Common Genetic Changes between Endometriosis and Ovarian Cancer

Obata, Koshiro; Hoshiai, Hiroshi

doi:10.1159/000052877

Cited by 87 publications

(54 citation statements)

References 10 publications

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“…They are genetically stable and are characterized by mutations in a number of different genes, including KRAS, BRAF, PTEN and b-catenin. 3,22,23 Type II tumors are rapidly growing highly aggressive neoplasms for which precursor lesions arising from Fimbria are currently under intensive studies. 24 Type II tumors include high-grade serous carcinoma, carcinosarcoma and undifferentiated carcinoma.…”

Section: Discussionmentioning

confidence: 99%

HMGA2: A biomarker significantly overexpressed in high-grade ovarian serous carcinoma

et al. 2010

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Ovarian carcinoma consists of a group of histologically heterogeneous diseases involving distinct tumorigenic pathways. High-grade papillary serous carcinoma of the ovary is commonly associated with p53 mutations. HMGA2, an oncofetal protein, is found to be overexpressed in ovarian cancer. To study the function of HMGA2 in ovarian cancer, it is important to know which subtypes of ovarian cancer are associated with HMGA2 overexpression. In this study, we collected six different types of ovarian cancer and examined HMGA2 expression by immunohistochemistry, along with HMGA1, p53 and Ki-67. We found that HMGA2 overexpression was significantly higher in high-grade papillary serous carcinoma (64%) and carcinosarcoma (60%) than in other types of ovarian cancers (7-23%). HMGA2 overexpression was moderately associated with dominant p53 mutations (R ¼ 0.51). In addition, the microRNA in situ analysis revealed that let-7b, the HMGA2-negative regulators, were significantly lost in high-grade serous carcinoma. Our findings suggest that HMGA2 is an important molecular change significantly related to high-grade papillary serous carcinoma and is less common in other histological types of ovarian cancer.

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Section: Discussionmentioning

confidence: 99%

HMGA2: A biomarker significantly overexpressed in high-grade ovarian serous carcinoma

et al. 2010

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“…LOH commonly indicates regions of TSG inactivation, and has been identified in endometriosis and endometriosis-derived cell lines at 5q, 6q, 9p, 10q, 11q, 22q, p16 (Ink4), galactose-1-phosphate uridy ltransferase, p53 and apolipoprotein All (Jiang et al 1996, Obata & Hoshiai 2000, Thomas & Campbell 2000, Goumenou et al 2001. Importantly, cases with ovarian cancer adjacent to endometriosis or arising from endometriosis showed common genetic LOH alterations in the endometriosis and cancer, indicating a possible malignant genetic transition spectrum between endometriosis and cancer (Jiang et al 1998.…”

Section: Loss Of Heterozygosity (Loh)mentioning

confidence: 99%

Endometriosis and the neoplastic process

Varma¹,

Rollason²,

Gupta³

et al. 2004

Reproduction

186

146

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Endometriosis is a frequent disorder that commonly presents with infertility and pelvic pain. Although the precise aetiology of endometriosis is unclear, it is generally considered to involve multiple genetic, environmental, immunological, angiogenic and endocrine processes. Genetic factors have been implicated in endometriosis but the susceptibility genes remain largely unknown. Although endometriosis is a benign disorder, recent studies of endometriosis suggest endometriosis could be viewed as a neoplastic process. Evidence to support this hypothesis includes the increased susceptibility to develop ovarian clear-cell and endometrioid cancers in the presence of endometriosis, and molecular similarities between endometriosis and cancer. In this article we discuss (i) the evidence suggesting that endometriosis might be viewed as a neoplastic process, and (ii) the implications of this hypothesis for elucidating the pathogenesis of endometriosis and developing novel methods of diagnostic classification and individualised treatments.

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“…Loss of PTEN function may even precede acquisition of cytological atypia, a histopathological feature long thought to distinguish the threshold between benign and premalignant endometrial disease. 21 Clear cell and endometrioid ovarian adenocarcinomas may also share deletion of the PTEN locus 41,42 with premalignant (endometriosis) tissues. 42 In contrast, PTEN inactivation in melanoma, 8 prostate carcinoma, 43 and glioblastoma, 11,13 is a marker for an aggressive subset of tumors likely to metastasize.…”

Section: Early and Late Effects: Tumor Initiation Versus Metastasismentioning

confidence: 99%

PTEN, a Protean Tumor Suppressor

Mutter

2001

The American Journal of Pathology

123

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The molecular biology of the PTEN tumor suppressor gene is as multifaceted as the range of sporadic human malignancies in which it has been implicated. Multiple mechanisms can inactivate PTEN in glioblastoma, melanoma, and carcinomas of the thyroid, breast, prostate, endometrium, and ovary. Initial impressions, based on mutational analysis alone, that ovarian cancer PTEN inactivation is infrequent bear revision in light of a 27% frequency of lost PTEN protein expression reported by Kurose and colleagues in this issue of The American Journal of Pathology.1 Only 8% of PTEN protein nonexpressing ovarian adenocarcinomas are explained by combined allelic imbalance (loss of heterozygosity) and mutation, suggesting that transcriptional silencing by epigenetic mechanisms may be yet an additional means of modifying PTEN activity. Although they show for ovarian carcinoma that PTEN function can be delimited by an identifiable and consistent repertoire of downstream effectors, such as the Akt pathway, the consequences of PTEN inactivation are nonuniform in different tissues. Thus, in the endometrium PTEN acts as a gatekeeper for initiation of carcinogenesis, yet in prostate cancer and melanoma it defines a much later event, metastasis. Tissue context determines the molecular events that inactivate PTEN and heavily modify the resultant phenotype.

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Common Genetic Changes between Endometriosis and Ovarian Cancer

Cited by 87 publications

References 10 publications

HMGA2: A biomarker significantly overexpressed in high-grade ovarian serous carcinoma

HMGA2: A biomarker significantly overexpressed in high-grade ovarian serous carcinoma

Endometriosis and the neoplastic process

PTEN, a Protean Tumor Suppressor

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