサイエンスコーパス: microsatellite instability

1 d molecular features, which include moderate microsatellite instability.

2 sults in hereditary cancers characterized by microsatellite instability.

3 Gialpha2-/- cancers have microsatellite instability.

4 ity, but not in cells from colon tumors with microsatellite instability.

5 we analysed colon cancer cell lines showing microsatellite instability.

6 ancer and to tumor characteristics including microsatellite instability.

7 een described in numerous cancers exhibiting microsatellite instability.

8 neoplasia, showing monoclonal expansion and microsatellite instability.

9 the more complex strategy of genotyping for microsatellite instability.

10 lite analysis for loss of heterozygosity and microsatellite instability.

11 ucity of p53 mutations in colon cancers with microsatellite instability.

12 d to compare directly lines with and without microsatellite instability.

13 wo of four AtMSH2-RNAi plants showed similar microsatellite instability.

14 ted in 18% (13 of 78) of CRC tissues without microsatellite instability.

15 rs for DNA mismatch repair deficiency and/or microsatellite instability.

16 ated with a loss of mismatch repair genes or microsatellite instability.

17 ts those genetic alterations contributing to microsatellite instability.

18 or without prior endoscopy to have CIMP and microsatellite instability.

19 BTB2; these were validated in 86 tumors with microsatellite instability.

20 MMR-positive patients with tumors exhibiting microsatellite instability (0.121); the difference was n

21 -negative patients with tumors exhibiting no microsatellite instability (0.211), and the lowest frequ

22 dine dehydrogenase, thymidine phosphorylase, microsatellite instability, 18q loss of heterozygosity,

23 BB2/HER2 point mutations (8.2% [26 of 317]), microsatellite instability (7.6% [13 of 170]), and high

24 otherapy in colon cancer patients exhibiting microsatellite instability, a hallmark of MMR deficiency

25 y event in the normal human aging process is microsatellite instability accumulation in normal human

26 Genotyping for microsatellite instability alone and immunohistochemical

27 the very high frequency of lung cancers with microsatellite instability among chromate workers.

28 he tumor characteristics of all 455 cases by microsatellite instability analysis, in addition to a pa

29 mmunohistochemistry of MLH1, MSH2, and MSH6; microsatellite instability analysis; and hypermethylatio

30 2% (37 of 116) of the colorectal tumors with microsatellite instability analyzed, and evidence of pro

31 used to determine survival associations for microsatellite instability and 5-fluorouracil treatment

32 MLH1 silencing results in microsatellite instability and a hypermutable phenotype.

33 pylori status, tumor site, patient survival, microsatellite instability and BRAF and KRAS mutations.

34 donors > 45 years had a greater frequency of microsatellite instability and CD34(+) progenitors lacki

35 hat have been identified in colon cancer are microsatellite instability and chromosome instability.

36 eviously demonstrated an association between microsatellite instability and decreased CDK2-AP1 (p12(D

37 consenting probands and families, including microsatellite instability and DNA mismatch repair immun

38 A high frequency of microsatellite instability and evidence of MSH2 loss in

39 We examined microsatellite instability and expression of the MMR gen

40 tumors from patients with LS were tested for microsatellite instability and immunohistochemistry (IHC

41 atures of the sebaceous neoplasms, including microsatellite instability and immunohistochemistry, wit

42 sh HNPCC cases whose colon cancers exhibited microsatellite instability and in 63 healthy Jews as a c

43 Allelic imbalance, specifically microsatellite instability and loss of heterozygosity, w

44 Immunohistochemistry and microsatellite instability and MLH1 methylation assays w

45 orrelation of hypermethylated miR-129-2 with microsatellite instability and MLH1 methylation status (

46 Microsatellite instability and MLH1 promoter methylation

47 includes defective DNA mismatch repair with microsatellite instability and POLE mutations in approxi

48 ted DNA polymerases and a distinct impact of microsatellite instability and replication repair defici

49 of consecutive colorectal cancers have high microsatellite instability and that, of this 12%, 25% ha

50 tumoral features, including KRAS, BRAF, p53, microsatellite instability and the CpG island methylatio

51 BRAF V600E mutation has been associated with microsatellite instability and the CpG island methylator

52 CRC) are commonly classified into those with microsatellite instability and those that are microsatel

53 ression levels were strongly associated with microsatellite instability and tumor location in the gas

54 SBA cases (91%), and the higher incidence of microsatellite instability and tumor mutational burden i

55 istory, and tumor characteristics, including microsatellite instability and tumor site.

