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Main Category: Fertility
Also Included In: Diabetes; Cancer / Oncology
Article Date: 26 Sep 2012 - 0:00 PDT Current ratings for:
News From The Journal Of Clinical Investigation: September 24, 2012
New insight into hyperporlactinemia-associated infertility
Hyperprolactinemia, the presence of abnormally high levels of the hormone prolactin, is a well-established cause of infertility in women in their 20s and 30s. This hormone imbalance is frequently associated with low levels of gonadotrophic-releasing hormone (GnRH), a lack of ovulation, and a decrease in menstruation; however, the molecular mechanisms by which excess prolactin causes infertility are unclear. In this issue of the Journal of Clinical Investigation, researchers led by Nadine Binart at the University of Paris report that high levels of prolactin block expression of kisspeptin, a protein hormone that induces secretion of GnRH. By administering kisspeptin, Binart and colleagues restored ovulation in mice with high levels of prolactin. In an accompanying article, Ursula Kaiser of Brigham and Women's Hospital in Boston discusses the implications of this research for the clinical treatment of infertility in patients with hyperprolactinemia.
TITLE: Hyperprolactinemia-induced ovarian acyclicity is reversed by kisspeptin administration
View this article at: http://www.jci.org/articles/view/63937?key=280ce0bc284f919d41a1
ACCOMPANYING THE ATTENDING PHYSICIAN
TITLE: Hyperprolactinemia and infertility: new insights
View this article at: http://www.jci.org/articles/view/64455?key=bfeda7b4e5e1fa11a4b3
GATA transcription factors regulate pancreas development
Type 1 diabetes is caused by the autoimmune destruction of insulin-producing pancreatic ß islets. Efforts to reverse the disease are focused on replacing these cells and current research is focused on identifying the factors that contribute to islet generation during embryonic development. In this issue of the Journal of Clinical Investigation two research teams led by Anabel Rojas at the Andalusian Center for Molecular Biology and Regenerative Medicine in Seville, Spain and Lori Sussel at Columbia University report that GATA4 and GATA6 transcription factors are required for development of the pancreas in mice. Mice deficient in both genes failed to develop a pancreas, exhibited hyperglycemia, and died shortly after birth, while mice deficient in only one of the genes had very minor defects. Mutations in GATA6 and GATA4 are frequently found in neonatal diabetic patients. In a companion commentary, Jorge Ferrer and colleagues at the Hospital Clinic of Barcelona, Spain discusses the transcriptional mechanisms that underlie pancreas formation and their relation to new regenerative therapies for type 1 diabetes.
TITLE: GATA4 and GATA6 control mouse pancreas organogenesis
View this article at: http://www.jci.org/articles/view/63240?key=c8a6bd31c727e2d3b763
ACCOMPANYING ARTICLE TITLE: Pancreas-specific deletion of mouse Gata4 and Gata6 causes pancreatic agenesis
View this article at: http://www.jci.org/articles/view/63352?key=fb768d6ab25676b91c54
ACCOMPANYING COMMENTARY TITLE: GATA believe it: new essential regulators of pancreas development
View this article at: http://www.jci.org/articles/view/65751?key=af40e461737fe0703fce
MicroRNA links oncogenic signaling pathways in glioblastoma
Glioblastomas, the most prevalent primary brain tumor, frequently exhibit alterations in a number of signaling pathways that promote growth and metastasis; however, targeting of single elements has been clinically disappointing as the cancer cells simply reduce their reliance on targeted pathway. In this issue of the Journal of Clinical Investigation researchers at the Zhongshan School of Medicine in Ghuangzhou, China report on a microRNA, miR-182, that links two oncogenic signaling pathways in glioblastoma. MicroRNAs are molecules that suppress the expression of target genes. Jun Li and colleagues found that miR-182 was over-expressed in human glioblastoma patients and was correlated with the hyperactivation of two different oncogenic signaling pathways. Expression of miR-182 repressed expression of multiple negative regulators of these pathways, leading to sustained activation and enhanced malignancy. In a companion commentary, Christine Eyler of Brigham and Women's Hospital in Boston and Jeremy Rich of the Cleveland Clinic discuss the necessity of identifying multiple molecular targets within a given cancer to develop effective therapies.
TITLE: TGF-ß induces miR-182 to sustain NF-?B activation in glioma subsets
View this article at: http://www.jci.org/articles/view/62339?key=f349f446cf2044913393
ACCOMPANYING COMMENTARY TITLE: Looking in the miR-ror: TGF-ß-mediated activation of NF-?B in glioma
View this article at: http://www.jci.org/articles/view/66058?key=e2a0f7a4caee9492bf27
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27 Sep. 2012.
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'News From The Journal Of Clinical Investigation: September 24, 2012'
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