Fenghuang Zhan
Professor
faculty
Internal Med, College of Medicine
Research Areas
Biography and Research Information
OverviewAI-generated summary
Fenghuang Zhan's research centers on the molecular mechanisms driving multiple myeloma progression and related hematologic malignancies. His work investigates how specific genes and molecular pathways contribute to tumor development, emphasizing gene expression regulation and its role in disease pathogenesis. Zhan has published on the function of HNRNPA2B1 in promoting multiple myeloma by stabilizing ILF3 mRNA, and the impact of CHEK1 and circCHEK1_246aa on chromosomal instability and bone lesion formation in this cancer. He also studies TRIP13's modulation of protein deubiquitination in B cell malignancies. His research extends to understanding the molecular landscape of smoldering myeloma and identifying evolutionary pathways leading to overt disease.
Beyond molecular mechanisms, Zhan's work addresses clinical aspects and outcomes in multiple myeloma. He has contributed to studies examining the risk of infections associated with bispecific antibody use and disparities in access to advanced therapies like CAR-T cells and bispecific antibodies for multiple myeloma patients. He is also involved in developing consensus recommendations for defining high-risk multiple myeloma. His federal grant funding from the NIH/National Cancer Institute supports his investigation into novel NEK2 signaling pathways in myeloma progression. With an h-index of 66 and over 18,000 citations from more than 400 publications, Zhan is a highly cited researcher in his field. He actively collaborates with researchers at the University of Arkansas for Medical Sciences, including John D. Shaughnessy Jr., Guido Tricot, Sharmilan Thanendrarajan, and Maurizio Zangari.
Metrics
- h-index: 67
- Publications: 429
- Citations: 19,103
Selected Publications
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Abstract LB220: Can dietary calcium prevent myeloma onset (2026)
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Clinical outcomes and risk factors of cytomegalovirus reactivation in teclistamab-treated multiple myeloma patients (2026)
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Peripheral blood immune cell profiling and response to BCMA CAR-T cell therapy in relapsed refractory multiple myeloma (2026)
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Proinflammatory GSDMD activation in live macrophages and DLBCL cells marks cognate interactions and better prognosis (2025)
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Polyclonal plasma cell (PolyPC) signature as a key indicator for predicting the progression of MGUS to multiple myeloma (2025)
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International Myeloma Society/International Myeloma Working Group Consensus Recommendations on the Definition of High-Risk Multiple Myeloma (2025)
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Long-Term Follow-Up of Patients With Multiple Myeloma Treated on Earlier Total Therapy Protocols (2025)
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Cystatin M/E Ameliorates Multiple Myeloma-Induced Hyper Osteolytic Bone Resorption (2025)
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Prior exposure to belantamab mafodotin influences outcomes with idecabtagene vicleucel in patients with multiple myeloma (2025)
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Targeting caseinolytic mitochondrial matrix peptidase, a novel contributor to the pathobiology of high-risk multiple myeloma (2025)
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Single-cell analysis of neoplastic plasma cells identifies myeloma pathobiology mediators and potential targets (2025)
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Long-term follow-up of Total Therapy IV: a phase 3 clinical trial for standard-risk multiple myeloma (2024)
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Multi-Omics Reveal Immune Microenvironment Alterations in Multiple Myeloma and Its Precursor Stages (2024)
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Prior Exposure to Belantamab Mafodotin Influences Outcomes with Idecabtagene Vicluecel in Patients with Multiple Myeloma (2024)
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Multi-omics reveal immune microenvironment alterations in multiple myeloma and its precursor stages (2024)
Federal Grants 1 $330,316 total
Grants & Funding
- NEK2 Over-expression Causes Drug Resistance in Myeloma NIH Principal Investigator
- Biological Validation of Candidate Myeloma Driver Genes NIH/Nat. Cancer Institute - Pass Through: Medical College of Wisconsin Principal Investigator
