Lineage plasticity in prostate cancer depends on JAK/STAT inflammatory signaling

Drug resistance in cancer is often linked to changes in tumor cell state or lineage, but the molecular mechanisms driving this plasticity remain unclear. Using murine organoid and genetically engineered mouse models, we investigated the causes of lineage plasticity in prostate cancer and its relatio...

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Veröffentlicht in:	Science (American Association for the Advancement of Science) 2022-09, Vol.377 (6611), p.1180-1191
Hauptverfasser:	Chan, Joseph M, Zaidi, Samir, Love, Jillian R, Zhao, Jimmy L, Setty, Manu, Wadosky, Kristine M, Gopalan, Anuradha, Choo, Zi-Ning, Persad, Sitara, Choi, Jungmin, LaClair, Justin, Lawrence, Kayla E, Chaudhary, Ojasvi, Xu, Tianhao, Masilionis, Ignas, Linkov, Irina, Wang, Shangqian, Lee, Cindy, Barlas, Afsar, Morris, Michael J, Mazutis, Linas, Chaligne, Ronan, Chen, Yu, Goodrich, David W, Karthaus, Wouter R, Pe'er, Dana, Sawyers, Charles L
Format:	Artikel
Sprache:	eng
Schlagworte:	Androgen Antagonists Animals Biological properties Biopsy Castration Cell Plasticity Drug Resistance, Neoplasm ErbB Receptors Fibroblast growth factor receptors Growth factors Humans Inflammation Janus kinase Janus Kinase Inhibitors - therapeutic use Janus Kinases - genetics Janus Kinases - metabolism Kinases Male Mice Molecular modelling Neoplasms, Experimental Organoids Plastic foam Plastic properties Plasticity Prostate cancer Prostatic Neoplasms - drug therapy Prostatic Neoplasms - pathology Signal Transduction Signaling STAT Transcription Factors - genetics STAT Transcription Factors - metabolism Tumors
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