Open AccessGastrointestinal stromal tumors (GIST): A model for molecule‐based diagnosis and treatment of solid tumors
Author(s) -
Kitamura Yukihiko,
Hirota Seiichi,
Nishida Toshirou
Publication year - 2003
Publication title -
cancer science
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.035
H-Index - 141
eISSN - 1349-7006
pISSN - 1347-9032
DOI - 10.1111/j.1349-7006.2003.tb01439.x
Subject(s) - imatinib mesylate , gist , interstitial cell of cajal , imatinib , cancer research , tyrosine kinase , medicine , tyrosine kinase inhibitor , gastrointestinal tract , abl , stromal tumor , pdgfra , myeloid leukemia , stromal cell , pathology , immunohistochemistry , receptor , cancer
Gastrointestinal stromal tumor (GIST) is the most common mesenchymal tumor of the human gastrointestinal (GI) tract. The c‐kit receptor tyrosine kinase (KIT) is expressed by practically all GISTs, and gain‐of‐function mutations of KIT are present in most GISTs. Interstitial cells of Cajal (ICC) are the pacemaker of the peristaltic movement of the GI tract. Since signals through KIT are essential for development of ICC and since multiple GISTs develop from the hyperplastic lesion of ICCs in familial GIST patients with germ‐line mutations of KIT, GISTs are considered to originate from ICC. Imatinib mesylate, which was developed for treatment of chronic myeloid leukemia (CML), was found to be useful for treatment of GISTs. Imatinib mesylate inhibits BCR‐ABL fused tyrosine kinase that causes CML. Imatinib mesylate also inhibits the mutated KIT observed in most GISTs, and this explains the effectiveness of Imatinib mesylate on GISTs. GISTs appear to serve as a model for molecule‐based diagnosis and treatment of solid tumors. (Cancer Sci 2003; 94: 315–320)