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Atypical Endometrial Hyperplasia (atypical + endometrial_hyperplasia)
Selected AbstractsCoexistent atypical polypoid adenomyoma and complex atypical endometrial hyperplasia in the uterusDIAGNOSTIC CYTOPATHOLOGY, Issue 7 2010Ayako Horita M.D. Abstract We report a case of atypical polypoid adenomyoma (APA) concomitantly identified with complex atypical endometrial hyperplasia (CAH) in the uterus. Since an initial endometrial smear revealed atypical endometrial cells, a diagnosis of CAH was made. Even though a concomitantly performed uterine cervical smear contained both atypical epithelial and stromal cells, the diagnosis of APA was not initially made because the cytological criteria for APA had not been established. Histologically, we recognized both CAH in the uterine corpus and APA in the lower uterine segment in the hysterectomy material. Retrospectively, the cells in the first cervical smear were interpreted as part of APA because the same types of cells were observed in the intraoperative cytology sample. Although the APA and CAH lesions were interposed by normal endometrium, estrogen was suspected to be the common etiological factor. Reports regarding the cytology of APA are currently scarce. To our knowledge, this is the first report showing cytological presentation of association of APA with CAH in addition to the first cervical smear of APA containing both epithelial and stromal components. Identification of abnormal proliferation of epithelium and stromal cells of smooth muscle origin is useful in the cytological diagnosis of APA. Diagn. Cytopathol. 2010. © 2009 Wiley-Liss, Inc. [source] Stromal luteoma and nodular hyperthecosis of the bilateral ovaries associated with atypical endometrial hyperplasia of the uterusPATHOLOGY INTERNATIONAL, Issue 11 2009Sohsuke Yamada No abstract is available for this article. [source] Malignant transformation of atypical endometrial hyperplasia after progesterone therapy showing germ-cell tumor-like differentiationPATHOLOGY INTERNATIONAL, Issue 6 2004Masanori Yasuda A 31-year-old woman was treated for atypical endometrial hyperplasia (AEH) with high-dose medroxyprogesterone acetate (MPA) therapy to preserve fertility. The AEH was found by repeated cytologic and histologic examinations to have completely disappeared with the therapy, but 3 years after her last follow up she required emergency surgery to treat severe genital bleeding. The hysterectomied uterus consisted mostly of poorly differentiated adenocarcinoma, G3 endometrioid type. Minor AEH was present in the exophytic area, in which some glands were cystically dilated. Part of the AEH had transformed into other histologic features with germ-cell-like differentiation, demonstrated by immunohistochemical positive reaction of placental alkaline phosphatase, alpha-fetoprotein, and human chorionic gonadotrophin. Recurrent AEH had undergone malignant transformation, resulting in the development of well- and poorly differentiated adenocarcinoma and tumor exhibiting germ-cell-like differentiation. The patient died of a massive tumor extension 7 months after surgery. The AEH before MPA therapy and the recurrent tumors had genetically different characteristics based on evidence of a loss of heterozygosity, detected at D8S1132 (chromosomal locus, 8q22.1) in the latter but not in the former, by analysis of genetic alterations using microsatellite markers. [source] Concurrent endometrial carcinoma in women with a biopsy diagnosis of atypical endometrial hyperplasia,CANCER, Issue 4 2006A Gynecologic Oncology Group study Abstract BACKGROUND Adenocarcinoma of the endometrium is the most common gynecologic malignancy in the United States, accounting for approximately 36,000 diagnoses of invasive carcinoma annually. The most common histologic type, endometrioid adenocarcinoma (EC), accounts for 75,80% of patients. The objective of this work was to estimate the prevalence of concurrent carcinoma in women with a biopsy diagnosis of the precursor lesion, atypical endometrial hyperplasia (AEH). METHODS This prospective cohort study included women who had a community diagnosis of AEH. Diagnostic biopsy specimens were reviewed independently by