Dual bispecific protein engager-armed T cells targeting BCMA and B7-H3 overcome antigen heterogeneity in multiple myeloma.

Thanida Chanpong¹, Nunghathai Sawasdee¹, Kamonlapat Supimon¹, Thanich Sangsuwannukul², Thaweesak Chieochansin¹, Seiji Okada³, Pa-Thai Yenchitsomanus⁴, Mutita Junking⁵

¹Siriraj Center of Research Excellence for Cancer Immunotherapy (SiCORE-CIT), and Division of Molecular Medicine, Research Department, Faculty of Medicine Siriraj Hospital, Mahidol University, Bangkok, Thailand.

²Siriraj Center of Research Excellence for Cancer Immunotherapy (SiCORE-CIT), and Division of Molecular Medicine, Research Department, Faculty of Medicine Siriraj Hospital, Mahidol University, Bangkok, Thailand; Department of Molecular Medicine, Mayo Clinic, Rochester, MN, United States.

³Division of Hematopoiesis, Graduate School of Medical Sciences, and Joint Research Center for Human Retrovirus Infection, Kumamoto University, Kumamoto, Japan.

⁴Siriraj Center of Research Excellence for Cancer Immunotherapy (SiCORE-CIT), and Division of Molecular Medicine, Research Department, Faculty of Medicine Siriraj Hospital, Mahidol University, Bangkok, Thailand. Electronic address: pa-thai.yen@mahidol.ac.th.

⁵Siriraj Center of Research Excellence for Cancer Immunotherapy (SiCORE-CIT), and Division of Molecular Medicine, Research Department, Faculty of Medicine Siriraj Hospital, Mahidol University, Bangkok, Thailand. Electronic address: mutita.jun@mahidol.ac.th.

PubMed DOI

Abstract

Multiple myeloma (MM) remains an incurable plasma cell malignancy, with most patients ultimately progressing to relapsed or refractory MM (RRMM) despite therapeutic advances. Antigen heterogeneity and immune escape, particularly the loss of B-cell maturation antigen (BCMA), pose major challenges to effective immunotherapy. Notably, BCMA loss driven by alterations in TNFRSF17 occurs in a substantia…

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