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Microarray analysis identifies versican and CD9 as potent prognostic markers in gastric gastrointestinal stromal tumors
Author(s) -
Setoguchi Tomohiko,
Kikuchi Hirotoshi,
Yamamoto Masayoshi,
Baba Megumi,
Ohta Manabu,
Kamiya Kinji,
Tanaka Tatsuo,
Baba Satoshi,
GotoInoue Naoko,
Setou Mitsutoshi,
Sasaki Takeshi,
Mori Hiroki,
Sugimura Haruhiko,
Konno Hiroyuki
Publication year - 2011
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.1349-7006.2011.01872.x
Subject(s) - gist , versican , stromal tumor , metastasis , stromal cell , cancer research , epigenetics , cancer , biology , immunohistochemistry , tissue microarray , pathology , medicine , gene , extracellular matrix , genetics , proteoglycan
Although the main cause of gastrointestinal stromal tumor (GIST) is gain‐of‐function mutations in the c‐kit gene in the interstitial cells of Cajal, concomitant genetic or epigenetic changes other than c‐kit appear to occur in the development of metastasis. We sought to identify the genes involved in the metastatic process of gastric GIST. Microarray analysis was performed to compare gene expressions between three gastric GIST and four metastatic liver GIST. Expression levels were higher for 165 genes and lower for 146 genes in metastatic liver GIST. The upregulation of five oncogenes and downregulation of four tumor suppressor genes including versican and CD9 were confirmed by quantitative reverse transcriptional PCR. Immunohistochemistry in 117 GIST revealed that protein levels of versican and CD9 were higher and lower, respectively, in metastatic GIST. High expression of versican and low expression of CD9 in 104 primary gastric GIST correlated with poor disease‐free survival ( P  = 0.0078 and P  = 0.0018). In addition to the c‐kit gene mutation, genetic or epigenetic changes other than c‐kit play important roles in the metastatic process. In particular, versican and CD9 are potential prognostic markers in gastric GIST. ( Cancer Sci 2011; 102: 883–889)

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