Japanese Journal of Clinical Oncology, Vol 27, Issue 6 378-383, Copyright © 1997 by Foundation for Promotion of Cancer Research
S Fujita and K Sugano
We have examined the expression of c-met mRNA in tissue from 27 colorectal
cancers and ten liver metastases using the reverse transcriptase-polymerase
chain reaction method. The expression of c-met mRNA in these tissues was
quantified and the copy number of c-met mRNA to 10(8.0) copies of
beta-actin mRNA was calculated. Mean copy numbers of c-met mRNA in cancer
tissue and normal mucosa were 10(5.5) and 10(4.5) respectively. The c-met
expression of cancer was significantly higher than that of normal mucosa (P
< 0.0001). In 20 of 22 samples in which c-met expression of both tumor
and corresponding normal tissue were examined, c-met was overexpressed in
the cancer tissue. No correlation was found between c-met expression and
the clinicopathologic background. The mean copy numbers of c-met mRNA in
the tissue from the ten liver metastases and normal liver were 10(6.1) and
10(6.2) respectively. Although c-met expression in metastatic tissue was
higher than that in the primary cancer tissue, the increase was not
statistically significant. In three of four patients with synchronous liver
metastases, c-met was overexpressed in the metastatic tissue compared with
that in the corresponding primary cancer tissue. These results show that
c-met is overexpressed in both primary colorectal cancer and liver
metastases and suggest that c-met plays a role in the development of
colorectal cancer liver metastases.
ORIGINAL ARTICLE
Expression of c-met proto-oncogene in primary colorectal cancer and liver metastases
Department of Surgery, National Cancer Center Hospital, Tokyo, Japan.
![]()
CiteULike
Connotea
Del.icio.us What's this?
This article has been cited by other articles:
![]() |
H. Takeuchi, A. Bilchik, S. Saha, R. Turner, D. Wiese, M. Tanaka, C. Kuo, H.-J. Wang, and D. S. B. Hoon c-MET Expression Level in Primary Colon Cancer: A Predictor of Tumor Invasion and Lymph Node Metastases Clin. Cancer Res., April 1, 2003; 9(4): 1480 - 1488. [Abstract] [Full Text] [PDF] |
||||
