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Neoplasms are thought to progress to cancer through genetic instability generating cellular diversity and clonal expansions driven by selection for mutations in cancer genes. Despite advances in the study of molecular biology of cancer genes, relatively little is known about evolutionary mechanisms that drive neoplastic progression. It is unknown, for(More)
Alterations of the DNA methylation pattern have been related to generalized chromosomal disruption and inactivation of multiple tumor suppressor genes in neoplasia. To screen for tumor-specific alterations and to make a global assessment of methylation status in cancer cells, we have modified the methylated CpG island amplification method to generate easily(More)
DNA hypomethylation is a common trait of colorectal cancer. Studies in tumor cell lines and animal models indicate that genome-wide demethylation may cause genetic instability and hence facilitate or accelerate tumor progression. Recent studies have shown that DNA hypomethylation precedes genomic damage in human gastrointestinal cancer, but the nature of(More)
Defects in DNA repair may be responsible for the genesis of mutations in key genes in cancer cells. The tumor suppressor gene p53 is commonly mutated in human cancer by missense point mutations, most of them G:C to A:T transitions. A recognized cause for this type of change is spontaneous deamination of the methylcytosine. However, the persistence of a(More)
Various studies have suggested the existence of different pathways of tumor progression in colorectal cancer that associate with specific molecular, chromosomal, and clinicopathological features. We hypothesize that a comprehensive analysis of cumulated genomic damage in colorectal cancers would aid the characterization of different tumor progression(More)
OBJECTIVE Investigate the effects of 12 months of dietary weight loss and/or aerobic exercise on leukocyte telomere length in postmenopausal women. DESIGN AND METHODS Four hundred and thirty nine overweight or obese women (50-75 years) were randomized to: (i) dietary weight loss (N = 118); (ii) aerobic exercise (N = 117), (iii) diet + exercise (N = 117),(More)
Cancer cells progress through the accumulation of genetic alterations. Familial adenomatous polyposis (FAP) tumors provide an excellent model to unravel the molecular steps underlying malignant transformation. Global genomic damage was assessed in 56 adenomas and 3 carcinomas from six FAP patients and compared with that of sporadic adenomas and carcinomas.(More)
Various studies have suggested the existence of different pathways of tumor progression in colorectal cancer that associate with specific molecular , chromosomal, and clinicopathological features. We hypothesize that a comprehensive analysis of cumulated genomic damage in colorectal cancers would aid the characterization of different tumor progression(More)
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