The International Journal of Biochemistry & Cell Biology, Journal Year: 2008, Volume and Issue: 40(8), P. 1443 - 1451
Published: Jan. 1, 2008
Language: Английский
The International Journal of Biochemistry & Cell Biology, Journal Year: 2008, Volume and Issue: 40(8), P. 1443 - 1451
Published: Jan. 1, 2008
Language: Английский
Trends in Biochemical Sciences, Journal Year: 2011, Volume and Issue: 36(6), P. 320 - 328
Published: May 3, 2011
Language: Английский
Citations
1640Molecular and Cellular Endocrinology, Journal Year: 2009, Volume and Issue: 308(1-2), P. 32 - 38
Published: April 16, 2009
Language: Английский
Citations
339Clinical ophthalmology, Journal Year: 2017, Volume and Issue: Volume 11, P. 279 - 289
Published: Jan. 1, 2017
Uveal melanoma: epidemiology, etiology, and treatment of primary disease Benjamin A Krantz,1 Nikita Dave,2 Kimberly M Komatsubara,2 Brian P Marr,3,4 Richard D Carvajal5 1Division Hospital Medicine, 2Division Hematology/Oncology, Columbia University Medical Center, 3Ophthalmic Oncology Service, Memorial Sloan Kettering Cancer 4Department Ophthalmology, Weill Cornell College, 5Division New York, NY, USA Abstract: melanoma (UM) is the most common intraocular malignancy arises from melanocytes in iris, ciliary body, or choroid. Early diagnosis local crucial, as survival correlates with tumor size. However, approximately 50% patients will develop metastatic 6–12 months’ diagnosis. Genomic analyses have led to development gene-expression profiles that effectively predict progression; unfortunately, no adjuvant therapy has been shown prolong date. insights into molecular biology UM found frequent activating mutations genes encoding for G-protein α-subunit, GNAQ GNA11, improved understanding downstream signaling pathways MAPK, PI3K/Akt, Hippo afforded an array new targets this disease. Studies are under way rationally developed regimens targeting these pathways, novel agents development. We review diagnosis, management, surveillance trials way. Keywords: uveal melanoma, ocular GNAQ, MAP kinase, MEK
Language: Английский
Citations
334Nature Cell Biology, Journal Year: 2016, Volume and Issue: 18(10), P. 1065 - 1077
Published: Sept. 12, 2016
Language: Английский
Citations
322Biochimica et Biophysica Acta (BBA) - Molecular Cell Research, Journal Year: 2013, Volume and Issue: 1843(2), P. 398 - 435
Published: Nov. 2, 2013
Language: Английский
Citations
320Cancer Research, Journal Year: 2009, Volume and Issue: 69(16), P. 6539 - 6545
Published: Aug. 12, 2009
Abstract Recently, we identified a novel crosstalk between insulin and G protein–coupled receptor (GPCR) signaling pathways in human pancreatic cancer cells. Insulin enhanced GPCR through rapamycin-sensitive mTOR-dependent pathway. Metformin, the most widely used drug treatment of type 2 diabetes, activates AMP kinase (AMPK), which negatively regulates mTOR. Here, determined whether metformin disrupts Treatment cells (PANC-1, MIAPaCa-2, BxPC-3) with (10 ng/mL) for 5 minutes markedly increase intracellular [Ca2+] induced by agonists (e.g., neurotensin, bradykinin, angiotensin II). Metformin pretreatment completely abrogated insulin-induced potentiation Ca2+ but did not interfere effect alone. also agonist–induced growth, measured DNA synthesis, number cultured adherent or nonadherent conditions. Low doses (0.1–0.5 mmol/L) blocked stimulation anchorage-dependent anchorage-independent growth agonists. striking sustained phosphorylation AMPK at Thr172 selective inhibitor (compound C, μmol/L) reversed effects on [Ca2+]i indicating that acts activation. In view these results, tested inhibits growth. Administration significantly decreased MIAPaCa-2 PANC-1 xenografted flank nude mice. These results raise possibility could be potential candidate strategies cancer. [Cancer Res 2009;69(16):6539–45]
Language: Английский
Citations
315Trends in Endocrinology and Metabolism, Journal Year: 2010, Volume and Issue: 21(5), P. 294 - 301
Published: Jan. 15, 2010
Language: Английский
Citations
292Mediators of Inflammation, Journal Year: 2012, Volume and Issue: 2012, P. 1 - 18
Published: Jan. 1, 2012
Src kinase (Src) is a tyrosine protein that regulates cellular metabolism, survival, and proliferation. Many studies have shown plays multiple roles in macrophage-mediated innate immunity, such as phagocytosis, the production of inflammatory cytokines/mediators, induction migration, which strongly implies pivotal role functional activation macrophages. Macrophages are involved variety immune responses diseases including rheumatoid arthritis, atherosclerosis, diabetes, obesity, cancer, osteoporosis. Previous suggested for responses; however, recently, new functions been reported, implying not described. In this paper, we discuss recent regarding number these newly defined responses. Moreover, feasibility target development pharmaceutical drugs to treat diseases. We provide insights into reports related macrophage-related novel inhibitors with strong immunosuppressive anti-inflammatory properties, could be applied various
Language: Английский
Citations
268Molecular Cancer Therapeutics, Journal Year: 2014, Volume and Issue: 13(11), P. 2477 - 2488
Published: Oct. 17, 2014
The development of drug resistance by cancer cells is recognized as a major cause for failure and disease progression. PI3K/AKT/mTOR pathway aberrantly stimulated in many thus it has emerged target therapy. However, mTORC1 S6K also mediate potent negative feedback loops that attenuate signaling via insulin/insulin growth factor receptor other tyrosine kinase receptors. Suppression these causes overactivation upstream pathways, including PI3K, AKT, ERK potentially oppose the antiproliferative effects mTOR inhibitors lead to resistance. A corollary this concept release consequent compensatory promitogenic pathways response signal can circumvent mitogenic block imposed targeting only one pathway. Consequently, elucidation regulate outputs networks an area fundamental importance rational design effective anticancer combinations inhibitors. Here, we review undergo suppress inhibition underscore unintended activation clinically relevant mTOR, or PI3K/mTOR.
Language: Английский
Citations
261Pancreatology, Journal Year: 2011, Volume and Issue: 11(3), P. 279 - 294
Published: July 11, 2011
Language: Английский
Citations
243