56 thylation is associated with the presence of microsatellite instability and with absence of p53 mutat

57 to have tumors with MMR deficiency (based on microsatellite instability and/or absence of MMR protein

58 ch repair (MMR) deficiency was determined by microsatellite instability and/or immunohistochemistry.

59 nrolled in the study, 208 (19.5 percent) had microsatellite instability, and 23 of these patients had

60 lignancy; screening of cutaneous lesions for microsatellite instability, and absence of mismatch repa

61 ogenesis: the chromosomal instability (CIN), microsatellite instability, and CpG island methylator ph

62 BRAF- and KRAS-mutation status, microsatellite instability, and CpG island methylator ph

63 lead to sporadic CRC-chromosome instability, microsatellite instability, and DNA hypermethylation-als

64 ave tumor susceptibility, shorter life span, microsatellite instability, and DNA-damage response phen

65 ence (16%, 7 of 43), whereas BRAF wild type, microsatellite instability, and low MACC1 expression def

66 th loss of MSH2 expression, tumors with high microsatellite instability, and lower BMI.

67 of mutations in key regulatory cancer genes, microsatellite instability, and other genes that affect

68 cteristics (CpG island methylator phenotype, microsatellite instability, and the B-Raf protooncogene,

69 is frequently deleted in human tumors due to microsatellite instability-associated mutations.

70 fect in Exo1(-/-) cells also caused elevated microsatellite instability at a mononucleotide repeat ma

71 reatly elevated, and they frequently exhibit microsatellite instability at mono- and dinucleotide rep

72 n mutation of dinucleotide-repeat sequences (microsatellite instability) at nine loci in 16 or more p

73 A relapsed leukemia patient displayed microsatellite instability, but no genetic and epigeneti

74 Microsatellite instability can be found in approximately

75 ed human CRC tissues and cell lines that had microsatellite instability contained truncations in the

76 py, including tumor mutational burden (e.g., microsatellite instability), copy-number alterations, an

77 Neither PTEN loss nor microsatellite instability correlated with efficacy.

78 g for clinical and tumor features, including microsatellite instability, CpG island methylator phenot

79 n tumor molecular characteristics (including microsatellite instability, CpG island methylator phenot

80 uding PTGS2, phosphorylated AKT, KRAS, BRAF, microsatellite instability, CpG island methylator phenot

81 hort, two of which overlapped with the TCGA 'microsatellite instability/CpG island methylation phenot

82 approximately 20% that overlap greatly with microsatellite instability CRCs and some nonhypermutated

83 data were combined, providing rationale for microsatellite instability for 8 of the 9 cell lines in

84 ors, and beta-catenin and PTEN mutations and microsatellite instability for endometrioid tumors.

85 uding loss of the INK4a tumor suppressor and microsatellite instability from reduction of the DNA mis

86 on with a concrete example that involves the microsatellite instability gene MLH1.

87 Microsatellite instability had been determined previousl

88 However, the presence or absence of microsatellite instability has a major effect on the exp

89 The role of microsatellite instability has been a subject of discuss

90 T1 mRNA was not translated in CRC cells with microsatellite instability (HCT116).

91 oss of MMR protein expression (MMR-D) and/or microsatellite instability high (MSI-H) genotype.

92 Although sporadic microsatellite instability high tumors had the highest a

93 We identified 36 microsatellite instability-high (17.6%) and 168 non-micr

94 astatic DNA mismatch repair-deficient (dMMR)/microsatellite instability-high (MSI-H) colorectal cance

95 alyses showed no survival difference between microsatellite instability-high and non-microsatellite i

96 efit of 5-fluorouracil was different between microsatellite instability-high and non-microsatellite i

97 ween microsatellite instability-high and non-microsatellite instability-high groups (hazard ratio, 1.

98 ween microsatellite instability-high and non-microsatellite instability-high groups.

99 tellite instability-high (17.6%) and 168 non-microsatellite instability-high tumors (82.4%).

