Supriya Chakraborty

Research Assistant Professor

Levine Cancer Institute

United States

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Supriya Chakraborty is a Research Assistant Professor at Levine Cancer Institute in the United States. Her research focuses on chronic lymphocytic leukemia, examining the proliferation of malignant B cells, the impact of tumor microenvironment signals, and the therapeutic targeting of specific cellular complexes. Recent publications highlight her work on genetic mutations associated with immune escape and the role of the B-cell receptor in disease progression.

Articles (10)

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2024

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2024

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2023

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2023

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2022

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2022

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2021

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2021

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2020

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2020

Collaborators (4)

Meike Vogler

Goethe University Frankfurt

GERMANY

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Dimitar Efremov

Head of Molecular Hematology

Institute of Genetic and Molecular and Cellular Biology

ITALY

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Brijesh Singh Yadav

Nord University

NORWAY

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Silvia Deaglio

University of Turin

ITALY

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Supriya Chakraborty

Research Interests

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Articles (10)

T-bet suppresses proliferation of malignant B cells in chronic lymphocytic leukemia.

NFKBIE mutations are selected by the tumor microenvironment and contribute to immune escape in chronic lymphocytic leukemia.

Inhibition of MYC translation through targeting of the newly identified PHB-eIF4F complex as therapeutic strategy in CLL

CXCR4 Loss Reduces the Local Growth of Richter Syndrome Murine and Patient-Derived Xenograft Models and Impairs BCR and VLA-4 Activation

Macrophage- and BCR- but not TLR-derived signals support the growth of CLL and Richter Syndrome murine models in vivo

S135: CRISPR/CAS9 EDITING REVEALS DEPENDENCE OF HUMAN RICHTER SYNDROME AND MURINE CLL CELLS ON SIGNALS FROM B CELL RECEPTOR, CXCR4 RECEPTOR AND MACROPHAGES BUT NOT FROM TOLL-LIKE RECEPTORS IN VIVO

Chronic Lymphocytic Leukemia Cells with Mutated Nfkbie Are Positively Selected By Microenvironmental Signals and Display Reduced Sensitivity to Ibrutinib Treatment

B-cell receptor signaling and genetic lesions in TP53 and CDKN2A/CDKN2B cooperate in Richter transformation.

Combined Genetic Lesions in TP53 and CDKN2A/CDKN2B Drive B Cell Receptor-Dependent/Costimulatory Signal-Independent Proliferation in Richter Syndrome

BDA-366, a putative Bcl-2 BH4 domain antagonist, induces apoptosis independently of Bcl-2 in a variety of cancer cell models.

Collaborators (4)

Meike Vogler

Dimitar Efremov

Brijesh Singh Yadav

Silvia Deaglio

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