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Histopathology. 2014 Nov;65(5):684-92. doi: 10.1111/his.12475. Epub 2014 Aug 5.

Amplification and overexpression of CMET is a common event in brain metastases of non-small cell lung cancer.

Author information

1
Department of Internal Medicine 1, Medical University of Vienna, Vienna, Austria; Comprehensive Cancer Center, CNS Unit, Medical University of Vienna, Vienna, Austria.

Abstract

BACKGROUND:

CMET represents an emerging therapy target for monoclonal antibodies and tyrosine kinase inhibitors in non-small cell lung cancer (NSCLC).

METHODS:

We investigated CMET gene amplification status by fluorescence in-situ hybridization (FISH) and CMET protein expression by immunohistochemistry in a large series of 209 NSCLC brain metastases (BM; 165 adenocarcinoma, 20 squamous cell carcinoma, 11 adenosquamous carcinomas, 11 large cell carcinomas and two large cell neuroendocrine carcinomas) and correlated our results to clinic-pathological parameters and molecular data from previous studies.

RESULTS:

We found CMET gene amplification in 36/167 (21.6%) and CMET protein expression in 87/196 (44.4%) of evaluable BM. There was a strong correlation between the presence of CMET gene amplification and CMET protein expression (P < 0.001, chi-square test). Furthermore, presence of CMET amplification correlated positively with presence of ALK amplifications (P = 0.039, chi-square test) and high HIF1 alpha index (P = 0.013, Mann-Whitney U-test). Neither CMET expression nor CMET gene amplification status correlated with patient outcome parameters or known prognostic factors.

CONCLUSIONS:

CMET overexpression and CMET amplification are commonly found in NSCLC BM and may represent a promising therapeutic target.

KEYWORDS:

CMET; brain metastases; fluorescence in-situ hybridization; immunohistochemistry; lung cancer; prognosis

PMID:
25039982
DOI:
10.1111/his.12475
[Indexed for MEDLINE]

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