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10.1210/en.2016-1395 http://scihub22266oqcxt.onion/10.1210/en.2016-1395 C5007898!5007898 !27409646     free     free     free Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\27409646 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Endocrinology 2016 ; 157 (9 ): 3374-83 Nephropedia Template TP {{tp|p=27409646 |t=2016. Minireview: Lymphangioleiomyomatosis (LAM): The "Other" Steroid-Sensitive Cancer |pdf=|usr=}}{{27409646 }} gab.com Text Minireview: Lymphangioleiomyomatosis (LAM): The "Other" Steroid-Sensitive Cancer JO: Endocrinology http://www.kidney.de/pget.php?&tw=1&pmid=27409646 #FOAvip Lymphangioleiomyomatosis (LAM) is a devastating rare lung disease affecting primarily childbearing age women in which tumors consisting of abnormal smooth-muscle-like cells grow within the lungs and progressively lead to loss of pulmonary function. LAM cells metastasize to the lungs, predominantly through the lymphatics; however, the source of the LAM cell is still unknown. LAM cells contain inactivating mutations in genes encoding tuberous sclerosis 1 or 2, proteins that normally limit cell growth through suppression of mammalian target of rapamycin complex 1. As of today, sirolimus (an mammalian target of rapamycin complex 1 inhibitor) is the only treatment, available for LAM patients that is approved by the Food and Drug Administration; however, this drug and others in its class provide stabilization but not remission of LAM. One of the biggest problems in treating LAM is that both the origin of the LAM cells and the mechanism of the sexual dimorphism in LAM are still not understood. LAM cells express estrogen and progesterone receptors, and lung function declines during periods of high circulating estrogen levels. Moreover, numerous basic research studies find that estrogen is a key driving force in LAM cell proliferation, migration, and metastasis. In this review, we highlight recent insights regarding the role of steroid hormones in LAM and discuss possible explanations for the profound female sexual dimorphism of LAM. Twit Text FOAVip Minireview: Lymphangioleiomyomatosis (LAM): The "Other" Steroid-Sensitive Cancer ????Endocrinology http://www.kidney.de/pget.php?&tw=1&pmid=27409646 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27409646 #FOAvip English Wikipedia <ref>{{Cite pmid|27409646 }}</ref> Minireview: Lymphangioleiomyomatosis (LAM): The "Other" Steroid-Sensitive Cancer #MMPMID27409646 Prizant H ; Hammes SR Endocrinology 2016[Sep]; 157 (9 ): 3374-83 PMID27409646 show ga Lymphangioleiomyomatosis (LAM) is a devastating rare lung disease affecting primarily childbearing age women in which tumors consisting of abnormal smooth-muscle-like cells grow within the lungs and progressively lead to loss of pulmonary function. LAM cells metastasize to the lungs, predominantly through the lymphatics; however, the source of the LAM cell is still unknown. LAM cells contain inactivating mutations in genes encoding tuberous sclerosis 1 or 2, proteins that normally limit cell growth through suppression of mammalian target of rapamycin complex 1. As of today, sirolimus (an mammalian target of rapamycin complex 1 inhibitor) is the only treatment, available for LAM patients that is approved by the Food and Drug Administration; however, this drug and others in its class provide stabilization but not remission of LAM. One of the biggest problems in treating LAM is that both the origin of the LAM cells and the mechanism of the sexual dimorphism in LAM are still not understood. LAM cells express estrogen and progesterone receptors, and lung function declines during periods of high circulating estrogen levels. Moreover, numerous basic research studies find that estrogen is a key driving force in LAM cell proliferation, migration, and metastasis. In this review, we highlight recent insights regarding the role of steroid hormones in LAM and discuss possible explanations for the profound female sexual dimorphism of LAM. |Cathepsin K/metabolism [MESH] |Estrogens/*metabolism [MESH] |Female [MESH] |Humans [MESH] |Leiomyoma/pathology [MESH] |Leukocyte Elastase/metabolism [MESH] |Lung/pathology [MESH] |Lymphangioleiomyomatosis/*etiology/genetics/metabolism/pathology [MESH] |Lymphatic Metastasis [MESH] |Matrix Metalloproteinases/metabolism [MESH] |Progesterone/*metabolism [MESH] |Selective Estrogen Receptor Modulators [MESH] |Sex Characteristics [MESH] |Uterine Neoplasms/pathology [MESH]Minireview: Lymphangioleiomyomatosis (LAM): The "Other" Steroid-Sensit(epmc).pdf DeepDyve Pubget Overpricing