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Articles by H. T Lynch
Total Records ( 2 ) for H. T Lynch
  A Bellacosa , A. K Godwin , S Peri , K Devarajan , E Caretti , L Vanderveer , B Bove , C Slater , Y Zhou , M Daly , S Howard , K. S Campbell , E Nicolas , A. T Yeung , M. L Clapper , J. A Crowell , H. T Lynch , E Ross , L Kopelovich and A. G. Knudson

We hypothesized that cells bearing a single inherited "hit" in a tumor suppressor gene express an altered mRNA repertoire that may identify targets for measures that could delay or even prevent progression to carcinoma. We report here on the transcriptomes of primary breast and ovarian epithelial cells cultured from BRCA1 and BRCA2 mutation carriers and controls. Our comparison analyses identified multiple changes in gene expression, in both tissues for both mutations, which were validated independently by real-time reverse transcription-PCR analysis. Several of the differentially expressed genes had been previously proposed as cancer markers, including mammaglobin in breast cancer and serum amyloid in ovarian cancer. These findings show that heterozygosity for a mutant tumor suppressor gene can alter the expression profiles of phenotypically normal epithelial cells in a gene-specific manner; these detectable effects of "one hit" represent early molecular changes in tumorigenesis that may serve as novel biomarkers of cancer risk and as targets for chemoprevention. Cancer Prev Res; 3(1); 48–61

  H. T Lynch , T Jascur , S Lanspa and C. R. Boland

The DNA mismatch repair (MMR) system provides critical genetic housekeeping, and its failure is associated with tumorigenesis. Through distinct domains on the DNA MMR proteins, the system recognizes and repairs errors occurring during DNA synthesis, but signals apoptosis when the DNA damage cannot be repaired. Certain missense mutations in the MMR genes can selectively alter just one of these functions. This affects the clinical features of tumors associated with defective DNA MMR activity. New work reported by Xie et al. in this issue of the journal (beginning on page 1409) adds to the understanding of DNA MMR. Cancer Prev Res; 3(11); 1371–4. ©2010 AACR.

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