Molecular pathogenesis of endometriosis-associated clear cell carcinoma of the ovary (review).

Hiroshi Kobayashi, Kobayashi H, Hirotaka Kajiwara, Kajiwara H, Seiji Kanayama, Kanayama S, Yoshihiko Yamada, Yamada Y, Furukawa N, Naoto Furukawa, Taketoshi Noguchi, Noguchi T, Haruta S, Shoji Haruta, Shozo Yoshida, Yoshida S, Mariko Sakata, Sakata M, Toshiyuki Sado, Sado T, Hidekazu Oi, Oi H
Oncology reports · 2009 · vol. 22(2) , pp. 233–40 · PMID:19578761 · W2012910154
article OA: closed CC0 ⤵ 48 in-corpus citations
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This review summarizes current knowledge on the molecular pathogenesis of endometriosis-associated clear cell carcinoma of the ovary, highlighting genetic alterations from oxidative stress in ectopic endometrium as a key factor.

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Abstract

Epithelial ovarian cancer (EOC) is the leading cause of death in women with gynecological malignancies. Among EOC, clear cell carcinoma (CCC) and endometrioid adenocarcinoma (EAC) differ from the other histological types with respect to their clinical characteristics and carcinogenesis. Both tumor types are often associated with endometriosis. EAC is recently reported to be characterized by K-RAS activation and PTEN dysfunction. However, the molecular changes in CCC remain largely unknown. The aim of this review is to summarize the current knowledge on the molecular mechanisms involved in CCC tumorigenesis. The present article reviews the English language literature for biological, pathogenetic and pathophysiological studies on endometriosis-associated CCC of the ovary. Several recent studies of loss of heterozygosity (LOH), allelic loss, comparative genomic hybridization, mutation, methylation status, microarray gene-expression profiling and proteomics are discussed in the context of CCC biology. Retrograde menstruation or ovarian hemorrhage carries highly pro-oxidant factors, such as heme and iron, into the peritoneal cavity or ovarian endometrioma. A histologically normal ectopic endometrium bears genetic damages caused by iron-dependent oxidative stress. DNA damage or LOH caused by oxidative stress is a critical factor in the carcinogenic process. LOH studies have implicated the involvement of specific chromosomal regions (5q, 6q, 9p, 10q, 11q, 17q and 22q). Furthermore, the PTEN and APC (early event), p53, polo-like kinases, Emi1 and K-RAS (late event) genes may be involved in CCC carcinogenesis. The molecular pathology of CCC is heterogeneous and involves various putative precursor lesions and multiple pathways of development, possibly via genetic alteration by oxidative stress.

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Condition tags

endometriosisendometrioma

MeSH descriptors

Adenocarcinoma, Clear Cell Endometriosis Ovarian Neoplasms Adenocarcinoma, Clear Cell Cell Cycle Proteins Cell Cycle Proteins Endometriosis F-Box Proteins F-Box Proteins Female Genes, Tumor Suppressor Hepatocyte Nuclear Factor 1-beta Hepatocyte Nuclear Factor 1-beta Humans Loss of Heterozygosity Microsatellite Instability Ovarian Neoplasms Oxidative Stress Protein Kinases Protein Kinases

Citation neighborhood

Papers in the corpus that this work cites (lower rings, blue) and that cite this one (upper rings, green). Dot size scales with the paper's in-corpus citation count — bigger dot = more influential within the endo/adeno field. Click a dot to open that paper. [ expand to 2 hops ] — adds papers reached through this work's immediate citers/citees. Heavier; up to 60 extra dots.

Cited by (48)

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