Landscape of Genomic Mechanisms of Resistance to Selective RET Inhibitors in RET -Altered Solid Tumors: Analysis of the RETgistry Global Consortium

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Authors: Sarah Waliany, Alissa J. Cooper, Stephen V. Liu, O. Gautschi, Julia K. Rotow, Katherine E. Smith, Urs Weber, Dae Ho Lee, H. Loong, Jyoti D. Patel, Nathan A. Pennell, Misako Nagasaka
+26 more Shetal Patel, Daniel S. W. Tan, Benjamin J. Solomon, Tae Min Kim, Georg Pall, Jonathan W. Riess, Lova Sun, Martin Früh, Natalie F. Uy, Shirish Gadgeel, Jamie Feng, Andrew Do, Christina J. Falcon, Natasha B. Leighl, Christina S. Baik, G. Lai, S. Ignatius Ou, Kingsley S.Y. Cheung, Tejas Patil, Aaron S. Mansfield, Daniela Weiler, Beow Y. Yeap, Lori J. Wirth, Justin F. Gainor, Alexander D. Drilon, Jessica J. Lin
Cited by: 4
References: 53

Abstract

PURPOSE: Rearranged during transfection (RET) alterations are oncogenic drivers across solid tumors. Selective RET inhibitors (SRI) selpercatinib and pralsetinib have transformed outcomes for patients with RET-altered malignancies. Limited knowledge exists on genomic mechanisms of resistance to SRI. EXPERIMENTAL DESIGN: We established "RETgistry," a global consortium of patients with advanced RET-altered solid tumors who received SRI and underwent postprogression tissue or plasma biopsies assessed by next-generation sequencing. Frequencies of secondary RET resistance mutations and acquired non-RET gene alterations were determined. Progression-free survival (PFS) and time to treatment discontinuation (TTD) on first SRI were estimated with the Kaplan-Meier method. RESULTS: RETgistry included 109 patients with RET-altered advanced solid tumors (lung, n = 94; thyroid, n = 15) who underwent 143 post-SRI progression biopsies (tissue, 91; plasma, 52). The median PFS and TTD were 13.9 months [95% confidence interval (CI), 10.1-16.6] and 17.3 months (95% CI, 14-20.2), respectively. Secondary RET mutations were detected in 20 (14%) biopsies [lung cancer, 15 (12.4%) and thyroid carcinoma, 5 (22.7%)]. Common acquired off-target alterations involved MET (18.2%; amplification, 15%), TP53 (8.2%), APC (7.6%), KRAS (7.1%), KEAP1 (5.9%), and CDKN2A/B (5.3%). MET alterations were enriched in post-SRI versus pre-SRI specimens (full cohort, 17.6% vs. 2.0%, P = 0.022; lung cancer, 19.1% vs. 2.1%, P = 0.022). CONCLUSIONS: The prevalence of secondary RET mutations after SRI was low, underscoring a greater role for off-target resistance. Recurrent acquired alterations involving tumor suppressor genes or upstream regulators of MAPK and PI3K pathways were identified, most commonly MET amplification. Continued efforts to characterize SRI resistance biology are critical to guide the development of novel therapeutic strategies.

Fields of Study & Subjects

Lung Cancer Treatments and Mutations Thyroid Cancer Diagnosis and Treatment Cancer-related Molecular Pathways

Publication details

Journal / source
Clinical Cancer Research
Publisher
American Association for Cancer Research (AACR)
Volume
32
Issue
6
Pages
1157–1168
Publication date
15 January 2026
Language
EN