Asxl1 loss cooperates with oncogenic Nras in mice to reprogram the immune microenvironment and drive leukemic transformation. You X, Liu F, Binder M, Vedder A, Lasho T, Wen Z, Gao X, Flietner E, Rajagopalan A, Zhou Y, Finke C, Mangaonkar A, Liao R, Kong G, Ranheim EA, Droin N, Hunter AM, Nikolaev S, Balasis M, Abdel-Wahab O, Levine RL, Will B, Nadiminti KVG, Yang D, Geissler K, Solary E, Xu W, Padron E, Patnaik MM, Zhang J. Search PubMed for more publications by Jing Zhang Validate therapeutic strategies in preclinical models in vitro and in vivo Develop mechanism-based novel combination targeted therapies and immunotherapiesĤ.

Investigate disease mechanisms using multi-Omics approachģ.

Study how genetic mutations alter hematopoietic stem and progenitor cell functions to promote blood cancersĢ. We use these models along with cell lines and patient samples to:ġ. We generated and characterized multiple genetically engineered mouse models for oncogenic Ras-driven blood cancers, including juvenile monocytic leukemia, chronic myelomonocytic leukemia and its transformation to acute myeloid leukemia, multiple myeloma, and early T cell precursor acute lymphoblastic leukemia. The research program in my lab focuses on cell signaling, in particular Ras signaling, in hematopoiesis and leukemogenesis.

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Historical Issues: Grappling with Our Past.

Crow Institute for the Study of Evolution

Zhang jing jing