Increased prevalence of p53 overexpression from typical endometriosis to atypical endometriosis and ovarian cancer associated with endometriosis

Cuesta, Ricardo Sáinz de la; Izquierdo, M J; Cañamero, Marta; Granizo, Juan José; Manzarbeitia, Félix

doi:10.1016/s0301-2115(03)00367-1

Cited by 78 publications

(50 citation statements)

References 13 publications

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“…Bischoff et al 19 showed that chromosomal loss of the p53 locus frequently occurred in late-stage endometriosis. Sainz de la Cuesta et al 42 demonstrated an increased prevalence of p53 accumulation in the transition from typical to atypical endometriosis and to ovarian cancer. Nezhat et al 43 reported that p53 accumulation was found in 17% of benign endometriotic lesions adjacent to carcinoma, while no abnormal staining was found in endometriosis without carcinoma.…”

Section: Loh and Genetic Instabilitymentioning

confidence: 98%

Ovarian cancer in endometriosis: molecular biology, pathology, and clinical management

et al. 2009

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Recent molecular and pathological evidence suggests that endometriosis is a monoclonal, neoplastic disease. Moreover, endometriosis serves as a precursor of ovarian cancer (endometriosis-associated ovarian cancer; EAOC), especially of the endometrioid and clear cell subtypes. Although a variety of molecular events, such as p53 alteration, PTEN silencing, K-ras mutations, and HNF-1 activation, have been identified in EAOC, its precise carcinogenic mechanism remains poorly understood. Our recent data indicate that microenvironmental factors, including oxidative stress and inflammation, play an important role in the carcinogenesis and phenotype of EAOC. The management of endometriosis from the standpoint of EAOC is not standardized yet. To this end, clarification of the precise natural course and the risk factors that contribute to malignant transformation remain important goals. Among the phenotypes of EAOC, clear cell carcinoma, seems to require a specific treatment strategy, including molecular targeting.

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Section: Loh and Genetic Instabilitymentioning

confidence: 98%

Ovarian cancer in endometriosis: molecular biology, pathology, and clinical management

et al. 2009

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“…TP53 alterations occur frequently in late stage endometriosis (10). atypical endometriosis had p53 overexpression (31). Thus, p53 mutations may affect malignant transformation of endometriosis into EAC (16) 17q.…”

Section: Loh Involved In Clear Cell Carcinoma (Ccc) Of the Ovary: Thementioning

confidence: 99%

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

Kobayashi¹

2009

Oncol Rep

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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 prooxidant factors, such as heme and iron, into the peritoneal cavity or ovarian endometrioma. A histologically normal ectopic endometrium bears genetic damages caused by irondependent 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. the candidate tumor suppressor genes 7. Microsatellite instability in CCC 8. Genes specifically up-regulated in CCC 9. Clear cell adenofibroma-CCC sequence 10. Iron, oxidative stress and carcinogenesis 11. Conclusions IntroductionEpithelial ovarian cancer (EOC) is the leading cause of death in women with gynecological malignancies worldwide. The majority of patients present with stage III and IV disease, for which the 5-year survival rates are less than 20%. Most of the patients with EOC present with advanced disease that is not cured by surgery. Ninety per cent of EOC are derived from epithelium within inclusion cysts or from the ovarian surface epithelium and these neoplasms are classified into serous, mucinous, endometrioid adenocarcinoma (EAC), clear cell carcinoma (CCC) and other types (1).Molecular genetic alterations play a key role in carcinogenesis (1). High-grade serous carcinoma arises in a de novo fashion and is characterized by p53 mutations and BRCA1 and/or BRCA2 dysfunction. In contrast, low-grade serous carcinomas are characterized by activation of the RAS-RAF signaling pathway secondary to mutations in KRAS and BRAF in an adenoma-borderline tumor-carcinoma sequence. Similarly, mucinous carcinomas have also ...

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“…Overexpression of p53 in atypical endometriosis and cancer associated with endometriosis has been reported (Sainz de la Cuesta R et al, 2004). Thymosin beta 4 (Tb4) gene expression, an actin sequestering protein, was up-regulated in uterine adenomyosis(endometriosis of myometrium) in mice ( Kawahara R et al, 2003).…”

Section: Gene Expressionmentioning

confidence: 96%

Genetic Polymorphisms and Molecular Pathogenesis of Endometriosis

Kodati¹,

Hasan²

2012

Endometriosis - Basic Concepts and Current Research Trends

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Increased prevalence of p53 overexpression from typical endometriosis to atypical endometriosis and ovarian cancer associated with endometriosis

Cited by 78 publications

References 13 publications

Ovarian cancer in endometriosis: molecular biology, pathology, and clinical management

Ovarian cancer in endometriosis: molecular biology, pathology, and clinical management

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

Genetic Polymorphisms and Molecular Pathogenesis of Endometriosis

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