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HMGA2 overexpression in non‐small cell lung cancer
Author(s) -
Meyer Britta,
Loeschke Siegfried,
Schultze Anke,
Weigel Thomas,
Sandkamp Martin,
Goldmann Torsten,
Vollmer Ekkehard,
Bullerdiek Jörn
Publication year - 2007
Publication title -
molecular carcinogenesis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.254
H-Index - 97
eISSN - 1098-2744
pISSN - 0899-1987
DOI - 10.1002/mc.20235
Subject(s) - hmga2 , lung cancer , biology , immunohistochemistry , adenocarcinoma , lung , cancer , carcinoma , cancer research , pathology , medicine , gene , immunology , microrna , biochemistry , genetics
Lung cancer is still the leading cause of death from cancer worldwide primarily because of the fact that most lung cancers are diagnosed at advanced stages. Overexpression of the high mobility group protein HMGA2 has been observed in a variety of malignant tumors and often correlates with poor prognosis. Herein, HMGA2 expression levels were analyzed in matching cancerous and non‐cancerous lung samples of 17 patients with adenocarcinoma (AC) and 17 patients with squamous cell carcinoma (SCC) with real‐time quantitative RT‐PCR (qRT‐PCR). Transcript levels were compared to results obtained by immunohistochemistry (IHC). HMGA2 expression was detectable by qRT‐PCR in all samples tested and varied from 5422 to 16 991 545 copies per 250 ng total RNA in the carcinoma samples and from 289 to 525 947 copies in the non‐cancerous tissue samples. In 33/34 non‐small cell lung cancer (NSCLC) samples tested, an overexpression of HMGA2 was revealed with statistically highly significant differences between non‐neoplastic and tumor samples for both AC ( P  < 0.0001) as well as for SCC ( P  < 0.0001). Expression varies strongly and is increased up to 911‐fold for AC and up to 2504‐fold for SCC, respectively, with statistically significant higher increase in SCC ( P  < 0.05). The results presented herein indicate that HMGA2 overexpression is a common event in NSCLC and could serve as molecular marker for lung cancer. © 2007 Wiley‐Liss, Inc.

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