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

癌症研究 生物 遗传学 癌症 计算生物学 后天抵抗 PI3K/AKT/mTOR通路 基因组学 MAPK/ERK通路 突变 原癌基因蛋白质c-ret 基因 抑癌基因 抗性(生态学) 生物信息学 抗药性 基因组 上游(联网) 抑制器 信号转导 基因表达调控 系统生物学
作者
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,Shetal Patel,Daniel S. W. Tan,Benjamin J. Solomon,Tae Min Kim,Georg Pall,Jonathan W. Riess,Lova Sun,Martin Früh
出处
期刊:Clinical Cancer Research [American Association for Cancer Research]
卷期号:32 (6): 1157-1168 被引量:1
标识
DOI:10.1158/1078-0432.ccr-25-4382
摘要

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.
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