Premium
Comparative tyrosine‐kinase profiles in colorectal cancers: Enhanced arg expression in carcinoma as compared with adenoma and normal mucosa
Author(s) -
Chen WeiShone,
Kung HsingJien,
Yang WenKuang,
Lin Wenchang
Publication year - 1999
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/(sici)1097-0215(19991126)83:5<579::aid-ijc1>3.0.co;2-r
Subject(s) - receptor tyrosine kinase , tyrosine kinase , cancer research , platelet derived growth factor receptor , colorectal cancer , kinase , medicine , cancer , biology , receptor , microbiology and biotechnology , growth factor
There is strong evidence that tyrosine kinases are involved in the regulation of cellular growth and tumor progression. Over‐expressions of tyrosine kinases have been documented in a number of neoplasms. To study the roles of tyrosine kinases in colon cancer, we developed a tyrosine‐kinase‐expression profile for each of the four different stages of colon carcinogenesis, using normal colon mucosa, adenomatous polyps, primary carcinoma and hepatic metastases collected from the same patient. We identified 30 tyrosine kinases expressed in these tissues: they include 10 non‐receptor tyrosine kinases ( yes, fyn, lyn, brk, abl, arg, jak1, jak3, tyk2 and itk ), 17 receptor tyrosine kinases ( erbB2, PDGF‐Rα, PDGF‐Rβ, kit, c‐fms, met, ron, FGF‐R1, FGF‐R2, FGF‐R3, FGF‐R4, cek5, tie‐1, tkt, axl, sky and Ins‐R ), 2 dual kinases ( mek and sek ) and one possible novel kinase. Among these kinases, arg kinase appears to be expressed at a higher level in primary carcinoma and metastatic tumor than in adjacent normal mucosa or adenomatous polyp. This result was confirmed by extensive analysis of 50 additional matched sets of normal colon and colon‐tumor specimens, using arg ‐specific primers and RT‐PCR reactions. This study identifies a possible role for arg tyrosine kinase in colon carcinogenesis, especially in the transition from adenoma to carcinoma. Int. J. Cancer 83:579–584, 1999. © 1999 Wiley‐Liss, Inc.