- Novel NEK2 signaling pathways in myeloma progression NIH Principal Investigator
- Gene expression profiling vs MRD assessment in Myeloma NIH Co-Investigator
- U54 - Administrative Core NIH/Nat. Cancer Institute - Pass Through: Baylor College of Medicine Principal Investigator
- Center for Molecular Interactions in Cancer (CMIC) NIH Co-Investigator
- U54 - Bioinformatics Core NIH/Nat. Cancer Institute - Pass Through: Baylor College of Medicine Principal Investigator
- Targeting NEK2 Enables Immune Checkpoint Blockade in High-Risk/Relapsed Myeloma The Paula and Rodger Riney Foundation Principal Investigator
Collaboration Network
Top Collaborators
- The molecular make up of smoldering myeloma highlights the evolutionary pathways leading to multiple myeloma
- Risk of infections associated with the use of bispecific antibodies in multiple myeloma: a pooled analysis
- Geographic and Racial Disparities in Access to Chimeric Antigen Receptor–T Cells and Bispecific Antibodies Trials for Multiple Myeloma
- TRIP13 modulates protein deubiquitination and accelerates tumor development and progression of B cell malignancies
- Bispecific BCMA/CD24 CAR-T cells control multiple myeloma growth
Showing 5 of 50 shared publications
- Risk of infections associated with the use of bispecific antibodies in multiple myeloma: a pooled analysis
- TRIP13 modulates protein deubiquitination and accelerates tumor development and progression of B cell malignancies
- Bispecific BCMA/CD24 CAR-T cells control multiple myeloma growth
- Genetic Analysis of Multiple Myeloma Identifies Cytogenetic Alterations Implicated in Disease Complexity and Progression
- CST6 suppresses osteolytic bone disease in multiple myeloma by blocking osteoclast differentiation
Showing 5 of 48 shared publications
- The molecular make up of smoldering myeloma highlights the evolutionary pathways leading to multiple myeloma
- Risk of infections associated with the use of bispecific antibodies in multiple myeloma: a pooled analysis
- Geographic and Racial Disparities in Access to Chimeric Antigen Receptor–T Cells and Bispecific Antibodies Trials for Multiple Myeloma
- Bispecific BCMA/CD24 CAR-T cells control multiple myeloma growth
- Multi-omics reveal immune microenvironment alterations in multiple myeloma and its precursor stages
Showing 5 of 44 shared publications
- The molecular make up of smoldering myeloma highlights the evolutionary pathways leading to multiple myeloma
- Risk of infections associated with the use of bispecific antibodies in multiple myeloma: a pooled analysis
- Geographic and Racial Disparities in Access to Chimeric Antigen Receptor–T Cells and Bispecific Antibodies Trials for Multiple Myeloma
- Bispecific BCMA/CD24 CAR-T cells control multiple myeloma growth
- Multi-omics reveal immune microenvironment alterations in multiple myeloma and its precursor stages
Showing 5 of 43 shared publications
- The molecular make up of smoldering myeloma highlights the evolutionary pathways leading to multiple myeloma
- Risk of infections associated with the use of bispecific antibodies in multiple myeloma: a pooled analysis
- Geographic and Racial Disparities in Access to Chimeric Antigen Receptor–T Cells and Bispecific Antibodies Trials for Multiple Myeloma
- Bispecific BCMA/CD24 CAR-T cells control multiple myeloma growth
- Multi-omics reveal immune microenvironment alterations in multiple myeloma and its precursor stages
Showing 5 of 43 shared publications
- Risk of infections associated with the use of bispecific antibodies in multiple myeloma: a pooled analysis
- Geographic and Racial Disparities in Access to Chimeric Antigen Receptor–T Cells and Bispecific Antibodies Trials for Multiple Myeloma
- Bispecific BCMA/CD24 CAR-T cells control multiple myeloma growth
- Multi-omics reveal immune microenvironment alterations in multiple myeloma and its precursor stages
- High NEK2 expression in myeloid progenitors suppresses T cell immunity in multiple myeloma
Showing 5 of 37 shared publications
- Geographic and Racial Disparities in Access to Chimeric Antigen Receptor–T Cells and Bispecific Antibodies Trials for Multiple Myeloma
- TRIP13 modulates protein deubiquitination and accelerates tumor development and progression of B cell malignancies
- Bispecific BCMA/CD24 CAR-T cells control multiple myeloma growth
- Genetic Analysis of Multiple Myeloma Identifies Cytogenetic Alterations Implicated in Disease Complexity and Progression
- CST6 suppresses osteolytic bone disease in multiple myeloma by blocking osteoclast differentiation
Showing 5 of 27 shared publications
- The molecular make up of smoldering myeloma highlights the evolutionary pathways leading to multiple myeloma