100 re is improved survival in patients with non-microsatellite instability-high tumors after 5-fluoroura

101 Microsatellite instability-high tumors were significantl

102 Patients with non-microsatellite instability-high tumors who received 5-fl

103 Conversely, patients with microsatellite instability-high tumors who were treated

104 herapy that does not extend to patients with microsatellite instability-high tumors.

105 influence of 5-fluorouracil in patients with microsatellite instability-high tumors.

106 by the associations of CIMP-high cancer with microsatellite instability-high, DNMT3B-positive, and BR

107 between CGI methylation and hypermutability, microsatellite instability, IDH1 mutation, 19p gain and

108 s (CMSs) with distinguishing features: CMS1 (microsatellite instability immune, 14%), hypermutated, m

109 Mlh3 deficiency alone causes microsatellite instability, impaired DNA-damage response

110 ents, mutations of BRAF in 15% patients, and microsatellite instability in 26% patients.

111 ed in tumor progression of mouse models with microsatellite instability in a haplo-insufficient manne

112 ic SETD2 aberrations are not associated with microsatellite instability in ccRCC.

113 Microsatellite instability in colorectal cancer predicts

114 subject of discussion, and data suggest that microsatellite instability in inflammatory bowel disease

115 ng repeat sequences: DNMT1 deficiency causes microsatellite instability in mouse embryonic stem cells

116 is revealed that Immunoscore was superior to microsatellite instability in predicting patients' disea

117 matory bowel disease might be different from microsatellite instability in sporadic colorectal cancer

118 (EXO1, MSH2, and MSH6) were associated with microsatellite instability, increased number of somatic

119 In vitro studies suggest that microsatellite instability influences cell survival afte

120 Microsatellite instability is associated with 10% to 15%

121 While microsatellite instability is implicated in numerous gen

122 cing were used to establish the incidence of microsatellite instability, KLF6 and TP53 allelic imbala

123 arise either by a chromosomal instability or microsatellite instability mechanism.

124 stage II disease, molecular markers such as microsatellite instability might help select patients fo

125 AI at APAF-1 locus and microsatellite instability (MIN) in CRCs and adenomas we

126 Microsatellite instability (MIN) leads to by elevated po

127 ay MSI or abnormal IHC (often referred to as microsatellite instability [MIN] pathway).

128 non-polyposis colon cancer, Lynch syndrome, microsatellite instability, mismatch repair genes, and t

129 athology testings (for example, analyses for microsatellite instability, MLH1 promoter CpG island met

130 Most tumors showed microsatellite instability, more marked at dinucleotide

131 Frequent microsatellite instability MSI (MSI-H) occurring in huma

132 Case tissue samples were obtained for microsatellite instability (MSI) analyses.

133 l as from adjacent normal control tissue and microsatellite instability (MSI) analysis using 5 highly

134 ridization (aCGH), mutational profiling, and microsatellite instability (MSI) analysis.

135 Colorectal cancers (CRCs) with microsatellite instability (MSI) and a mismatch repair (

136 the H3K36 trimethyltransferase SETD2 display microsatellite instability (MSI) and an elevated spontan

137 reviously characterized genetic alterations (microsatellite instability (MSI) and APC gene mutation).

138 MP1) is a distinct phenotype associated with microsatellite instability (MSI) and BRAF mutation in co

139 Two major classes of genetic instability, microsatellite instability (MSI) and chromosome instabil

140 We characterized 100 sporadic CRCs for microsatellite instability (MSI) and CIN.

141 s have investigated the relationship between microsatellite instability (MSI) and colorectal cancer (

142 iffers by the molecular pathologic status of microsatellite instability (MSI) and expression of cell-

143 here tumors were available were screened for microsatellite instability (MSI) and expression of MSH2

144 In a subset of patients, we assessed microsatellite instability (MSI) and expression of the m

145 Tumors were analyzed for microsatellite instability (MSI) and for expression of M

146 R) status was accessed by testing tissue for microsatellite instability (MSI) and for hMLH1 and hMSH2

147 Microsatellite instability (MSI) and genomic hypermethyl

148 ounds using MMR mutation screening, aided by microsatellite instability (MSI) and immunohistochemistr

149 Most studies of microsatellite instability (MSI) and outcomes in endomet

150 te that genomic instability, as evidenced by microsatellite instability (MSI) and promoter methylatio

151 Heterogeneity for microsatellite instability (MSI) and promoter methylatio

152 r depletion of MutSalpha from cells leads to microsatellite instability (MSI) and resistance to DNA d

153 Colorectal cancers (CRCs) displaying DNA microsatellite instability (MSI) are associated with a f

154 Mismatch repair (MMR) deficiency (MMRD) and microsatellite instability (MSI) are prognostic for surv

155 MSH2, MSH6, and PMS2 protein expression and microsatellite instability (MSI) are well-established to

156 for loss of heterozygosity at BMPR2 and for microsatellite instability (MSI) at 5 loci.

