<p>Chimeric antigen receptor (CAR) T cell therapy for solid tumors is constrained by the scarcity of safe, uniformly expressed cell-surface targets. Here we identify glycoprotein NMB (GPNMB)—an MiT/TFE-family fusion-driven protein—as being highly, homogeneously and stably expressed in primary and relapsed alveolar soft-part sarcoma (ASPS) and translocation renal cell carcinoma. We develop a GPNMB-directed CAR T cell product, GCAR1, which demonstrates potent activity against patient-matched cells, organoids and xenograft models. Post hoc interim analysis of a first-in-human open-label, individual-participant trial (<a href="https://clinicaltrials.gov/ct2/show/NCT07104682">NCT07104682</a>) for a participant with relapsed/refractory, metastatic ASPS showed that GCAR1 induces stable disease for up to 3 months, accompanied by resolution of many nontarget lesions (primary endpoint), and is well tolerated. GCAR1 T cells expand in peripheral blood as a polyclonal population and remain detectable for 1 month. Spatial transcriptomics identified immunosuppressive niches in a treatment-resistant lesion and immune checkpoint blockade synergized with GCAR1 in a xenograft model. Altogether, our data provide a proof of concept for treating GPNMB-expressing solid tumors with GCAR1 and more broadly targeting surface antigens driven by oncogenic gene fusions with CAR T cell therapies.</p>

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GPNMB-directed CAR T cell therapy against MiT/TFE-family fusion-driven solid tumors

  • Franz J. Zemp,
  • Zackariah Breckenridge,
  • Hyojin Song,
  • Gurveer S. Gill,
  • Taye L. Louie,
  • Kiran Narta,
  • Hongrui Liu,
  • Yeon Suh,
  • Louisa Guignard,
  • Edna Ayerim Mandujano-Tinoco,
  • Nicolás Collao,
  • Joanna Pyczek,
  • Kristofor K. Ellestad,
  • Jada Curry,
  • Jethro Langley,
  • Cini John,
  • Laura K. Mah,
  • Jahanara Rajwani,
  • Danyel Evseev,
  • Madison Turk,
  • Sacha Benaoudia,
  • Jonathan Alex,
  • Victor Naumenko,
  • Varsha Thoppey Manoharan,
  • Mobina Kazemi Mehrabadi,
  • Harmony A. Smith,
  • Geneece N. Y. Gilbert,
  • Aaron Gillmor,
  • Ted B. Verhey,
  • Hayley M. Todesco,
  • Katalin Osz,
  • Bo-Young Ahn,
  • Ana Bogossian,
  • Colleen Anderson,
  • Saif Sikdar,
  • Shahrbano Rukunuddin,
  • Tarek A. Bismar,
  • Daniel Y. C. Heng,
  • Keith Lawson,
  • W. Marston Linehan,
  • Haley Pedersen,
  • Paul M. K. Gordon,
  • John B. McIntyre,
  • John MacGregor,
  • Livia Garzia,
  • Kathy Brodeur-Robb,
  • Lisa DiFrancesco,
  • Travis Ogilvie,
  • Patrick Schöffski,
  • Agnieszka Wozniak,
  • Robert A. Holt,
  • John Bell,
  • Donna L. Senger,
  • Victor Lewis,
  • Michael Monument,
  • Omar Khan,
  • Lou Baudrier,
  • Pierre Billon,
  • Vincent Gabriel,
  • Jeff Biernaskie,
  • Kyle Potts,
  • Kiril Trpkov,
  • Kevin Hay,
  • Jennifer Quizi,
  • Jennifer Chan,
  • Ramy Saleh,
  • Jan Willem Henning,
  • Nicole L. Prokopishyn,
  • Mona Shafey,
  • A. Sorana Morrissy,
  • Douglas J. Mahoney

摘要

Chimeric antigen receptor (CAR) T cell therapy for solid tumors is constrained by the scarcity of safe, uniformly expressed cell-surface targets. Here we identify glycoprotein NMB (GPNMB)—an MiT/TFE-family fusion-driven protein—as being highly, homogeneously and stably expressed in primary and relapsed alveolar soft-part sarcoma (ASPS) and translocation renal cell carcinoma. We develop a GPNMB-directed CAR T cell product, GCAR1, which demonstrates potent activity against patient-matched cells, organoids and xenograft models. Post hoc interim analysis of a first-in-human open-label, individual-participant trial (NCT07104682) for a participant with relapsed/refractory, metastatic ASPS showed that GCAR1 induces stable disease for up to 3 months, accompanied by resolution of many nontarget lesions (primary endpoint), and is well tolerated. GCAR1 T cells expand in peripheral blood as a polyclonal population and remain detectable for 1 month. Spatial transcriptomics identified immunosuppressive niches in a treatment-resistant lesion and immune checkpoint blockade synergized with GCAR1 in a xenograft model. Altogether, our data provide a proof of concept for treating GPNMB-expressing solid tumors with GCAR1 and more broadly targeting surface antigens driven by oncogenic gene fusions with CAR T cell therapies.