- TRIP13 modulates protein deubiquitination and accelerates tumor development and progression of B cell malignancies
- Bispecific BCMA/CD24 CAR-T cells control multiple myeloma growth
- Multi-omics reveal immune microenvironment alterations in multiple myeloma and its precursor stages
- CST6 suppresses osteolytic bone disease in multiple myeloma by blocking osteoclast differentiation
Showing 5 of 22 shared publications
- FOXM1 regulates glycolysis and energy production in multiple myeloma
- Bispecific BCMA/CD24 CAR-T cells control multiple myeloma growth
- Multi-omics reveal immune microenvironment alterations in multiple myeloma and its precursor stages
- CST6 suppresses osteolytic bone disease in multiple myeloma by blocking osteoclast differentiation
- Bispecific CAR-T Cells Targeting Both BCMA and CD24: A Potentially Treatment Approach for Multiple Myeloma
Showing 5 of 22 shared publications
- Bispecific BCMA/CD24 CAR-T cells control multiple myeloma growth
- Multi-omics reveal immune microenvironment alterations in multiple myeloma and its precursor stages
- High NEK2 expression in myeloid progenitors suppresses T cell immunity in multiple myeloma
- A gene signature can predict risk of MGUS progressing to multiple myeloma
- Three years of maintenance with VRD in multiple myeloma: results of total therapy IIIB with a 15-year follow-up
Showing 5 of 22 shared publications
- Expression of integrin β-7 is epigenetically enhanced in multiple myeloma subgroups with high-risk cytogenetics
- Bifunctional Inhibitor Reveals NEK2 as a Therapeutic Target and Regulator of Oncogenic Pathways in Lymphoma
- PHF19 inhibition as a therapeutic target in multiple myeloma
- Figure S9 from Bifunctional Inhibitor Reveals NEK2 as a Therapeutic Target and Regulator of Oncogenic Pathways in Lymphoma
- Figure S6 from Bifunctional Inhibitor Reveals NEK2 as a Therapeutic Target and Regulator of Oncogenic Pathways in Lymphoma
Showing 5 of 21 shared publications
- Bifunctional Inhibitor Reveals NEK2 as a Therapeutic Target and Regulator of Oncogenic Pathways in Lymphoma
- Concomitant Deletion of Short Arm (del 1p) and Amplification or Gain (1q21) of Chromosome 1 By Fluorescence in Situ Hybridization (FISH) Is Associated with Poor Clinical Outcome
- Figure S9 from Bifunctional Inhibitor Reveals NEK2 as a Therapeutic Target and Regulator of Oncogenic Pathways in Lymphoma
- Figure S6 from Bifunctional Inhibitor Reveals NEK2 as a Therapeutic Target and Regulator of Oncogenic Pathways in Lymphoma
- Table S9 from Bifunctional Inhibitor Reveals NEK2 as a Therapeutic Target and Regulator of Oncogenic Pathways in Lymphoma
Showing 5 of 20 shared publications
- Bifunctional Inhibitor Reveals NEK2 as a Therapeutic Target and Regulator of Oncogenic Pathways in Lymphoma
- Figure S9 from Bifunctional Inhibitor Reveals NEK2 as a Therapeutic Target and Regulator of Oncogenic Pathways in Lymphoma
- Figure S6 from Bifunctional Inhibitor Reveals NEK2 as a Therapeutic Target and Regulator of Oncogenic Pathways in Lymphoma
- Table S9 from Bifunctional Inhibitor Reveals NEK2 as a Therapeutic Target and Regulator of Oncogenic Pathways in Lymphoma
- Table S12 from Bifunctional Inhibitor Reveals NEK2 as a Therapeutic Target and Regulator of Oncogenic Pathways in Lymphoma
Showing 5 of 19 shared publications
- Bifunctional Inhibitor Reveals NEK2 as a Therapeutic Target and Regulator of Oncogenic Pathways in Lymphoma
- Figure S9 from Bifunctional Inhibitor Reveals NEK2 as a Therapeutic Target and Regulator of Oncogenic Pathways in Lymphoma
- Figure S6 from Bifunctional Inhibitor Reveals NEK2 as a Therapeutic Target and Regulator of Oncogenic Pathways in Lymphoma
- Table S9 from Bifunctional Inhibitor Reveals NEK2 as a Therapeutic Target and Regulator of Oncogenic Pathways in Lymphoma
- Table S12 from Bifunctional Inhibitor Reveals NEK2 as a Therapeutic Target and Regulator of Oncogenic Pathways in Lymphoma
Showing 5 of 19 shared publications
- Bifunctional Inhibitor Reveals NEK2 as a Therapeutic Target and Regulator of Oncogenic Pathways in Lymphoma
- Figure S9 from Bifunctional Inhibitor Reveals NEK2 as a Therapeutic Target and Regulator of Oncogenic Pathways in Lymphoma
- Figure S6 from Bifunctional Inhibitor Reveals NEK2 as a Therapeutic Target and Regulator of Oncogenic Pathways in Lymphoma
- Table S9 from Bifunctional Inhibitor Reveals NEK2 as a Therapeutic Target and Regulator of Oncogenic Pathways in Lymphoma
- Table S12 from Bifunctional Inhibitor Reveals NEK2 as a Therapeutic Target and Regulator of Oncogenic Pathways in Lymphoma
Showing 5 of 19 shared publications
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