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Finally, the present results demonstrate a recurrent SDHB mutation in normal PBMCs and leukemic T cells.
The current study describes identification of substantial levels of SDHB transcripts carrying a recurrent R46X mutation in normal PBMCs.
No information exists on the actual rate of Kras mutation in normal human tissues and we cannot rule out species-specific differences.
These data again indicate the presence of oncogenic cell stress and p53 upregulation and/or mutation in normal epithelial and dysplastic cells adjacent to invasive cancers within inclusion cysts, but not elsewhere within the same ovarian tissues.
Genetic analyses of DNA from the normal epithelium and dysplasia adjacent to the carcinomas revealed the presence of the corresponding tumor-associated TP53 mutation in normal epithelium in two of five cases, and in dysplasia but not normal epithelium in two additional cases (Supplemental Table S2).
In order to rule out the presence of observed mutation in normal population, an assay was utilized for large scale mutation detection using PCR-RFLP technique.
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We have also experimentally tested whether RASSF1A (genomic DNA, exons1 and 2) harbored mutations in normal tissues and found one mutated clone out of 14 in normal kidney (normal control to T356, see section "Frequent mutations in RASSF1A in human carcinomas").
We describe here approaches for characterizing somatic mutations in normal and non-tumor disease tissues.
Prevalence of pSCNA in peripheral blood predicted survival, implying that mutations in normal tissues might have consequences for cancer patients.
Of the 12 PIK3CA wild-type cases, LNA-PCR sequencing detected three additional H1047R mutations in "normal" breast tissue and one E545K in usual ductal hyperplasia.
Researchers proposed that HSP90 allows the flies to store many genetic mutations in normal times but express them only in tough times.
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