Allelotyping of endometriosis with adjacent ovarian carcinoma reveals evidence of a common lineage

X Jiang, Jiang X, Xiuxian Jiang, Sarah J. Morland, S J Morland, Morland SJ, Hitchcock A, Andrew Hitchcock, A Hitchcock, E J Thomas, Thomas EJ, Eric J. Thomas, I G Campbell, Ian Campbell
Cancer research · 1998 · vol. 58(8) , pp. 1707–12 · PMID:9563487 · W2127853347
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This study found common genetic alterations in synchronous endometriosis and ovarian carcinoma cases, supporting the hypothesis that endometriosis can be the clonal precursor of these malignancies.

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Abstract

Endometriosis is a common gynecological disease in which tissue similar to the endometrium proliferates at sites outside the uterine cavity. Malignant transformation of endometriosis to endometrioid and clear cell ovarian carcinomas has been documented in histological studies, but no molecular genetic evidence exists to support that endometriosis is the clonal precursor of such malignancies. We examined 14 cases of endometriosis synchronous with ovarian cancer for loss of heterozygosity on 12 chromosome arms, X chromosome inactivation, and TP53 mutation to determine whether they shared genetic alterations. In all four of the cases where the carcinoma had arisen within endometriosis and in five of the seven cases where the carcinoma was adjacent to the endometriosis, common genetic lesions were detected, consistent with a common lineage. A TP53 mutation was also detected in one case of endometriosis adjacent to carcinoma. These findings support the numerous histological observations that endometrioid and clear cell ovarian carcinomas may arise through malignant transformation of endometriotic lesions.

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Condition tags

endometriosis

MeSH descriptors

Alleles Alleles Carcinoma Endometriosis Ovarian Neoplasms Adult Adult Aged Aged Aged, 80 and over Aged, 80 and over Carcinoma Carcinoma Carcinoma Carcinoma Cell Lineage Cell Lineage Chromosome Deletion Chromosome Deletion Clone Cells

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 (11)

Cited by (50)

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