RESUMO
El tumor trofoblástico del lecho placentario es un tumor excepcional, con no más de 100 casos referidos en la bibliografía. Se trata de una enfermedad neoplásica del trofoblasto intermedio, con capacidad metastatizante en pocos casos. Se presenta el caso de una paciente de 30 años, con una amenorrea de 10+4 semanas y que acudió a urgencias maternales aquejada de sangrado vaginal. Las exploraciones, bioquímica y ecografía fueron compatibles con el diagnóstico de enfermedad trofoblástica, y después de varios legrados ya apareció este raro diagnóstico anatomopatológico. Tras recidiva tumoral se decide histerectomía simple previo estudio de extensión tumoral negativo, y el diagnóstico de tumor trofoblástico del lecho placentario se confirmó en la pieza. Un año después la paciente sigue clínica y analíticamente libre de enfermedad
Placental-site trophoblastic tumor is exceptionally uncommon, with no more than a hundred cases reported in the literature. It is a neoplastic disorder of the middle trophoblast, with metastatic potential in a few cases. Our patient was a 30-year-old woman with amenorrhea of 10 weeks and 4 days' duration who attended the maternity emergency service complaining of vaginal bleeding. Physical examination, laboratory tests and ultrasonographic findings were compatible with a diagnosis of trophoblastic disease. After several curettages, this rare histopathological diagnosis was made. The tumor recurred and negative tumoral extension study and simple hysterectomy were performed. Analysis of the surgical specimen confirmed the diagnosis of placental-site trophoblastic tumor. After 1 year, laboratory tests show no recurrence and the patient is clinically disease-free
Assuntos
Feminino , Adulto , Humanos , Tumor Trofoblástico de Localização Placentária/patologia , Doença Trofoblástica Gestacional/patologia , Amenorreia/etiologia , Hemorragia Uterina/etiologia , Lactogênio Placentário/análise , Diagnóstico DiferencialRESUMO
Diploid yeast cells switch from mitosis to meiosis when starved of essential nutrients. While G1 cyclins play a key role in initiating the mitotic cell cycle, entry into meiosis depends on Ime1, a transcriptional activator regulated by both nutritional and cell-type signals. We show here that G1 cyclins downregulate IME1 transcription and prevent the accumulation of the Ime1 protein within the nucleus, which results in repression of early-meiotic gene expression. As G1-cyclin deficient cells do not require nutrient starvation to undergo meiosis, G1 cyclin would exert its role by transmitting essential nutritional signals to Ime1 function. The existence of a negative cross-talk mechanism between mitosis and meiosis may help explain why these two developmental options are incompatible in budding yeast.
Assuntos
Ciclinas/fisiologia , Proteínas Fúngicas/fisiologia , Fase G1/fisiologia , Meiose/fisiologia , Mitose/fisiologia , Proteínas Nucleares/fisiologia , Proteínas de Saccharomyces cerevisiae , Saccharomyces cerevisiae/citologia , Saccharomyces cerevisiae/fisiologia , Fatores de Transcrição , Núcleo Celular/fisiologia , Meios de Cultura , Ciclinas/genética , Proteínas Fúngicas/genética , Fase G1/genética , Expressão Gênica , Genes Fúngicos , Meiose/genética , Mitose/genética , Proteínas Nucleares/genética , Fase S/genética , Fase S/fisiologia , Saccharomyces cerevisiae/genética , Transdução de Sinais , Transativadores/genética , Transativadores/fisiologiaRESUMO
Nutrients are among the most important trophic factors in all organisms. When deprived of essential nutrients, yeast cells use accumulated reserves to complete the current cycle and arrest in the following G1 phase. We show here that the Cln3 cyclin, which has a key role in the timely activation of SBF (Swi4-Swi6)- and MBF (Mbp1-Swi6)-dependent promoters in late G1, is down-regulated rapidly at a post-transcriptional level in cells deprived of the nitrogen source. In addition to the fact that Cln3 is degraded faster by ubiquitin-dependent mechanisms, we have found that translation of the CLN3 mRNA is repressed approximately 8-fold under nitrogen deprivation conditions. As a consequence, both SBF- and MBF-dependent expression is strongly down-regulated. Mainly because of their transcriptional dependence on SBF, and perhaps with the contribution of similar post-transcriptional mechanisms to those found for Cln3, the G1 cyclins Cln1 and 2 become undetectable in starved cells. The complete loss of Cln cyclins and the sustained presence of the Clb-cyclin kinase inhibitor Sic1 in starved cells may provide the molecular basis for the G1 arrest caused by nitrogen deprivation.
