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Articles by A de la Chapelle
Total Records ( 2 ) for A de la Chapelle
  K Guda , L Natale , J Lutterbaugh , G. L Wiesner , S Lewis , S. M Tanner , J Tomsic , L Valle , A de la Chapelle , R. C Elston , J Willis and S. D. Markowitz
 

Recently, germline allele-specific expression (ASE) of the gene encoding for transforming growth factor-β type I receptor (TGFBR1) has been proposed to be a major risk factor for cancer predisposition in the colon. Germline ASE results in a lowered expression of one of the TGFBR1 alleles (>1.5-fold), and was shown to occur in ~20% of informative familial and sporadic colorectal cancer (CRC) cases. In the present study, using the highly quantitative pyrosequencing technique, we estimated the frequency of ASE in TGFBR1 in a cohort of affected individuals from familial clusters of advanced colon neoplasias (cancers and adenomas with high-grade dysplasia), and also from a cohort of individuals with sporadic CRCs. Cases were considered positive for the presence of ASE if demonstrating an allelic expression ratio <0.67 or >1.5. Using RNA derived from lymphoblastoid cell lines, we find that of 46 informative Caucasian advanced colon neoplasia cases with a family history, only 2 individuals display a modest ASE, with allelic ratios of 1.65 and 1.73, respectively. Given that ASE of TGFBR1, if present, would likely be more pronounced in the colon compared with other tissues, we additionally determined the allele ratios of TGFBR1 in the RNA derived from normal-appearing colonic mucosa of sporadic CRC cases. We, however, found no evidence of ASE in any of 44 informative sporadic cases analyzed. Taken together, we find that germline ASE of TGFBR1, as assayed in lymphoblastoid and colon epithelial cells of colon cancer patients, is a relatively rare event. [Cancer Res 2009;69(12):4959–61]

  S Volinia , M Galasso , S Costinean , L Tagliavini , G Gamberoni , A Drusco , J Marchesini , N Mascellani , M. E Sana , R Abu Jarour , C Desponts , M Teitell , R Baffa , R Aqeilan , M. V Iorio , C Taccioli , R Garzon , G Di Leva , M Fabbri , M Catozzi , M Previati , S Ambs , T Palumbo , M Garofalo , A Veronese , A Bottoni , P Gasparini , C. C Harris , R Visone , Y Pekarsky , A de la Chapelle , M Bloomston , M Dillhoff , L. Z Rassenti , T. J Kipps , K Huebner , F Pichiorri , D Lenze , S Cairo , M. A Buendia , P Pineau , A Dejean , N Zanesi , S Rossi , G. A Calin , C. G Liu , J Palatini , M Negrini , A Vecchione , A Rosenberg and C. M. Croce
 

We studied miRNA profiles in 4419 human samples (3312 neoplastic, 1107 nonmalignant), corresponding to 50 normal tissues and 51 cancer types. The complexity of our database enabled us to perform a detailed analysis of microRNA (miRNA) activities. We inferred genetic networks from miRNA expression in normal tissues and cancer. We also built, for the first time, specialized miRNA networks for solid tumors and leukemias. Nonmalignant tissues and cancer networks displayed a change in hubs, the most connected miRNAs. hsa-miR-103/106 were downgraded in cancer, whereas hsa-miR-30 became most prominent. Cancer networks appeared as built from disjointed subnetworks, as opposed to normal tissues. A comparison of these nets allowed us to identify key miRNA cliques in cancer. We also investigated miRNA copy number alterations in 744 cancer samples, at a resolution of 150 kb. Members of miRNA families should be similarly deleted or amplified, since they repress the same cellular targets and are thus expected to have similar impacts on oncogenesis. We correctly identified hsa-miR-17/92 family as amplified and the hsa-miR-143/145 cluster as deleted. Other miRNAs, such as hsa-miR-30 and hsa-miR-204, were found to be physically altered at the DNA copy number level as well. By combining differential expression, genetic networks, and DNA copy number alterations, we confirmed, or discovered, miRNAs with comprehensive roles in cancer. Finally, we experimentally validated the miRNA network with acute lymphocytic leukemia originated in Mir155 transgenic mice. Most of miRNAs deregulated in these transgenic mice were located close to hsa-miR-155 in the cancer network.

 
 
 
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