Molecular-genetic analysis of clonal intratumoral heterogeneity on colorectal adenocarcinomas

• Published in: Molekuliarnaia biologiia Vol. 42; no. 6; p. 1040
• Main Authors: Nemtsova, M N, Pal'tseva, E M, Babaian, A Iu, Mikhaĭlenko, D S, Babenko, O V, Samofalova, O Iu, Tsar'kov, P V, Zaletaev, D V
• Format: Journal Article
• Language: Russian
• Published: Russia (Federation) 01-11-2008
• Subjects: Adenocarcinoma - genetics; Adenocarcinoma - metabolism; Aged; Chromosomal Instability - genetics; Chromosomes, Human - genetics; Chromosomes, Human - metabolism; Colorectal Neoplasms - genetics; Colorectal Neoplasms - metabolism; Cyclin D; Cyclin-Dependent Kinase Inhibitor p16; Cyclins - genetics; Cyclins - metabolism; Female; Humans; Loss of Heterozygosity; Male; Microsatellite Repeats - genetics; Middle Aged; Neoplasm Proteins - genetics; Neoplasm Proteins - metabolism; Oncogene Protein p21(ras) - genetics; Oncogene Protein p21(ras) - metabolism; Point Mutation; Retinoblastoma Protein - genetics; Retinoblastoma Protein - metabolism
• ISSN: 0026-8984

We have examined the existence of intratumoral genetic heterogeneity for LOH on chromosomes 9p21 (p16, p15, p19), 13p14 (RB1), 10q23 (PTEN), 17p (TP53), microsatellite instability and K-RAS point mutations on four different segments of sporadic colorectal cancers. The intratumoral genetic heterogenity was detected in 9/11 (81%) colorectal adenocarcinomas and morphologically validated. These results show that colorectal cancer is highly heterogeneous for these molecular markers. Furthermore, the analysis has shown the order (succession) of the appearance of these molecular anomalies during tumorigenesis on sporadic CRC, and supposed, that K-RAS point mutations, and anomalies of p16-RB1-cyclin D pathway could occur before LOH on 10q23 (PTEN) and microsatellite instability during tumor progression.