Yubin Kang

Positions:

Professor of Medicine

Medicine, Hematologic Malignancies and Cellular Therapy
School of Medicine

Member of the Duke Cancer Institute

Duke Cancer Institute
School of Medicine

Education:

M.D. 1991

Shanghai Second Medical University (China)

Fellow, Hematology, Oncology, Cellular Therpay

Duke University School of Medicine

Grants:

Plerixafor for allogeneic hematopoietic stem cell transplantation

Administered By
Medicine, Hematologic Malignancies and Cellular Therapy
Awarded By
National Institutes of Health
Role
Principal Investigator
Start Date
End Date

A PHASE 2, MULTICENTER, MULTI-COHORT, OPEN-LABEL STUDY OF POMALIDOMIDE IN COMBINATION WITH LOW-DOSE DEXAMETHASONE OR POMALIDOMIDE IN COMBINATION WITH LOW-DOSE DEXAMETHASONE AND DARATUMUMAB IN SUBJECTS WITH RELAPSED OR REFRACTORY MULTIPLE MYELOMA

Administered By
Duke Cancer Institute
Awarded By
Celgene Corporation
Role
Principal Investigator
Start Date
End Date

Clinical characteristics, JAK2 status, and macrophage infiltration in multiple myeloma patients with marrow fibrosis

Administered By
Medicine, Hematologic Malignancies and Cellular Therapy
Awarded By
Incyte Corporation
Role
Principal Investigator
Start Date
End Date

Clinical Trial of ABC294640 in Patients with Refractory Multiple Myeloma

Administered By
Medicine, Hematologic Malignancies and Cellular Therapy
Awarded By
Apogee Biotechnology Corporation
Role
Principal Investigator
Start Date
End Date

Phase I study of Pomolidomide, Bortezomib, and Dexamethasone (PVD) as First-Line treatment of AL Amyloidosis or Light Chain Deposition Disease

Administered By
Duke Cancer Institute
Awarded By
Karmanos Cancer Center
Role
Principal Investigator
Start Date
End Date

Publications:

Chimeric antigen receptor (CAR) T-cell therapy for multiple myeloma.

Although treatment outcomes of multiple myeloma patients have improved significantly during the last two decades, myeloma is still an incurable disease. There are newly emerging immunotherapies to treat multiple myeloma including monoclonal antibodies, antibody-drug conjugate, bispecific antibodies, and chimeric antigen receptor (CAR) T cell therapy. Impressive response rate and clinical efficacy in heavily pretreated myeloma patients led to the FDA approval of the first myeloma CAR-T therapy in March 2021. Among many different targets for myeloma CAR-T therapies, B Cell Maturation Antigen (BCMA) has been the most successful target so far, but other targets which can be used either for single-target or dual-target CAR-T's are actively being explored. Clinical efficacy and safety of current myeloma CAR-T therapies will be presented here. Potential mechanisms leading to resistance include clearance of CAR-T cells, antigenic escape, and immunosuppressive tumor microenvironment. Novel strategies to enhance myeloma CAR-T will also be described. In this article, we provide a comprehensive review of the current data and the future directions of myeloma CAR-T therapies.
Authors
MLA Citation
Choi, Taewoong, and Yubin Kang. “Chimeric antigen receptor (CAR) T-cell therapy for multiple myeloma.Pharmacol Ther, Sept. 2021, p. 108007. Pubmed, doi:10.1016/j.pharmthera.2021.108007.
URI
https://scholars.duke.edu/individual/pub1497860
PMID
34582835
Source
pubmed
Published In
Pharmacol Ther
Published Date
Start Page
108007
DOI
10.1016/j.pharmthera.2021.108007

PIM Kinases in Multiple Myeloma.

Multiple myeloma (MM) remains an incurable disease and novel therapeutic agents/approaches are urgently needed. The PIM (Proviral insertion in murine malignancies) serine/threonine kinases have 3 isoforms: PIM1, PIM2, and PIM3. PIM kinases are engaged with an expansive scope of biological activities including cell growth, apoptosis, drug resistance, and immune response. An assortment of molecules and pathways that are critical to myeloma tumorigenesis has been recognized as the downstream targets of PIM kinases. The inhibition of PIM kinases has become an emerging scientific interest for the treatment of multiple myeloma and several PIM kinase inhibitors, such as SGI-1776, AZD1208, and PIM447 (formerly LGH447), have been developed and are under different phases of clinical trials. Current research has been focused on the development of a new generation of potent PIM kinase inhibitors with appropriate pharmacological profiles reasonable for human malignancy treatment. Combination therapy of PIM kinase inhibitors with chemotherapeutic appears to create an additive cytotoxic impact in cancer cells. Notwithstanding, the mechanisms by which PIM kinases modulate the immune microenvironment and synergize with the immunomodulatory agents such as lenalidomide have not been deliberately depicted. This review provides a comprehensive overview of the PIM kinase pathways and the current research status of the development of PIM kinase inhibitors for the treatment of MM. Additionally, the combinatorial effects of the PIM kinase inhibitors with other targeted agents and the promising strategies to exploit PIM as a therapeutic target in malignancy are highlighted.
Authors
Wu, J; Chu, E; Kang, Y
MLA Citation
Wu, Jian, et al. “PIM Kinases in Multiple Myeloma.Cancers (Basel), vol. 13, no. 17, Aug. 2021. Pubmed, doi:10.3390/cancers13174304.
URI
https://scholars.duke.edu/individual/pub1496027
PMID
34503111
Source
pubmed
Published In
Cancers
Volume
13
Published Date
DOI
10.3390/cancers13174304

