RABL6A inhibits tumor-suppressive PP2A/AKT signaling to drive pancreatic neuroendocrine tumor growth

Hyperactivated AKT/mTOR signaling is a hallmark of pancreatic neuroendocrine tumors (PNETs). Drugs targeting this pathway are used clinically, but tumor resistance invariably develops. A better understanding of factors regulating AKT/mTOR signaling and PNET pathogenesis is needed to improve current...

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Veröffentlicht in:	The Journal of clinical investigation 2019-04, Vol.130 (4), p.1641-1653
Hauptverfasser:	Umesalma, Shaikamjad, Kaemmer, Courtney A, Kohlmeyer, Jordan L, Letney, Blake, Schab, Angela M, Reilly, Jacqueline A, Sheehy, Ryan M, Hagen, Jussara, Tiwari, Nitija, Zhan, Fenghuang, Leidinger, Mariah R, O'Dorisio, Thomas M, Dillon, Joseph, Merrill, Ronald A, Meyerholz, David K, Perl, Abbey L, Brown, Bart J, Braun, Terry A, Scott, Aaron T, Ginader, Timothy, Taghiyev, Agshin F, Zamba, Gideon K, Howe, James R, Strack, Stefan, Bellizzi, Andrew M, Narla, Goutham, Darbro, Benjamin W, Quelle, Frederick W, Quelle, Dawn E
Format:	Artikel
Sprache:	eng
Schlagworte:	AKT protein Biomedical research Cancer therapies Cancer treatment Care and treatment Cell cycle Cell growth Development and progression Drug delivery Drug resistance Everolimus G1 phase Gene expression Kinases Metastasis Neuroendocrine tumors Novels Pancreas Pancreatic cancer Pathogenesis Patient outcomes Patients Phase transitions Phosphatase Phosphatases Phosphoprotein phosphatase Phosphorylation Protein phosphatase Proteins Sunitinib TOR protein Tumor suppressor genes Tumors
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