three gynecologic pathologists who used International Society of Gynecologic Pathologists/World Health Organization criteria. Study participants underwent hysterectomy within 12 weeks of entry onto protocol without interval treatment. The hysterectomy slides also were reviewed by the study pathologists, and their findings were used in the subsequent analyses. RESULTS Between November 1998 and June 2003, 306 women were enrolled on the study. Of these, 17 women were not included in the analysis: Two patients had unreadable slides because of poor processing or insufficient tissue, 2 patients had only slides that were not endometrial, the slides for 5 patients were not available for review, and 8 of the hysterectomy specimens were excluded because they showed evidence of interval intervention, either progestin effect or ablation. In total, 289 patients were included in the current analysis. The study panel review of the AEH biopsy specimens was interpreted as follows: 74 of 289 specimens (25.6%) were diagnosed as less than AEH, 115 of 289 specimens (39.8%) were diagnosed as AEH, and 84 of 289 specimens (29.1%) were diagnosed as endometrial carcinoma. In 5.5% (16 of 289 specimens), there was no consensus on the biopsy diagnosis. The rate of concurrent endometrial carcinoma for analyzed specimens was 42.6% (123 of 289 specimens). Of these, 30.9% (38 of 123 specimens) were myoinvasive, and 10.6% (13 of 123 specimens) involved the outer 50% of the myometrium. Among the women who had hysterectomy specimens with carcinoma, 14 of 74 women (18.9%) had a study panel biopsy consensus diagnosis of less than AEH, 45 of 115 women (39.1%) had a study panel biopsy consensus diagnosis of AEH, and 54 of 84 women (64.3%) had a study panel diagnosis of carcinoma. Among women who had no consensus in their biopsy diagnosis, 10 of 16 women (62.5%) had carcinoma in their hysterectomy specimens. CONCLUSIONS The prevalence of endometrial carcinoma in patients who had a community hospital biopsy diagnosis of AEH was high (42.6%). When considering management strategies for women who have a biopsy diagnosis of AEH, clinicians and patients should take into account the considerable rate of concurrent carcinoma. Cancer 2006. © 2006 American Cancer Society. [source] Preventive Effects of Isoflavones, Genistein and Daidzein, on Estradiol-17,-related Endometrial Carcinogenesis in MiceCANCER SCIENCE, Issue 7 2001Zenglin Lian The effects of isoflavones (genistein and daidzein) on endometrial carcinogenesis in mice were investigated in two experiments. In the short-term experiment (2 weeks), single subcutaneous (s.c.) administration of genistein [1 mg/30 g body weight (b.w.)] significantly decreased the levels of estradiol-l7, (E2) (5 ppm in diet)-induced expression of c-jun, interleukin-l, (IL-l,) and tumor necrosis factor-a (TNF-a) mRNAs in the uteri of ovariectomized mice (P<0.005, P<0.05 and P<0.01, respectively). Daidzein significantly inhibited E2-induced expression of c-fos and IL-l, (P<0.01, P<0.01 respectively). In the long-term experiment (30 weeks), 140 female ICR mice were given N-methyl-N-nitrosourea-containing solution (1 mg/100 g b.w.) and normal saline (as controls) into their left and right uterine corpora, respectively. They were divided into six groups; group 1 was given E2 (in diet) alone. Group 2 was given E2 and genistein (1 mg/30 g b.w., s.c., every four weeks). Group 3 was exposed to E2 and daidzein (1 mg/30 g b.w., s.c., every four weeks). Groups 4 and 5 respectively received genistein and daidzein, and were kept on the basal diet. Group 6 was kept on the basal diet and served as a control. At the termination of the experiment, incidences of endometrial adenocarcinoma and atypical endometrial hyperplasia of the group given E2 and genistein or daidzein were significantly lower than of the group with E2 alone (P<0.01 and P<0.05, respectively). It is suggested that both genistein and daidzein have an inhibitory effect on estrogen-related endometrial carcinogenesis in mice, possibly by suppressing expression of estrogen-induced estrogen-related genes c-fos and c-jun, and internal cytokines IL-l, and TNF-, through a cytokine and estrogen receptor-mediated pathway. [source] | ||||||||||||||||||||||