Molecular heterogeneity in urothelial carcinoma and determinants of clinical benefit to PD-L1 blockade.
СтатьяНазвание и аннотация: Перевод в очереди
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Hamidi Habib, Senbabaoglu Yasin, Beig Niha, Roels Juliette, Manuel Cyrus, Guan Xiangnan, Koeppen Hartmut, Assaf Zoe June, Nabet Barzin Y, Waddell Adrian, Yuen Kobe, Maund Sophia, Sokol Ethan, Giltnane Jennifer M, Schedlbauer Amber, Fuentes Eloisa, Cowan James D, Kadel Edward E, Degaonkar Viraj, Andreev-Drakhlin Alexander, Williams Patrick, Carter Corey, Gupta Suyasha, Steinberg Elizabeth, Loriot Yohann, Bellmunt Joaquim, Grivas Petros, Rosenberg Jonathan, van der Heijden Michiel S, Galsky Matthew D, Powles Thomas, Mariathasan Sanjeev, Banchereau Romain
Аннотация
Checkpoint inhibitors targeting programmed cell death protein 1 (PD-1)/programmed death-ligand 1 (PD-L1) have revolutionized cancer therapy across many indications including urothelial carcinoma (UC). Because many patients do not benefit, a better understanding of the molecular mechanisms underlying response and resistance is needed to improve outcomes. We profiled tumors from 2,803 UC patients from four late-stage randomized clinical trials evaluating the PD-L1 inhibitor atezolizumab by RNA sequencing (RNA-seq), a targeted DNA panel, immunohistochemistry, and digital pathology. Machine learning identifies four transcriptional subtypes, representing luminal desert, stromal, immune, and basal tumors. Overall survival benefit from atezolizumab over standard-of-care is observed in immune and basal tumors, through different response mechanisms. A self-supervised digital pathology approach can classify molecular subtypes from H&E slides with high accuracy, which could accelerate tumor molecular profiling. This study represents a large integration of UC molecular and clinical data in randomized trials, paving the way for clinical studies tailoring treatment to specific molecular subtypes in UC and other indications.