open access

Vol 42, No 3 (2004)
Original paper
Submitted: 2011-12-19
Published online: 2004-10-21
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K-RAS point mutation, and amplification of C-MYC and C-ERBB2 in colon adenocarcinoma.

Wiesław Kruszewski, Renata Kowara, Robert Rzepko, Cezary Warezak, Jacek Zieliński, Grzegorz Gryglewski, Andrzej Kopacz, Tomasz Jastrzebski, Tadeusz Pawełczyk
Folia Histochem Cytobiol 2004;42(3):173-179.

open access

Vol 42, No 3 (2004)
ORIGINAL PAPERS
Submitted: 2011-12-19
Published online: 2004-10-21

Abstract

The routine multidisciplinary management of colon cancer is based mainly on tumor staging, histology, grading and vascular invasion. In this approach, important individual information derived from molecular characteristics of the tumor may be missed, especially since significant heterogeneity of molecular aberrations in cancer cells has been observed, and recognition of every of relationships between them may be of value. K-RAS, C-MYC and C-ERBB2 are protooncogenes taking part in carcinogenesis and tumor progression in the colon. They influence cell proliferation, differentiation and survival. K-RAS point mutation, as well as amplification of C-MYC and C-ERBB2 were searched in 84 primary colon adenocarcinomas resected with curative intent. Multiplex polymerase-chain reaction and restriction fragment length polymorphism were performed to assess codon 12 K-RAS point mutation. Amplification of C-MYC and C-ERBB2 genes was evaluated by densitometry after agarose gel separation of the respective multiplex PCR products. No relation was found among mutated and/or amplified genes, and between searched molecular aberrations and pathoclinical features. In multivariate analysis, nodal status appeared to be the only independent prognostic indicator. In colon adenocarcinoma, codon 12 K-RAS point mutation and amplification of C-MYC and C-ERBB2 seem to occur independently in the process of tumor progression. Amplification of C-ERBB2 tends to associate with more advanced stage of disease. Concomitant occurrence of codon 12 K-RAS mutation, C-MYC and C-ERBB2 amplification was of no prognostic value in respect to survival.

Abstract

The routine multidisciplinary management of colon cancer is based mainly on tumor staging, histology, grading and vascular invasion. In this approach, important individual information derived from molecular characteristics of the tumor may be missed, especially since significant heterogeneity of molecular aberrations in cancer cells has been observed, and recognition of every of relationships between them may be of value. K-RAS, C-MYC and C-ERBB2 are protooncogenes taking part in carcinogenesis and tumor progression in the colon. They influence cell proliferation, differentiation and survival. K-RAS point mutation, as well as amplification of C-MYC and C-ERBB2 were searched in 84 primary colon adenocarcinomas resected with curative intent. Multiplex polymerase-chain reaction and restriction fragment length polymorphism were performed to assess codon 12 K-RAS point mutation. Amplification of C-MYC and C-ERBB2 genes was evaluated by densitometry after agarose gel separation of the respective multiplex PCR products. No relation was found among mutated and/or amplified genes, and between searched molecular aberrations and pathoclinical features. In multivariate analysis, nodal status appeared to be the only independent prognostic indicator. In colon adenocarcinoma, codon 12 K-RAS point mutation and amplification of C-MYC and C-ERBB2 seem to occur independently in the process of tumor progression. Amplification of C-ERBB2 tends to associate with more advanced stage of disease. Concomitant occurrence of codon 12 K-RAS mutation, C-MYC and C-ERBB2 amplification was of no prognostic value in respect to survival.
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About this article
Title

K-RAS point mutation, and amplification of C-MYC and C-ERBB2 in colon adenocarcinoma.

Journal

Folia Histochemica et Cytobiologica

Issue

Vol 42, No 3 (2004)

Article type

Original paper

Pages

173-179

Published online

2004-10-21

Bibliographic record

Folia Histochem Cytobiol 2004;42(3):173-179.

Authors

Wiesław Kruszewski
Renata Kowara
Robert Rzepko
Cezary Warezak
Jacek Zieliński
Grzegorz Gryglewski
Andrzej Kopacz
Tomasz Jastrzebski
Tadeusz Pawełczyk

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