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Altered patterns of transcription of the septin gene, SEPT9 , in ovarian tumorigenesis
Author(s) -
Scott Michael,
McCluggage W. Glenn,
Hillan Kenneth J.,
Hall Peter A.,
Russell S.E. Hilary
Publication year - 2005
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/ijc.21486
Subject(s) - serous fluid , pathology , carcinogenesis , biology , cystadenocarcinoma , serous carcinoma , malignancy , ovarian carcinoma , ovarian cancer , cancer research , medicine , cancer , genetics
Ovarian carcinoma represents the most lethal gynaecological malignancy. A variety of morphological subtypes are recognised ( e.g . serous, mucinous, endometrioid), which may be benign, borderline or malignant. While their relationship is controversial, knowledge of the molecular mechanisms of ovarian tumorigenesis may help resolve this issue and perhaps identify early markers of disease. Perturbed patterns of expression of the SEPT9 gene on chromosome 17q25.3 have been implicated in a variety of tumour types including both breast and ovarian neoplasia. In preliminary studies, we showed that SEPT9 mRNA was upregulated in a bank of ovarian tumours, which included benign, borderline and malignant tumours, and reported increased levels of one splice variant, SEPT9 _v4*. We now describe a comprehensive analysis of SEPT9 expression specifically in serous and mucinous ovarian tumours (benign, borderline and malignant), using cDNA microarray, semi‐ and quantitative RTPCR of microdissected archival tumour material. Our data show consistent and specific overexpression of both SEPT9 _v1 and SEPT9 _v4* transcripts in the epithelial component of ovarian tumours. These transcripts show highest levels of expression in serous and mucinous borderline tumours. SEPT9 _v1 is also upregulated in both serous and mucinous carcinomas. Interestingly, highest levels of expression are observed in serous borderline and low‐grade tumours rather than high‐grade in keeping with a model of progression of benign, borderline and low‐grade serous tumours. © 2005 Wiley‐Liss, Inc.