MPN-specific antigens and anti-MPN T cell receptors

Current understanding

MPN-mutant clones (JAK2 V617F, CALR frameshift, MPL) generate neoantigens that may be presented on HLA and recognized by cognate T cell receptors, providing a basis for adaptive immune surveillance of the malignant clone. Systematically mapping MPN-specific antigens and their cognate TCRs from patient bone marrow and blood is an emerging effort intended to enable TCR-based adoptive immunotherapy, complementing checkpoint blockade and NK-cell strategies. Evidence remains observational and early-stage, with antigen-TCR pairs and their functional anti-clonal activity still to be validated.

Evidence log

• 2026-09-28 — Mutant CALR-peptide Based Vaccine in Patients With Mutated CALR Myeloproliferative Neoplasm: cross-connection with calr-mutations: A mutant CALR peptide vaccine operationalizes the shared CALR frameshift neoantigen as an active immunization target, bridging CALR neoepitope biology with MPN-directed T cell immunotherapy strategies. (novelty: 4)
• 2026-06-24 — Chimeric Antigen Receptor T Cell Therapy Redirected to CD4 (CD4CAR)as a Second Line Treatment for Chronic Myelomonocytic Leukemia, CMML.: cross-connection with cd4-car-t-cell-therapy-cmml: Both pursue T-cell-mediated elimination of MPN/CMML clones but differ in target recognition: CD4CAR engages a lineage surface antigen (CD4) via a synthetic CAR independent of HLA, while MPN-TCR strategies rely on HLA-restricted recognition of mutation-derived neoantigens. (novelty: 4)
• June 12-15 — Advancing Frontiers in Myeloproliferative Neoplasms - EHA 2025 Congress Review: cross-connection with calr-mutations: INCA035784, a T cell-redirecting antibody targeting mutant CALR, operationalizes the CALR neoepitope as a T cell-engageable antigen, bridging CALR mutation biology with anti-MPN T cell immunotherapy approaches. (novelty: 3)
• 2026-05-15 — Identification of MPN-specific Antigens and Anti-MPN TCRs in Myeloproliferative Neoplasm: cross-connection with calr-mutations: CALR frameshift mutations generate a shared neoantigenic C-terminal peptide, making CALR-mutant MPN a leading source of candidate antigens for anti-MPN TCR discovery. (novelty: 4)

Open questions

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