Selina Chen-Kiang
· Professor of Microbiology & ImmunologyCornell University · Microbiology and Immunology
Active 1977–2025
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About
Selina Chen-Kiang is a Professor of Microbiology and Immunology at Weill Cornell Medicine. Her research focuses on cell cycle control and apoptosis as major determinants of homeostasis in physiologic response and cancer. She aims to define the mechanisms underlying cell cycle control of B cell immunity and tumorigenesis by combining genetic, molecular, and biochemical approaches. Her work specifically investigates how the cell cycle integrates antigen and cytokine signals to regulate B cell activation, expansion, and terminal differentiation into antibody-secreting plasma cells, as well as how the cell cycle is coupled to apoptotic control in B cell immunity. Her research has identified key regulators such as p18INK4c, a G1 cyclin-dependent kinase inhibitor, which is required for the generation of antibody-secreting plasma cells and the survival of plasma cell precursors, marking a significant contribution to understanding cell cycle control of B cell immunity. She studies how antigen and cytokine signaling pathways, including BLyS, CD40 ligand, IL-4, and IL-6, modulate the timing and magnitude of antibody responses through cell cycle control. Additionally, her work addresses how loss of cell cycle checkpoints contributes to the development of multiple myeloma, an incurable plasma cell cancer, by identifying disrupted molecular interactions and cell cycle regulation in malignant plasma cells and their microenvironment.
Selected publications
Clinical Cancer Research · 2021-01-25 · 71 citations
articleOpen accessAbstract Purpose: Recent preclinical data suggest that cyclin-dependent kinase 4/6 (CDK4/6) inhibition may be harnessed to sensitize estrogen receptor–positive (ER+) breast cancer to radiotherapy. However, these findings were obtained in human ER+ breast cancer cell lines exposed to subclinical doses of CDK4/6 inhibitors with limited attention to treatment schedule. We investigated the activity of radiotherapy combined with the prototypic CDK4/6 inhibitor palbociclib placing emphasis on therapeu…
Nature Communications · 2023 · 32 citations
Richter's Transformation (RT) is a poorly understood and fatal progression of chronic lymphocytic leukemia (CLL) manifesting histologically as diffuse large B-cell lymphoma. Protein arginine methyltransferase 5 (PRMT5) is implicated in lymphomagenesis, but its role in CLL or RT progression is unknown. We demonstrate herein that tumors uniformly overexpress PRMT5 in patients with progression to RT. Furthermore, mice with B-specific overexpression of hPRMT5 develop a B-lymphoid expansion with incr…
PRMT5 supports multiple oncogenic pathways in mantle cell lymphoma
Blood · 2023-06-02 · 27 citations
articleOpen accessMantle cell lymphoma (MCL) is an incurable B-cell malignancy with an overall poor prognosis, particularly for patients that progress on targeted therapies. Novel, more durable treatment options are needed for patients with MCL. Protein arginine methyltransferase 5 (PRMT5) is overexpressed in MCL and plays an important oncogenic role in this disease via epigenetic and posttranslational modification of cell cycle regulators, DNA repair genes, components of prosurvival pathways, and RNA splicing re…
Blood Advances · 2023-06-16 · 15 citations
articleOpen accessMantle cell lymphoma (MCL) is an incurable B-cell malignancy that comprises up to 6% of non-Hodgkin lymphomas diagnosed annually and is associated with a poor prognosis. The average overall survival of patients with MCL is 5 years, and for most patients who progress on targeted agents, survival remains at a dismal 3 to 8 months. There is a major unmet need to identify new therapeutic approaches that are well tolerated to improve treatment outcomes and quality of life. The protein arginine methyl…
Resistance to PRMT5-targeted therapy in mantle cell lymphoma
Blood Advances · 2023-10-02 · 11 citations
articleOpen accessABSTRACT: Mantle cell lymphoma (MCL) is an incurable B-cell non-Hodgkin lymphoma, and patients who relapse on targeted therapies have poor prognosis. Protein arginine methyltransferase 5 (PRMT5), an enzyme essential for B-cell transformation, drives multiple oncogenic pathways and is overexpressed in MCL. Despite the antitumor activity of PRMT5 inhibition (PRT-382/PRT-808), drug resistance was observed in a patient-derived xenograft (PDX) MCL model. Decreased survival of mice engrafted with thes…
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