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BLOCKADE OF TUMOR-INTRINSIC TGF-B SIGNALING DRIVES HYPERPROGRESSION IN SMALL CELL LUNG CANCER
Journal article   Open access

BLOCKADE OF TUMOR-INTRINSIC TGF-B SIGNALING DRIVES HYPERPROGRESSION IN SMALL CELL LUNG CANCER

Brett A. Schroeder, Chirayu Mohindroo, Anna-Lena Meinhardt, Nobuyuki Takahashi, Yang Zhang, Min-Jung Lee, Sarthak Sahoo, Renee N Donahue, Rajesh Kumar, Michael Nirula, …
Cancer discovery
04/22/2026
DOI: 10.1158/2159-8290.CD-25-1454
PMID: 42018154
url
https://doi.org/10.1158/2159-8290.CD-25-1454View
Published (Version of record) Open Access

Abstract

Stromal immunosuppressive pathways are key modulators of response to immune checkpoint inhibitors, but their tumor-intrinsic consequences remain incompletely defined. We conducted a clinical trial of bintrafusp alfa, a bifunctional PD-L1/TGF-β inhibitor, in small cell lung cancer. Among 34 evaluable patients, 18% had partial responses, 20% stable disease, and 62% progressive disease; 38% of progressors met criteria for hyperprogressive disease (HPD). HPD was also observed across other tumor types (n=450), in higher frequencies with bintrafusp than PD-(L)1 blockade alone. Blood and tumor profiling showed that HPD correlated with systemic immune suppression and elevated TGF-β signaling. Functional studies demonstrated that tumor-intrinsic TGF-β signaling restrains proliferation in a subset of SCLC; pathway blockade triggers hyperproliferation. External validation across cell lines and tumor samples confirmed a tumor-intrinsic TGF-β–high transcriptional state associated with inferior survival. Together, these findings identify a context-dependent, growth-constraining function of TGF-β and support tumor-intrinsic biomarker-guidance while targeting stromal immunosuppressive pathways.

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