157 Identifying microsatellite instability (MSI) by partitioning DNA int

158 Microsatellite instability (MSI) caused by mismatch repa

159 These were found in microsatellite instability (MSI) cell lines and 43% of M

160 Cancer cells showing microsatellite instability (MSI) demonstrate a high freq

161 To date, two forms of microsatellite instability (MSI) have been described in

162 Patients with colorectal tumors with microsatellite instability (MSI) have better prognoses t

163 Colorectal cancers (CRC) with microsatellite instability (MSI) have clinical, patholog

164 developed a three-marker assay that assigns microsatellite instability (MSI) in a multiplex polymera

165 nal spectrum, and functional consequences of microsatellite instability (MSI) in cancer genomes.

166 S. cerevisiae and also induced high rates of microsatellite instability (MSI) in human cells.

167 ting the prognostic and predictive impact of microsatellite instability (MSI) in human colon carcinom

168 Microsatellite instability (MSI) is a clonal change in t

169 Microsatellite instability (MSI) is a hallmark of cancer

170 Microsatellite instability (MSI) is a hallmark of mismat

171 Microsatellite instability (MSI) is a hypermutable pheno

172 Microsatellite instability (MSI) is a molecular phenotyp

173 Microsatellite instability (MSI) is an important indicat

174 Microsatellite instability (MSI) is displayed by approxi

175 umulation of DNA replication errors known as microsatellite instability (MSI) is the hallmark lesion

176 Microsatellite instability (MSI) of DNA is a hallmark fe

177 ctal cancers (CRCs) are classified as having microsatellite instability (MSI) or chromosomal instabil

178 pe of genomic instability that they exhibit, microsatellite instability (MSI) or chromosomal instabil

179 However, it is unclear whether microsatellite instability (MSI) or immunohistochemistry

180 be screened for Lynch syndrome (LS) through microsatellite instability (MSI) or immunohistochemistry

181 median [range] age, 60.0 [19.0-75.0] years), microsatellite instability (MSI) phenotype, KRAS, and BR

182 amilial CRC unstratified with respect to the microsatellite instability (MSI) phenotype.

183 Microsatellite instability (MSI) refers to the hypermuta

184 Colorectal cancers with microsatellite instability (MSI) represent 15% of all co

185 rt of 273 sporadic CRCs by determining their microsatellite instability (MSI) status.

186 All tumors underwent microsatellite instability (MSI) testing.

187 myelodysplastic syndrome (MDS) exhibited the microsatellite instability (MSI) that is diagnostic for

188 ffective in selecting for cells with reduced microsatellite instability (MSI) that is inherent in mis

189 rited defects in DNA mismatch repair and the microsatellite instability (MSI) tumor phenotype.

190 We sought to determine whether tumor microsatellite instability (MSI) typing along with immun

191 mycosis fungoides samples were analyzed for microsatellite instability (MSI) using the panel of mark

192 or and plasma MGMT promoter methylation, and microsatellite instability (MSI) were examined in 14 of

193 n (CBP) gene together are mutated in >85% of microsatellite instability (MSI)+ colon cancer cell line

194 eling family, in 83% of gastric cancers with microsatellite instability (MSI), 73% of those with Epst

195 ed UVRAG(FS) in colorectal cancer (CRC) with microsatellite instability (MSI), and promotes tumorigen

196 , p21, beta-catenin, LINE-1 hypomethylation, microsatellite instability (MSI), and the CpG island met

197 (CRC) cell lines and in primary tumors with microsatellite instability (MSI), but not in microsatell

198 omic instability are common in colon cancer: microsatellite instability (MSI), chromosome instability

199 proposed, based on specific combinations of microsatellite instability (MSI), CpG island methylator

200 s are resistant to genotoxic agents and have microsatellite instability (MSI), due to accumulation of

