Palash Chandra Maity

Research Group Leader (Third-party Funded Program) Experimental Cancer Research @Universitätsklinikum Ulm

Ulm, DE
MOBILE NUMBERS
+91 *********19

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WORK HISTORY

Jun 2022 — Present

Research Group Leader (Third-party Funded Program) Experimental Cancer Research @Universitätsklinikum Ulm

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Founded and lead an independently funded research program (Fritz Thyssen Stiftung, 2023–2026) on receptor-driven signaling in B-cell malignancies and Immunotherapy.• Develop signal-centric models of lymphomagenesis integrating BCR, CD19, and chemokine receptor crosstalk (IJMS 2025; Cell Commun Signal 2025).• Investigate CD19–CXCR4–BCR signaling circuits in DLBCL, MZL and Waldenström’s macroglobulinemia.• Define secreted IgM as an autocrine conditioning and survival signal in IgM-associated lymphomas (Nat Commun 2025; Leukemia 2026).• Translate quantitative signaling principles into rational combinatorial immunotherapy strategies.• Integrate engineered receptor systems and CRISPR perturbation in lymphoma models and primary patient material to identify functional biomarkers (Method Mol Biol 2025).

EDUCATION

N/A

University of Calcutta

Bachelor's degree, Chemistry

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University of Calcutta

Master's degree, Genetics

ABOUT PALASH CHANDRA MAITY

I am an independent translational immunologist working on B-cell malignancies, with a mechanistic focus on receptor-centric signaling and its consequences for disease behavior, therapeutic response, and biomarker logic. My work starts with an immunological hypothesis and is driven by identifying which signaling nodes genuinely constrain malignant B-cell survival, spatial organization, and treatment resistance in patients.Scientifically, my core expertise lies in B-cell receptor (BCR) biology, its isotype-specific signaling properties, and its functional integration with chemokine receptors, adhesion systems, and microenvironmental cues. A central contribution of my work has been to show how qualitatively distinct receptor inputs are decoded into discrete, non-interchangeable cellular decisions, rather than behaving as linear or purely quantitative signaling cascades. This receptor-centric framework underpins both my disease models and my approach to receptor-targeted immunotherapeutic strategies.My work is shaped by experience across inflammatory signaling, CRO-based antibody development, molecular immunology and independent cancer immunology, with a consistent emphasis on mechanistic sufficiency over descriptive complexity. I operate across molecular mechanism, experimental logic, and translational interpretation, and I am selective by design: the early elimination of biologically weak hypotheses is integral to how I work.I function best in environments that value intellectual leadership, disease credibility, and mechanistic rigor over hierarchy or output volume. I am interested in academic, hybrid, or translational settings where deep immunology is expected to shape decisions, not merely accompany them.

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