Phase I, Dose Escalation Study of Naive T-Cell Depleted Donor Lymphocyte Infusion Following Allogeneic Stem Cell Transplantation

Authors
Maung, KK; Chen, BJ; Rizzieri, DA; Gasparetto, C; Sullivan, K; Long, GD; Engemann, AM; Waters-Pick, B; Nichols, KR; Lopez, R; Kang, Y; Sarantopoulos, S; Sung, AD; Chao, NJ; Horwitz, ME
MLA Citation
Maung, Ko Ko, et al. “Phase I, Dose Escalation Study of Naive T-Cell Depleted Donor Lymphocyte Infusion Following Allogeneic Stem Cell Transplantation.” Biology of Blood and Marrow Transplantation, vol. 25, no. 3, 2019.
URI
https://scholars.duke.edu/individual/pub1468272
Source
wos-lite
Published In
Biology of Blood and Marrow Transplantation : Journal of the American Society for Blood and Marrow Transplantation
Volume
25
Published Date

Overall survival of patients with triple-class refractory multiple myeloma treated with selinexor plus dexamethasone vs standard of care in MAMMOTH.

Authors
Cornell, R; Hari, P; Tang, S; Biran, N; Callander, N; Chari, A; Chhabra, S; Fiala, MA; Gahvari, Z; Gandhi, U; Godby, K; Gupta, R; Jagannath, S; Jagosky, M; Kang, Y; Kansagra, A; Kauffman, M; Kodali, S; Kumar, SK; Lakshman, A; Liedtke, M; Lonial, S; Ma, X; Malek, E; Mansour, J; McGehee, EF; Neppalli, A; Paul, B; Richardson, P; Scott, EC; Shacham, S; Shah, J; Siegel, DS; Umyarova, E; Usmani, SZ; Varnado, W; Vij, R; Costa, L
MLA Citation
Cornell, Robert, et al. “Overall survival of patients with triple-class refractory multiple myeloma treated with selinexor plus dexamethasone vs standard of care in MAMMOTH.Am J Hematol, vol. 96, no. 1, Jan. 2021, pp. E5–8. Pubmed, doi:10.1002/ajh.26010.
URI
https://scholars.duke.edu/individual/pub1461157
PMID
32974944
Source
pubmed
Published In
Am J Hematol
Volume
96
Published Date
Start Page
E5
End Page
E8
DOI
10.1002/ajh.26010

Multiple Myeloma, Version 3.2021, NCCN Clinical Practice Guidelines in Oncology.

Multiple myeloma is a malignant neoplasm of plasma cells that accumulate in bone marrow, leading to bone destruction and marrow failure. This manuscript discusses the management of patients with solitary plasmacytoma, smoldering multiple myeloma, and newly diagnosed multiple myeloma.
Authors
Kumar, SK; Callander, NS; Adekola, K; Anderson, L; Baljevic, M; Campagnaro, E; Castillo, JJ; Chandler, JC; Costello, C; Efebera, Y; Faiman, M; Garfall, A; Godby, K; Hillengass, J; Holmberg, L; Htut, M; Huff, CA; Kang, Y; Hultcrantz, M; Larson, S; Liedtke, M; Martin, T; Omel, J; Shain, K; Sborov, D; Stockerl-Goldstein, K; Weber, D; Keller, J; Kumar, R
MLA Citation
Kumar, Shaji K., et al. “Multiple Myeloma, Version 3.2021, NCCN Clinical Practice Guidelines in Oncology.J Natl Compr Canc Netw, vol. 18, no. 12, Dec. 2020, pp. 1685–717. Pubmed, doi:10.6004/jnccn.2020.0057.
URI
https://scholars.duke.edu/individual/pub1468630
PMID
33285522
Source
pubmed
Published In
J Natl Compr Canc Netw
Volume
18
Published Date
Start Page
1685
End Page
1717
DOI
10.6004/jnccn.2020.0057