201 omarkers, including major mutational events, microsatellite instability (MSI), epigenetic features, p

202 We also looked for microsatellite instability (MSI), germline mutations in

203 luding the CpG island methylation phenotype, microsatellite instability (MSI), LINE-1 hypomethylation

204 from NRG/GOG0210 patients were assessed for microsatellite instability (MSI), MLH1 methylation, and

205 Microsatellite instability (MSI), the spontaneous loss o

206 smatch repair plays a key role in preventing microsatellite instability (MSI), which is a hallmark of

207 roximately 15% of colorectal cancers exhibit microsatellite instability (MSI), which leads to accumul

208 Microsatellite instability (MSI), which occurs in 15% of

209 sor Bax is frequently mutated in tumors with microsatellite instability (MSI).

210 ions that define this syndrome and result in microsatellite instability (MSI).

211 development and is inversely associated with microsatellite instability (MSI).

212 ct classes: chromosome instability (CIN) and microsatellite instability (MSI).

213 They die of invasive GI tumors that display microsatellite instability (MSI).

214 mined these associations stratified by tumor microsatellite instability (MSI).

215 mismatch repair genes and hence demonstrate microsatellite instability (MSI).

216 ctive DNA mismatch repair (MMR) indicated by microsatellite instability (MSI).

217 cular manifestation of this repair defect is microsatellite instability (MSI).

218 R)-deficient colorectal tumours that exhibit microsatellite instability (MSI).

219 DNA methylation that direct the increase in microsatellite instability (MSI).

220 n as the microsatellite mutator phenotype or microsatellite instability (MSI).

221 f genomic instability: chromosomal (CIN) and microsatellite instability (MSI).

222 d synovium, we analyzed synovial tissues for microsatellite instability (MSI).

223 site endonuclease; and (b) the prevalence of microsatellite instability (MSI).

224 tations in gastrointestinal neoplasms having microsatellite instability (MSI).

225 loss of heterozygosity of chromosome 9p; and microsatellite instability (MSI).

226 of recurrent indels that may serve to detect microsatellite instability (MSI).

227 Tumors are characterized by microsatellite instability (MSI).

228 cers have mismatch repair gene mutations and microsatellite instability (MSI).

229 3, MGMT, MINT1, MINT31, p14 [ARF], and WRN); microsatellite instability (MSI); the CpG island methyla

230 otype), including simple repeat instability [microsatellite instability (MSI)] are a signature of MMR

231 ectal cancer (CRC) cells with high levels of microsatellite instability (MSI-H) accumulate mutations

232 ght to determine the frequency of high-level microsatellite instability (MSI-H) and the mutational an

233 The role of high-degree microsatellite instability (MSI-H) as a marker to predic

234 ated with genesis or progression of frequent microsatellite instability (MSI-H) cancers.

235 Colon cancers with high-frequency microsatellite instability (MSI-H) develop frameshift mu

236 Colorectal tumors manifesting high-frequency microsatellite instability (MSI-H) develop genetically a

237 Colorectal cancers with high levels of microsatellite instability (MSI-H) have an unexplained l

238 with colon cancer who demonstrate high-level microsatellite instability (MSI-H) or defective DNA mism

239 CIMP is probably the cause of high-frequency microsatellite instability (MSI-H) sporadic CRCs, its ro

240 equently occurred in colon cancers with high microsatellite instability (MSI-H).

241 sus workshop for detection of high-frequency microsatellite instability (MSI-H).

242 tween methylation of hMLH1 and high-level of microsatellite instability (MSI-H): methylation of hMLH1

243 l cancer cells frequently have low levels of microsatellite instability (MSI-L) and elevated microsat

244 ensity was significantly higher in low-level microsatellite instability (MSI-L) than in non-MSI-L can

245 rity (81%) of A/J tumors displayed low-level microsatellite instability (MSI-L) when analysed using m

246 yzed by direct sequencing in 141 tumors with microsatellite instability (MSI-positive) and 107 micros

247 al/family history of cancer or polyps, tumor microsatellite instability [MSI], mismatch repair [MMR]

248 ed on combinations of tumor markers: type 1 (microsatellite instability [MSI]-high, CpG island methyl

249 odds ratio, 2.19; 95% CI, 1.14 to 4.21) and microsatellite instability (multivariate odds ratio, 2.1

