全职PI
叶浩彬

  青年研究员

  电话:021-31242095

  邮箱:haobin_ye@fudan.edu.cn

  地址:复旦大学2号交叉学科楼C7023室


个人简介

2016-2020年 科罗拉多大学医学院 血液系 博士后

2015年    罗切斯特大学 病理学 博士

主要研究方向

白血病干细胞代谢;白血病细胞微环境;肿瘤(白血病)引发的机体代谢紊乱;靶向代谢治疗白血病。

荣誉及获奖情况

  • 2018年   美国血液学会优秀摘要

  • 2015年   美国血液学会优秀摘要

代表性成果

  1. Ye H, Minhajuddin M, Krug A, Pei S, Culp-Hill R, Amaya M, Inguva, A Ponder J, Bloois E D, Schniedewind B, Amaya M L, Inguva A, Stevens B M, Pollyea D A, Christians U, D'Alessandro A, Jordan C T. The hepatic microenvironment uniquely protects leukemia cells through induction of growth and survival pathways mediated by LIPG. Cancer Discovery  2020 (*共同通讯作者).

  2. Jones C L, Stevens B M, Pollyea D A, Culp-Hill R, Reisz J A, Nemkov T, Gehrke S, Gamboni F, Krug A, Winters A, Pei S, Gustafson A, Ye H, Inguva A, Amaya M, Minhajuddin M, Abbott D, Becker M W, DeGregori J, Smith C A, D'Alessandro A, Jordan C T. Nicotinamide Metabolism Mediates Resistance to Venetoclax in Relapsed Acute Myeloid Leukemia Stem Cells. Cell Stem Cell 2020.

  3. Pei S, Pollyea D A, Gustafson A, Stevens B M, Minhajuddin M, Fu R, Riemondy K A, Gillen A E, Sheridan R M, Kim J, Costello J C, Amaya M L, Inguva A, Winters A, Ye H, Krug A, Jones C L, Adane B, Khan N, Ponder J, Schowinsky J, Abbott D, Hammes A, Myers J R, Ashton J/M, Nemkov T, D'Alessandro A, Gutman J A, Ramsey H E, Savona M R, Smith C A, Jordan C T. Monocytic subclones confer resistance to venetoclax-based therapy in acute myeloid leukemia patients. Cancer Discovery, 2020, DOI: 10.1158/2159-8290.CD-19-0710.

  4. Adane B, Ye H, Khan N, Pei S, Minhajuddin M, Stevens B M, Zaberezhnyy V, Gasparetto M, Kelly K, Ho T C, Myers J R, Ashton J M, Siegenthaler J, Campbell E, Pollyea D A, Becker M W, Jordan  CT. The hematopoietic oxidase NOX2 regulates self-renewal of leukemic stem cells. Cell Reports, 2019, 27(1): 238-254.e6.

  5. Ye H, Adane B, Khan N, Alexeev E, Nusbacher N, Minhajuddin M, Stevens B M, Winters A C, Lin X, Ashton J M, Purev E, Xing L, Pollyea D A, Lozupone C A, Serkova N J, Colgan S P, Jordan C T. Subversion of systemic glucose metabolism as a mechanism to support the growth of leukemia cells. Cancer Cell, 2018, 34(4):659-673.e6(Selected into Best of Cancer Cell 2018) . Highlight: Sabotaging the host, Nature Reviews Cancer 2018.

  6. Jones C L, Stevens B M, D'Alessandro A, Reisz J A, Culp-Hill R, Nemkov T, Pei S, Khan N, Adane B, Ye H, Krug A, Reinhold D, Smith C, DeGregori J, Pollyea D A, Jordan C T. Inhibition of amino acid metabolism selectively targets human leukemia stem cells. Cancer Cell, 2018, 34(5): 724-740.e4.

  7. Ye H, Adane B, Khan N, Sullivan T, Minhajuddin M, Gasparetto M, Stevens B M, Pei S, Balys M, Ashton J M, Klemm D J, Woolthuis C M, Stranahan A W, Park C Y, Jordan C T. Leukemic stem cells evade chemotherapy by metabolic adaptation to an adipose tissue niche. Cell Stem Cell, 2016, 19(1): 23-37(Featured article). Highlight: Leukaemia cells hide in fat tissue, Nature 2016.

  8. Pei S, Minhajuddin M, Callahan K P, Balys M, Ashton J M, Neering S J, Lagadinou E D, Corbett C, Ye H, Jordan C T. Targeting aberrant glutathione metabolism to eradicate human acute myelogenous leukemia cells. J Biol Chem, 2013, 288(47): 33542-33558.

  9. Zheng FJ, Ye H, Wu M S, Lian Y F, Qian C N, Zeng Y X. Repressing malic enzyme 1 redirects glucose metabolism, unbalances the redox state, and attenuates migratory and invasive abilities in nasopharyngeal carcinoma cell lines. Chin J Cancer, 2012, 31(11): 519-531.