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(American Journal of Pathology. 2000;156:791-795.)
© 2000 American Society for Investigative Pathology

Short Communications

KIT Extracellular and Kinase Domain Mutations in Gastrointestinal Stromal Tumors

Marcia L. Lux*, Brian P. Rubin*, Tara L. Biase*, Chang-Jie Chen*, Timothy Maclure*, George Demetri{dagger}, Sheng Xiao*, Samuel Singer{dagger}{ddagger}§, Christopher D.M. Fletcher*{dagger} and Jonathan A. Fletcher*{dagger}

From the Departments of Pathology*
and Surgery,{ddagger}
Brigham and Women’s Hospital; the Department of Pediatric Oncology,{dagger}
Dana-Farber Cancer Institute and Children’s Hospital; and the Departments of Pathology,*
Surgery,§
and Pediatrics,{dagger}
Harvard Medical School, Boston, Massachusetts

Gastrointestinal stromal tumors (GISTs) are the most common mesenchymal neoplasms arising in the gastrointestinal tract. GISTs express the KIT receptor tyrosine kinase, and many cases have activating mutations in the KIT juxtamembrane region. We now report an analysis of KIT cDNA and genomic sequences in eight GISTs that lack juxtamembrane region mutations. Six cases contained heterozygous exon 9 mutations in which six nucleotides, encoding Ala-Tyr, were duplicated. The other two cases contained homozygous exon 13 missense mutations, resulting in substitution of Glu for Lys642, that were associated with constitutive KIT tyrosine phosphorylation. Sequence analysis of DNAs from nonneoplastic companion tissues revealed that both the exon 9 and exon 13 mutations were somatic. These are the first descriptions, in any tumor, of mutations in KIT exons encoding the C-terminal end of the extracellular domain and the first part of the split kinase domain. These findings indicate that KIT may be activated by mutations in at least three domains—extracellular, juxtamembrane, and kinase—in GISTs.




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