z-logo
open-access-imgOpen Access
Immunohistochemical and genetic features of gastric and metastatic liver gastrointestinal stromal tumors: Sequential analyses
Author(s) -
Kikuchi Hirotoshi,
Yamashita Kimihiro,
Kawabata Toshiki,
Yamamoto Masayoshi,
Hiramatsu Yoshihiro,
Kondo Kenji,
Baba Megumi,
Ohta Manabu,
Kamiya Kinji,
Tanaka Tatsuo,
Suzuki Shohachi,
Kitagawa Kyoko,
Kitagawa Masatoshi,
Sugimura Haruhiko,
Konno Hiroyuki
Publication year - 2006
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.1349-7006.2006.00154.x
Subject(s) - gist , medicine , cd117 , pathology , stromal tumor , pdgfra , immunohistochemistry , stomach , imatinib mesylate , imatinib , loss of heterozygosity , cd34 , stromal cell , cancer research , biology , gene , allele , biochemistry , stem cell , myeloid leukemia , genetics
Metastatic gastrointestinal stromal tumors (GIST) have an extremely poor prognosis; however, their immunohistochemical and genetic features have not been assessed satisfactorily and the mechanisms responsible for their high malignant potential remain unclear. We examined the immunohistochemical differences between gastric GIST and metastatic lesions in the liver of four patients who had undergone a postgastrectomy hepatectomy for metachronous liver metastases. We also carried out genetic analysis of the tumors in three of the four cases. In all cases, the immunoreactivity profiles, including KIT (CD117), CD34, smooth muscle actin (SMA), desmin, S‐100 and vimentin, were similar between the gastric and metastatic tumors, but the Ki67 labeling index in the metastatic GIST was higher than that of the primary GIST. Interestingly, in the case who had received neoadjuvant imatinib therapy before gastrectomy, its therapeutic effect was observed in most of the primary lesion, with the exception of a specific small area with high cellularity. Genetic analysis revealed no acquired mutations in the c‐kit or PDGFRA genes in the metastatic lesions in any of the patients, but loss of heterozygosity (LOH) of the c‐kit gene was observed mainly in the metastatic tumors in two of the three cases. Furthermore, in the case of neoadjuvant imatinib therapy, LOH of the c‐kit gene was shown in the high cellularity area in the primary lesion and metastatic liver GIST. It is suggested that LOH of the c‐kit gene is an important event that leads to imatinib resistance and metastatic progression of GIST. In conclusion, both gastric and metastatic GIST had almost the same immunohistochemical features, except for their proliferative activity, and LOH of the c‐kit gene played an important role in the process of liver metastasis. ( Cancer Sci 2006; 97: 127 – 132)

The content you want is available to Zendy users.

Already have an account? Click here to sign in.
Having issues? You can contact us here