Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2003 Apr;94(4):315-20.
doi: 10.1111/j.1349-7006.2003.tb01439.x.

Gastrointestinal stromal tumors (GIST): a model for molecule-based diagnosis and treatment of solid tumors

Yukihiko Kitamura  1 , Seiichi Hirota, Toshirou Nishida
Affiliations
Review

Gastrointestinal stromal tumors (GIST): a model for molecule-based diagnosis and treatment of solid tumors

Yukihiko Kitamura et al. Cancer Sci. 2003 Apr.

Erratum in

  • Cancer Sci. 2003 Oct;94(10):930

Abstract

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 germline 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.

PubMed Disclaimer

References

    1. Hirota S, Isozaki K, Moriyama Y, Hashimoto K, Nishida T, Ishiguro S, Kawano K, Hanada M, Kurata A, Takeda M, Tunio GM, Matsuzawa Y, Kanakura Y, Shinomura Y, Kitamura Y. Gain‐of‐function mutations of c‐kit in human gastrointestinal stromal tumors. Science 1998; 279: 577–80. - PubMed
    1. O'Leary T, Berman JJ. Gastrointestinal stromal tumors: answers and questions. Hum. Pathol 2002; 33: 456–8. - PubMed
    1. Heinrich MC, Rubin BP, Longley BJ, Fletcher JA. Biology and genetic aspects of gastrointestinal stromal tumors: KIT activation and cytogenetic alterations. Hum. Pathol 2002; 33: 484–95. - PubMed
    1. Kindblom LG, Remotti HE, Aldenborg F, Meis‐Kindblom JM. Gastrointestinal pacemaker cell tumor (GIPACT): gastrointestinal stromal tumors show phenotypic characteristics of the interstitial cells of Cajal. Am J Pathol 1998; 152: 1259–69. - PMC - PubMed
    1. Thomsen L, Robinson TL, Lee JC, Farraway LA, Hughes MJ, Andrews DW, Huizinga JD. Interstitial cells of Cajal generate a rhythmic pacemaker current. Nat Med 1998; 4: 848–51. - PubMed

MeSH terms