Molecular mechanisms and biological plausibility underlying the malignant transformation of endometriosis: a critical analysis

Paola Viganó, Paola Viganò, Edgardo Somigliana, Chiodo I, I. Chiodo, Ilda Chiodo, Abbiati A, Annalisa Abbiati, Paolo Vercellini
Human Reproduction Update · 2005 · vol. 12(1) , pp. 77–89 · doi:10.1093/humupd/dmi037 · PMID:16172112 · W2129869328
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This analysis evaluates the limited and discordant biological evidence for endometriosis as a preneoplastic condition, examining clonal expansion and genetic changes that might link it to ovarian cancer.

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Abstract

Although population-based studies have unequivocally reported an increased risk of ovarian cancer in women with endometriosis, the biological evidence supporting the idea of endometriosis as a preneoplastic condition is scanty and not well substantiated. The fundamental features of human neoplasms (monoclonal growth, genetic changes, mutations in tumour suppressor genes and replicative advantage) have been evaluated in endometriotic lesions but results obtained are discordant. It is plausible that ectopic glands may expand monoclonally but the entity of this phenomenon is debated. According to some allelotyping studies, from one-third to one-half of endometriosis lesions would harbour somatic genetic changes in chromosomal regions supposed to contain genes involved in ovarian tumourigenesis, especially for the endometrioid histotype. These findings would be consistent with the progression model for carcinogenesis from the benign precursor to ovarian cancer but they could not be unequivocally replicated. Gene mutational studies are rare in this context. A single group has found missense mutations and deletions of PTEN gene in about 20% of ovarian endometriotic cysts. Moreover, in a model of genetically engineered mice harbouring an oncogenic allele of K-ras resulting in benign lesions reminiscent of endometriosis, a conditional deletion of PTEN caused the progression towards the endometrioid tumour. Based on these data, the causal link between endometriosis and ovarian endometrioid/clear cell carcinomas remains to be defined both in terms of entity of association and of underlying molecular mechanisms.

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Condition tags

endometriosis

MeSH descriptors

Endometriosis Endometriosis Ovarian Neoplasms Animals Chromosome Aberrations Cytogenetic Analysis Endometriosis Female Genes, Tumor Suppressor Humans In Situ Hybridization, Fluorescence Loss of Heterozygosity Mice Mutation Oncogenes Oncogenes Ovarian Neoplasms Ovarian Neoplasms PTEN Phosphohydrolase PTEN Phosphohydrolase

Citation neighborhood (2-hop)

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. Outer rings show 2-hop neighbours — papers reached through the immediate citers/citees. [ collapse to 1-hop ]

References (100)

Cited by (50)

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