Research Lab Overview

The Bin Zhang Lab advances precision medicine for patients with hematologic malignancies by uncovering and therapeutically targeting the mechanisms that sustain leukemia stem cells (LSCs). These cells can survive treatment, maintain disease and drive relapse. The laboratory investigates how LSCs interact with the bone marrow niche, how their self-renewal and treatment resistance are regulated and how these processes promote progression to aggressive disease, including blast-crisis chronic myeloid leukemia (CML) and secondary acute myeloid leukemia (AML).

The Zhang Lab integrates basic and translational research across CML, AML and acute lymphoblastic leukemia (ALL). Its discoveries have revealed how microRNAs regulate LSC survival and shape the protective bone marrow microenvironment. Using diverse genetically engineered mouse models and patient-derived xenografts, the team identifies therapeutic vulnerabilities and develops strategies to eliminate LSCs while preserving normal hematopoiesis. The laboratory also develops targeted immunotherapies, including chimeric antigen receptor (CAR) T cells and bispecific antibodies, to overcome treatment resistance and achieve durable disease control.

Research Highlights

What Is the Role of miR-126 in Normal Hematopoiesis and Leukemogenesis?

The Zhang Lab investigates how miR-126 regulates normal hematopoietic stem cells and leukemia stem cells. The team's studies identified miR-126 as a key regulator of LSC quiescence and self-renewal and established a CpG-anti-miR-126 therapeutic strategy to disrupt LSC maintenance and enhance treatment sensitivity. These discoveries led to the development of miRisten, a first-in-class miR-126 inhibitor currently undergoing clinical testing in AML (NCT07025564).

What Is the Role of miR-142 in Leukemia Transformation?

The Zhang Lab investigates how miR-142 deficiency drives clonal hematopoietic cell transformation and establishes an immunosuppressive bone marrow microenvironment. The team examines how these processes promote progression from clonal myeloid disorders to secondary AML, drive the evolution of chronic-phase CML to blast crisis and increase B-cell acute lymphoblastic leukemia (B-ALL) aggressiveness. The lab also develops and evaluates a CpG-conjugated miR-142 mimic to restore miR-142 activity and prevent or reverse disease progression.

How Can We Develop Targeted Immunotherapies for Leukemia?

In collaboration with the groups of John Williams, Ph.D., Christine Brown, Ph.D., and Guido Marcucci, M.D., the Zhang Lab develops CAR T cell and bispecific antibody therapies targeting leukemia cells and LSCs. These strategies aim to overcome therapeutic resistance and enhance antileukemic activity while preserving normal hematopoietic cells.

Principal Investigator: Bin Zhang, M.D., Ph.D.

Dr. Zhang is a Professor in the Department of Hematologic Malignancies Translational Science and the Gehr Family Center for Leukemia Research at City of Hope. Her research investigates how microRNAs reprogram both clonal and nonclonal hematopoietic cells to promote leukemic transformation and disease progression. She also develops novel immunotherapies for myeloid and lymphoid malignancies.

Full bio

Lab Members

Dan Dan Zhao

Staff Scientist

Dr. Zhao is a Staff Scientist at City of Hope, where her research

Alex earned his B.A. in Cellular and Molecular Biology from

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Our Publications

Longitudinal single cell RNA-sequencing reveals evolution of micro- and macro-states in chronic myeloid leukemia.

Frankhouser D, Zhao D, Fu YH, Dey A, Chen Z, Irizarry J, Ambriz JR, Branciamore S, O'Meally D, Trent J, Forman S, Kuo YH, MacLean A, Zhang B, Rockne R, Marcucci G.

Loss of endothelial miR-126 drives age-related decline in hematopoiesis.

Zhao D, Nguyen LX, Gong X, Chen F, Zhao X, Chen MH, Marcucci G, Zhang B.

MicroRNA-142 improves IL1RAP CAR-T cell activity in acute myeloid leukemia.

Harada K, Zhao D, Park M, Chen F, Xu Y, Zhang Y, Zhou Y, Parcutela B, Jewel Y, Munoz A, Amanam I, Nguyen L, Chen J, Ghoda L, Forman S, Williams J, Zhang B, Marcucci G.

miR-142 deficit in T cells during blast crisis promotes chronic myeloid leukemia immune escape.

Chen F, Zhao D, Xu Y, Zhang Y, Chen MH, Pathak KV, Hansen N, Lovell B, Liang Y, Estrella K, Wang WL, Ghoda L, Rockne R, Wu X, Ali H, Yu J, Caligiuri MA, Forman SJ, Trent JM, Kuo YH, Li L, Swiderski P, Zhang J, Kortylewski M, Nguyen LX, Pirrotte P, Boldin M, Marcucci G, Zhang B.

Homoharringtonine synergizes with venetoclax in early T-cell progenitor acute lymphoblastic leukemia: bench and bed.

Suo S, Sun S, Nguyen LX, Qian J, Li F, Zhao D, Yu W, Lou Y, Zhu H, Tong T, Yang M, Huang X, Zhao S, Qiao J, Liang C, Wang H, Zhang Y, Zhang X, Hoang DH, Chen F, Kang H, Valerio M, Sun J, Ghoda L, Li L, Marcucci G, Zhang B, Jin J.