RESUMO
The aim of this study was to evaluate the effect of hormone replacement therapy (HRT) on the expression of Ki-67, bcl-2 and c-erb.B2 in endometrial polyps during menopause. Sixteen patients using HRT and 24 untreated controls with endometrial polyps were enrolled in this study. Polypectomy was carried out by hysteroscopy. The presence of c-erb.B2, bcl-2 and Ki-67 expression was determined by immunohistochemistry. HRT was found to decrease Ki-67 and bcl-2 expression in endometrial polyps without affecting the c-erb.B2 staining reaction. HRT may cause endometrial polyp involution by decreasing proliferation and stimulating apoptosis.
Assuntos
Neoplasias do Endométrio/metabolismo , Terapia de Reposição de Estrogênios , Noretindrona/análogos & derivados , Pólipos/metabolismo , Administração Cutânea , Administração Oral , Idoso , Estudos de Casos e Controles , Estradiol/farmacologia , Estrogênios Conjugados (USP)/farmacologia , Feminino , Humanos , Imuno-Histoquímica , Antígeno Ki-67/metabolismo , Acetato de Medroxiprogesterona/farmacologia , Menopausa , Pessoa de Meia-Idade , Noretindrona/farmacologia , Acetato de Noretindrona , Proteínas Proto-Oncogênicas c-bcl-2/metabolismo , Receptor ErbB-2/metabolismo , Estudos RetrospectivosRESUMO
Our objective was to investigate the presence of focal p53 expression in relation to proliferation rates in adenomyotic lesions during the menstrual cycle and in women on oral contraception. Fifty-nine perimenopausal patients with menorrhagia and adenomyosis were submitted to endometrial resection. The procedure was carried out during menstruation (n = 14), during the proliferative phase (n = 15), during the luteal phase (n = 20) or following the use of oral contraceptives (n = 10). The number of Ki-67-positive cells was low during menstruation, during the luteal phase and following the use of progestins. In the proliferative phase, on the other hand, there was a significant increase in the percentage of Ki-67-positive cells. Focal p53 expression was detected mainly during the proliferative phase of the menstrual cycle when proliferation rates were high. PTEN expression was detected in all cases irrespective of the phase of the menstrual cycle or use of oral contraception. We conclude that proliferation rates in adenomyotic lesions undergo marked cyclic variations and this affects the percentage of cases showing focal p53 expression in the glandular epithelium.
Assuntos
Anticoncepcionais Orais Combinados , Endometriose/patologia , Endométrio/citologia , Ciclo Menstrual , Adulto , Divisão Celular , Feminino , Humanos , Pessoa de Meia-Idade , Estudos RetrospectivosRESUMO
OBJECTIVE: To determine whether or not the presence of c-erbB2 over-expression in endometrial polyps affects the percentage of cells positive for Ki-67 proliferation marker. METHODS: Thirty-five patients with endometrial polyps were submitted to polypectomy by hysteroscopy. Ki-67 and c-erbB2 over-expression were investigated in the polyps by immunohistochemistry. RESULTS: The presence of c-erbB2 over-expression by immunohistochemistry was observed in 80% of endometrial polyps and was associated with higher proliferation rates as determined by the number of positive Ki-67 cell nuclei. In c-erbB2-negative polyps, the proliferation rates were low. CONCLUSION: Ki-67 and c-erbB2 over-expression are frequent in endometrial polyps in post-menopausal women.
Assuntos
Neoplasias do Endométrio/metabolismo , Antígeno Ki-67/metabolismo , Pólipos/metabolismo , Receptor ErbB-2/metabolismo , Idoso , Idoso de 80 Anos ou mais , Divisão Celular , Neoplasias do Endométrio/patologia , Feminino , Humanos , Histeroscopia , Imuno-Histoquímica , Pessoa de Meia-Idade , Pólipos/patologia , Pós-MenopausaRESUMO
STUDY OBJECTIVE: To determine whether types I and II endometrial carcinomas have different precursor lesions recognized at hysteroscopy and immunohistochemistry. DESIGN: Single center case study (Canadian Task Force classification II-2). SETTING: A private, university affiliated hospital. PATIENTS: One hundred forty-six postmenopausal women with endometrial pathology diagnosed by hysteroscopy and biopsy. INTERVENTION: Hysteroscopy and immunohistochemical determination of p53 overexpression. MEASUREMENTS AND MAIN RESULTS: The number of cells showing p53 overexpression was low in endometrial polyps, hyperplasia, and G1 endometrioid carcinomas. A marked increase was seen only in high-grade G2-G3 endometrioid carcinomas and in cases of uterine papillary serous carcinoma. In the latter, strong p53 overexpression was detected in early forms still confined to endometrial polyps. Hysteroscopy could not differentiate between high- and low-grade endometrioid carcinomas. CONCLUSION: The p53-driven pathway plays an important role in the origin of papillary serous carcinoma but not in G1 endometrioid cancer that evolves from estrogen-stimulated endometrium. However, this pathway is important for progression of low-grade endometrioid carcinomas to higher-grade tumors.
Assuntos
Neoplasias do Endométrio/metabolismo , Histeroscopia , Proteína Supressora de Tumor p53/metabolismo , Núcleo Celular/metabolismo , Núcleo Celular/patologia , Cistadenocarcinoma Papilar/metabolismo , Cistadenocarcinoma Papilar/patologia , Hiperplasia Endometrial/metabolismo , Hiperplasia Endometrial/patologia , Neoplasias do Endométrio/patologia , Feminino , Expressão Gênica , Humanos , Imuno-Histoquímica , Pessoa de Meia-Idade , Pólipos/metabolismo , Pólipos/patologia , Neoplasias Uterinas/metabolismo , Neoplasias Uterinas/patologiaRESUMO
OBJECTIVE: To detect the presence of testosterone and estrogen receptors in the stroma and glandular epithelium in the malignant and non-malignant endometrium. METHODS: One hundred and forty-five consecutively-enrolled peri- or postmenopausal patients were submitted to diagnostic or operative hysteroscopy. These patients either had a history of abnormal uterine bleeding or they were asymptomatic with an endometrial echo greater than 4 mm. The presence of estrogen and testosterone receptors was determined in endometrial samples by immunohistochemistry, using monoclonal antibodies and a streptavidin-biotin peroxidase complex system with diamino benzidine as the chromogen. RESULTS: Testosterone receptors were detected mainly in the stroma in the non-malignant endometrial lesions and in the atypical glandular epithelium in cases of estrogen-positive endometrial carcinomas. CONCLUSIONS: The presence of testosterone receptors in estrogen receptor positive endometrial carcinomas may be involved in the mechanism of cell proliferation in these tumors. The strong staining reaction for testosterone receptors in the endometrial glands can be considered one of the features of invasive malignancy.