Objective: Atypical endometrial hyperplasia (AEH) has been associated with the presence of concomitant endometrial carcinoma (EC). The aim of this study is to examine the frequency of coexisting endometrial carcinoma ...Objective: Atypical endometrial hyperplasia (AEH) has been associated with the presence of concomitant endometrial carcinoma (EC). The aim of this study is to examine the frequency of coexisting endometrial carcinoma when atypical endometrium hyperplasia was found upon biopsy. We also evaluated the influence of preoperative diagnostic techniques (pipelle and dilation and curettage (D&C)), and the value of transvaginal ultrasound in detecting unexpected tumor invasion. Study design: Between January 1992 and December 2003, at the Department of Obstetrics and Gynecology, University of Parma, and Policlinico S. Matteo, Pavia, 70 consecutive patients subjected to total hysterectomy with a histological diagnosis of AEH were retrospectively selected. 52/70 patients underwent vaginal hysterectomy, with bilateral salpingo-oophorectomy (BSO)whereas 18/70 had abdominal hysterectomy with BSO within 8 weeks since the diagnosis of AEH. Results: We found in 30 of the 70 patients with atypical endometrial hyperplasia in the biopsy coexisting endometrial carcinoma (43%). No differences in diagnostic accuracy between the pipelle method and D&C were found. Conclusion: Transvaginal ultrasound was not a feasible method for predicting EC. After a follow-up of an average of 5 years there was, neither in the abdominal operated patients nor in the vaginal operated patients, a recurrence of disease.展开更多
Background. In this paper, we report a case of primary squamous cell carcinoma of the endometrium (PSCCE) with immunohistochemical and molecular study to evaluate the phenotype and to define the etiopathogenesis of th...Background. In this paper, we report a case of primary squamous cell carcinoma of the endometrium (PSCCE) with immunohistochemical and molecular study to evaluate the phenotype and to define the etiopathogenesis of this tumor. Case history. A 72- year- old woman was admitted to the Department of Obstetric and Gynecology for weight loss and pelvic mass. Abdominal ultrasonography disclosed the abdominopelvic mass with solid, cystic, and calcified areas. The patient underwent exploratory laparotomy. Intraoperative findings showed an enlarged uterus with perforation of its wall. The surface of omentum was covered with small white nodules. Pathological examination showed features of PSCCE. Immunohistochemical analysis with antibodies for estrogen and progesterone receptors disclosed negativity of neoplastic elements. Immunostaining with p53 tumor- suppressor protein showed the mutation of p53 tumor- suppressor protein as a strong nuclear positivity. Molecular study by polymerase chain reaction (PCR) amplification of tumor DNA did not show any signal for human papilloma virus (HPV) DNA. Conclusion. In summary, unlike the example reported in the literature by others, in the present case we demonstrated that PSCCE is not due to HPV infection, but probably to other pathogenetic mechanisms, which cause a mutation of p53 tumor- suppressor gene. Thus, it is reasonable to conclude that both HPV infection and unclear carcinogenic factors, responsible of p53 tumor- suppressor gene mutation, may cause PSCCE.展开更多
文摘Objective: Atypical endometrial hyperplasia (AEH) has been associated with the presence of concomitant endometrial carcinoma (EC). The aim of this study is to examine the frequency of coexisting endometrial carcinoma when atypical endometrium hyperplasia was found upon biopsy. We also evaluated the influence of preoperative diagnostic techniques (pipelle and dilation and curettage (D&C)), and the value of transvaginal ultrasound in detecting unexpected tumor invasion. Study design: Between January 1992 and December 2003, at the Department of Obstetrics and Gynecology, University of Parma, and Policlinico S. Matteo, Pavia, 70 consecutive patients subjected to total hysterectomy with a histological diagnosis of AEH were retrospectively selected. 52/70 patients underwent vaginal hysterectomy, with bilateral salpingo-oophorectomy (BSO)whereas 18/70 had abdominal hysterectomy with BSO within 8 weeks since the diagnosis of AEH. Results: We found in 30 of the 70 patients with atypical endometrial hyperplasia in the biopsy coexisting endometrial carcinoma (43%). No differences in diagnostic accuracy between the pipelle method and D&C were found. Conclusion: Transvaginal ultrasound was not a feasible method for predicting EC. After a follow-up of an average of 5 years there was, neither in the abdominal operated patients nor in the vaginal operated patients, a recurrence of disease.
文摘Background. In this paper, we report a case of primary squamous cell carcinoma of the endometrium (PSCCE) with immunohistochemical and molecular study to evaluate the phenotype and to define the etiopathogenesis of this tumor. Case history. A 72- year- old woman was admitted to the Department of Obstetric and Gynecology for weight loss and pelvic mass. Abdominal ultrasonography disclosed the abdominopelvic mass with solid, cystic, and calcified areas. The patient underwent exploratory laparotomy. Intraoperative findings showed an enlarged uterus with perforation of its wall. The surface of omentum was covered with small white nodules. Pathological examination showed features of PSCCE. Immunohistochemical analysis with antibodies for estrogen and progesterone receptors disclosed negativity of neoplastic elements. Immunostaining with p53 tumor- suppressor protein showed the mutation of p53 tumor- suppressor protein as a strong nuclear positivity. Molecular study by polymerase chain reaction (PCR) amplification of tumor DNA did not show any signal for human papilloma virus (HPV) DNA. Conclusion. In summary, unlike the example reported in the literature by others, in the present case we demonstrated that PSCCE is not due to HPV infection, but probably to other pathogenetic mechanisms, which cause a mutation of p53 tumor- suppressor gene. Thus, it is reasonable to conclude that both HPV infection and unclear carcinogenic factors, responsible of p53 tumor- suppressor gene mutation, may cause PSCCE.
