Yubin Ge

Yubin Ge, Ph.D.
Associate Professor of Oncology
421 E. Canfield Street, Suite 3128
Detroit, MI 48201

Mentoring: Daniel Luedtke ( Year 3 )

Research Interests: 
Acute myeloid leukemia (AML) biology and leukemogenesis
Translational studies of AML, pancreatic cancer, diffuse intrinsic pontine glioma (DIPG), and neuroblastoma
Research Description:
Research in the Ge laboratory spans the basic biology and development of acute myeloid leukemia (AML) in children and adults, to combinational therapies and translational studies with primary patient specimens. Leukemia is the most common form of childhood cancer and cancer is the leading cause of death from disease of American children. Hence, improving leukemia therapy is of utmost importance in pediatric health. This is particularly relevant to AML in which progress has lagged significantly in comparison to childhood acute lymphoblastic leukemia. AML is even more challenging to treat in the elderly due to decreased tolerability to intensive therapy and increased therapy-related mortality. Resistance to cytarabine- and anthracycline-based chemotherapy is a major cause of treatment failure in this disease. Therefore, new therapies for patients with AML are urgently needed to overcome drug resistance, decrease relapse rates, and reduce short- and long-term adverse effects of treatment. The Ge laboratory studies have been focusing on the molecular basis for the remarkable synergism between histone deacetylase (HDAC) inhibitors (HDACIs) and standard chemotherapy drugs used for treating AML, and identification of the relevant HDAC isoforms. He is also working in collaboration with Dr. Zhihui Qin developing HDACI hybrid compounds and prodrugs for the treatment of leukemia. Another focus of the Ge laboratory is the use of Bcl-2 inhibitors for the treatment of AML. His studies have focused on the underlying molecular mechanisms of resistance to Bcl-2 inhibitors, specifically ABT-199, and identifying therapeutic targets for combination therapies with ABT-199 to overcome intrinsic resistance. In addition to AML, the Ge laboratory is also developing novel combinational therapies in preclinical models of pancreatic cancer, Diffuse Intrinsic Pontine Glioma (DIPG), and neuroblastoma.

Selected Publications:

Zhao J, Xie C, Edwards H, Wang G, Taub JW, and Ge Y*. Histone deacetylases 1 and 2 cooperate in regulating BRCA1, CHK1, and RAD51 expression in acute myeloid leukemia cells. Oncotarget. 2017;8:6319-29.

Schwartz J, Niu X, Walton E, Hurley L, Lin H, Edwards H, Taub JW, Wang Z, and Ge Y*. Synergistic anti-leukemic interactions between ABT-199 and Panobinostat in acute myeloid leukemia ex vivo. Am J Transl Res. 2016;8:3893-902.

Liao Y, Niu X, Chen B, Edwards H, Xu L, Xie C, Polin L, Taub JW, Ge Y*, and Qin Z*. Synthesis and antileukemic activities of piperlongumine and HDAC inhibitor hybrids against acute myeloid leukemia cells. J Med Chem. 2016;59:7974-90.

Ahsan S, Ge Y, and Tainsky M. Combinatorial therapeutic targeting of BMP2 and MEK1/2 pathways in NF1-associated malignant peripheral nerve sheath tumors. Oncotarget. 2016;7:57171-185.

Niu X, Zhao J, Ma J, Xie C, Edwards H, Wang G, Caldwell JT, Chu R, Wang Z, Lin H, Taub J, and Ge Y*. Binding of released Bim to Mcl-1 is a mechanism of intrinsic resistance to ABT-199 which can be overcome by combination with daunorubicin or cytarabine in acute myeloid leukemia cells. Clin Cancer Res. 2016;22:4440-51.

Zhao J, Niu J, Li X, Edwards H, Wang G, Wang Y, Taub JW, Lin H, and Ge Y*. Inhibition of CHK1 enhances cell death induced by the Bcl-2-selective inhibitor ABT-199 in acute myeloid leukemia cells. Oncotarget. 2016;7:34785-99.

Qi W, Zhang W, Edwards H, Chu R, Madlambayan GJ, Taub JW, Wang Z, Wang Y, Li C, Lin H, and Ge Y*. Synergistic anti-leukemic interactions between panobinostat and MK-1775 in acute myeloid leukemia ex vivo. Cancer Biol Ther. 2015;16:1784-93.

Shaham L, Vendarmini E,  Ge Y,  Goren Y, Tijssen M,  Birger Y, McNulty M, Geron I, Schwartzman O, Goldberg L, Chou ST, Pitman H, Weiss MJ, Michaeli S, Sredni B, Göttgens B, Crispino J, Taub JW, and Izraeli S. MiR-486-5p is an oncomiR in the myeloid leukemias of Down Syndrome. Blood. 2015;125:1292-301.

Xie C, Edwards, Caldwell JT, Wang G, Taub JW, and Ge Y*. Obatoclax potentiates the cytotoxic effect of cytarabine on acute myeloid leukemia cells by enhancing DNA damage. Mol Oncol. 2015;9:409-21.  

Wang G, Niu X, Zhang W, Caldwell JT, Edwards H, Chen W, Taub JW, Zhao L, and Ge Y*. Synergistic antitumor interactions between MK-1775 and panobinostat in preclinical models of pancreatic cancer. Cancer Lett. 2015;356:656-68.

Qi W, Xie C, Li C, Caldwell JT, Edwards H, Taub JW, Wang Y, Lin H, and Ge Y*. CHK1 plays a critical role in the anti-leukemic activity of the wee1 inhibitor MK-1775 in acute myeloid leukemia cells. J Hematol Oncol. 2014;7:53.

Caldwell JT, Edwards H, Buck SA, Ge Y*, and Taub JW*. Targeting the wee1 Kinase for Treatment of Pediatric Down Syndrome Acute Myeloid Leukemia. Pediatr Blood Cancer. 2014; 61:1767-73. [Featured on the cover for the issue].

Chen S, Wang G, Niu X, Zhao J, Tan W, Wang H, Zhao L, and Ge Y*. Combination treatment with AZD2281 (Olaparib) and GX15-070 (Obatoclax) results in synergistic antitumor activities in preclinical models of pancreatic cancer. Cancer Lett. 2014; 348:20-8.

Niu X, Wang G, Wang Y, Caldwell JT, Edwards H, Xie C, Taub JW, Li C, Lin H, and Ge Y*. Acute myeloid leukemia cells harboring MLL fusion genes or with the acute promyelocytic leukemia phenotype are sensitive to the Bcl-2 selective inhibitor ABT-199. Leukemia. 2014;28:1557-60.

Education and Training
PhD (1998): Jilin University, Changchun, China

Cancer Biology Courses Taught:
CB7210 Fundamentals of Cancer Biology
CB7240 Principles of Cancer Therapy
CB7300 Special Topics F31 Grant Writing Course

CB7460 Mechanism of Neoplasia: Alterations to Cellular Signaling
CB7700 Recent Developments in Cancer Biology (Course Co-Director)