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2.
Reprod Biol Endocrinol ; 11: 91, 2013 Sep 12.
Artigo em Inglês | MEDLINE | ID: mdl-24028152

RESUMO

BACKGROUND: Although some studies have reported a potential connection between ovulation induction therapy (OIT) and malignant ovarian diseases, the results have been inconclusive. In the present study, we sought to determine whether women undergoing OIT at our in vitro fertilization (IVF) clinic, especially those with severe ovarian hyperstimulation syndrome (OHSS) and suspicious cytologic findings, were at risk for developing malignant ovarian tumours after treatment. METHODS: Patients who underwent OIT at our IVF clinic were enrolled in this study and assessed for any evidence of malignant ovarian tumours. Patients who developed severe OHSS as a result of OIT were treated with a culdocentesis. Cells from the ascitic fluid were cytologically scored for abnormality and malignancy. Peripheral blood samples were obtained from patients with severe OHSS to determine serum levels of the tumour markers (CA-125 and HE4) that were used to calculate the Risk for Ovarian Malignancy Algorithm (ROMA) index. RESULTS: Follow-up data were available for 1,353 of the 1,587 patients (85%) who underwent OIT at our IVF clinic between January 2006 and December 2012. Twenty-three patients (1.4%) were hospitalized with OHSS. Culdocentesis was performed 16 times in nine patients with severe OHSS (age range, 23-34 years; mean, 27.1 years). Although cytological examination of the ascitic cells of these patients suggested malignant ovarian neoplasia, over the course of the observation period, the ovarian volume gradually decreased and became normal. Subsequent cytological and histological examinations failed to find evidence of any malignant tumours in these nine patients. None of the 1,353 participants who underwent OIT developed any malignant ovarian tumours during the study period. Moreover, none of the 462 patients who were in our ovarian tumour registry were also participants in the IVF program. CONCLUSIONS: The presence of atypical cells in the ascitic fluid of women with severe OHSS does not likely indicate malignancy; therefore, radical surgical intervention is not justified. The risk of malignancy is minimal shortly after OIT. At our centre, OIT has not been associated with any cases of ovarian tumour.


Assuntos
Líquido Ascítico/patologia , Síndrome de Hiperestimulação Ovariana/patologia , Neoplasias Ovarianas/complicações , Algoritmos , Antígeno Ca-125/sangue , Culdoscopia , Feminino , Seguimentos , Humanos , Síndrome de Hiperestimulação Ovariana/complicações , Síndrome de Hiperestimulação Ovariana/cirurgia , Neoplasias Ovarianas/patologia , Indução da Ovulação/efeitos adversos , Proteínas/metabolismo , Medição de Risco , Proteína 2 do Domínio Central WAP de Quatro Dissulfetos
3.
J Steroid Biochem Mol Biol ; 103(2): 196-9, 2007 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-17097286

RESUMO

PTEN phosphatase, a product of PTEN tumor suppressor gene, exists in cells in phosphorylated and unphosphorylated form and has a central role in regulation of PI3K/Akt signalling which is involved in non-genomic action of estradiol. The purpose of this study was to analyze the level of total PTEN and phosphoPTEN parallel to phosphoAkt in leiomyoma and adjacent myometrium during menstrual cycle and at menopause. The expression of total PTEN in leiomyoma and myometrium did not change throughout the experiments. However, the level of phosphoPTEN was increased in leiomyoma during menstrual cycle. The phosphorylation of PTEN in myometrium was lower during secretory phase than that of proliferative phase. The phosphoAkt was abundant in leiomyoma, and its expression was higher during menstrual cycle than in myometrium. The phosphorylation of PTEN was directly related to phosphoAkt, suggesting a direct link between the inactivation of PTEN and activation of Akt. At the decline of sexual steroids, at menopause, no differences were observed in the expression of studied proteins between the two types of tissues. Our results suggest that the altered phosphorylation of PTEN protein and the consequent activation of survival signals may contribute to the pathomechanism of leiomyoma.


Assuntos
Leiomioma/metabolismo , PTEN Fosfo-Hidrolase/metabolismo , Proteínas Quinases/metabolismo , Neoplasias Uterinas/metabolismo , Adulto , Estudos de Casos e Controles , Feminino , Expressão Gênica , Humanos , Pessoa de Meia-Idade , Proteína Oncogênica v-akt/metabolismo , Fosforilação
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