250 al cancer biomarkers and are associated with microsatellite instability, namely MLH1, PMS2, MSH2, MSH

251 d from chromosomal instability neoplasia and microsatellite instability neoplasia CRC subtypes and to

252 Some colorectal and endometrial tumors with microsatellite instability not attributable to MLH1 hype

253 e previously shown that distinct patterns of microsatellite instability occur in upper and lower urin

254 individuals' tumor tissue demonstrated high microsatellite instability of di- and tetranucleotides (

255 (HR: 1.99; 95% CI: 1.10, 3.56) but not with microsatellite instability or CpG island methylator phen

256 ) CRIS-A: mucinous, glycolytic, enriched for microsatellite instability or KRAS mutations; (ii) CRIS-

257 independent of tumor staging, site location, microsatellite instability or stability, and patient tre

258 chromosomal gains or losses, a high level of microsatellite instability, or the presence of Helicobac

259 by age at diagnosis, family history of CRC, microsatellite instability, or tumor site at either locu

260 ance of oncogenic BRAF mutation coupled with microsatellite instability, p16Ink4a inactivation, and p

261 me-wide copy-number variation and a moderate microsatellite instability phenotype compared with Msh2/

262 etween smoking cessation and cancer risks by microsatellite instability (Pheterogeneity = 0.02), DNMT

263 In a panel of 40 samples from microsatellite instability-positive colon cancer patient

264 lopment and clinical behavior of a subset of microsatellite instability-positive endometrial, colon,

265 r contributing to phenotypic variation among microsatellite instability-positive tumors.

266 Archival tissues were analyzed for microsatellite instability, PTEN status, and 487-gene se

267 eatures and is responsible for most cases of microsatellite instability related to hMLH1 inactivation

268 nal effects of mutations at other regions of microsatellite instability should be evaluated.

269 This endogenous microsatellite instability, shown for the first time in

270 potent indicator of tumor recurrence beyond microsatellite-instability staging that could be an impo

271 MIRMMR predicts microsatellite instability status in cancer samples usin

272 The microsatellite instability status of a patient's colorec

273 Tumor microsatellite instability status was available for 95 p

274 on (right sided), poor differentiation, high microsatellite instability status, and a positive first-

275 canonical CIMP-related loci and 7 new loci), microsatellite instability status, and BRAF/KRAS mutatio

276 with the tumor's clinicopathologic details, microsatellite instability status, and subsequent behavi

277 Fresh-frozen tissue, microsatellite instability status, clinical parameters,

278 Patterns of concurrent mutations, microsatellite instability status, CpG island methylatio

279 2, TP53, CpG island methylator phenotype, or microsatellite instability status.

280 umor's progression stage, origin, and likely microsatellite instability status.

281 gene expression that correlated with patient microsatellite instability status.

282 in these double somatic tumors than in other microsatellite-instability subgroups.

283 TR mutations are found in human cancers with microsatellite instability, suggesting that ATR haploins

284 In stage II disease, for example, microsatellite instability supports observation after su

285 For HNPCC, 80%-95% can be identified by microsatellite instability testing.

286 protein loss, supported by BRAF mutation and microsatellite instability testing.

287 In recurrent disease, the absence of microsatellite instability (the standard marker for MMR

288 d ratio (HR); calculations were adjusted for microsatellite instability; the CpG island methylator ph

289 icrosatellite-stable tumors from tumors with microsatellite instability, thus potentially improving c

290 for clinical and tumoral features, including microsatellite instability, TP53 (p53), PTGS2 (cyclooxyg

291 ated, and family characteristics, as well as microsatellite instability, tumor MMR immunostaining, an

292 owever, the mechanistic relationship between microsatellite instability, tumor-infiltrating immune ce

293 s of CpG island methylator phenotype (CIMP), microsatellite instability, v-raf murine sarcoma viral o

294 DNA microsatellite instability was also assessed using a pan

295 Archival DNA was extracted, and microsatellite instability was assessed by National Canc

296 Microsatellite instability was observed in all VCMsh2 st

297 As expected, significant microsatellite instability was observed in six of six tu

298 or homing were observed, but an increase in microsatellite instability was seen in the MSH2-/- early

299 Genotyping of the tumor for microsatellite instability was the primary screening met

300 ts whose screening results were positive for microsatellite instability, we searched for germ-line mu