Endometrioid Carcinoma

Mutation of P-catenin has been reported in approximately one third of cases,45,46 and mutation of PTEN in 20%, rising to 46% in tumors with 10q23 loss of heterozygosity.47 These mutations are generally detected in well-differentiated stage I tumors with a favorable prognosis, suggesting that inactivation of these genes is an early event. Moreover, similar molecular genetic alterations, including loss of heterozygos-ity at 10q23 and mutations in PTEN, have been reported in endometriosis, atypical endometriosis, and ovarian endometrioid carcinoma in the same specimen.48-52 The molecular genetic findings together with the morphologic data showing a frequent association of endometriosis with endometrioid adenofibromas, atypical proliferative (borderline) tumors, adjacent to invasive well-differentiated endometri-oid carcinoma, suggest a stepwise tumor progression toward the development of endometrioid carcinoma.

A previous study shows that mouse model expressing oncogenic KRAS or conditional PTEN deletion within the ovarian surface epithelium gave rise to preneoplastic ovarian lesions similar to endometriosis and in some mice to endometrioid carcino-mas.53 More recently, Dr. Cho's research team has further generated new transgenic mice that conditionally express mutant PTEN and P-catenin. Upon induction of the mutations, all mice develop endometrioid carcinomas.54 Hence, P-catenin and PTEN mutations play an important role in the development of endometrioid carcinoma of the ovary.

51 Tips for Dealing with Endometriosis

51 Tips for Dealing with Endometriosis

Do you have Endometriosis? Do you think you do, but aren’t sure? Are you having a hard time learning to cope? 51 Tips for Dealing with Endometriosis can help.

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