Alimentary tractK-ras-2 G-C and G-T transversions correlate with DNA aneuploidy in colorectal adenomas☆
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Cited by (43)
Intragenic Mutations in Thyroid Cancer
2008, Endocrinology and Metabolism Clinics of North AmericaCitation Excerpt :The mutations associated with thyroid tumors involve predominantly codon 61 of N-RAS and, to a less extent, of H-RAS [17,30,34,35]. Giaretti and colleagues [37–39] showed that activating mutations of K-RAS were involved in the control of chromosome stability in aneuploidy in colorectal tumors. Fagin [40] advanced that a similar mechanism, also involving RAS, might cause aneuploidy in follicular thyroid tumors.
Aneuploidy arises at early stages of Apc-driven intestinal tumorigenesis and pinpoints conserved chromosomal loci of allelic imbalance between mouse and human
2007, American Journal of PathologyCitation Excerpt :The occurrence of KRAS mutations already at early adenoma stages36–38 suggests the possibility that this oncogene may partly contribute to CIN. In fact, few studies have reported positive correlations between KRAS mutations and aneuploidization.39,40 It has been postulated that constitutive KRAS activation may induce genomic instability via the mitogen-activated protein kinase (MAPK) pathway, which affects G1 and G2/M cell-cycle transit times and apoptosis.41
Mutant KRAS, chromosomal instability and prognosis in colorectal cancer
2005, Biochimica et Biophysica Acta - Reviews on CancerAneuploidy: A report of an ECETOC task force
1998, Mutation Research - Reviews in Mutation ResearchChromosome 20 aberrations at the diploid-aneuploid transition in sporadic colorectal cancer
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2008, Journal of Cellular Biochemistry
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Supported by grants from the Italian National Research Council, (CNR 92.02331.PF39), Italian Association for Cancer Research, and European Community.