본문으로 건너뛰기
← 뒤로

ADC target profiling in NSCLC: Generalizable AI separates TROP-2 and cMET phenotypes.

1/5 보강
Clinical cancer research : an official journal of the American Association for Cancer Research 2026
Retraction 확인
출처

Anders P, Sextro M, Lingelbach K, Standvoss K, Pandhe S, Ghosh S, Böhm C, Tietz S, Krupar R, Tharun L, Eich ML, Ribbat-Idel J, Ramberger E, Liang X, Aumiller V, Merkelbach-Bruse S, Quaas A, Frost N, Schlachtenberger G, Heldwein M, Keilholz U, Hekmat K, Rückert JC, Büttner R, Grohe C, Horst D, Alber M, Ruff L, Klauschen F, Dernbach G, Seegerer P, Schallenberg S

📝 환자 설명용 한 줄

[BACKGROUND] Antibody drug conjugates (ADCs) targeting TROP-2 and cMET are entering clinical trials in NSCLC.

이 논문을 인용하기

BibTeX ↓ RIS ↓
APA Anders P, Sextro M, et al. (2026). ADC target profiling in NSCLC: Generalizable AI separates TROP-2 and cMET phenotypes.. Clinical cancer research : an official journal of the American Association for Cancer Research. https://doi.org/10.1158/1078-0432.CCR-25-4513
MLA Anders P, et al.. "ADC target profiling in NSCLC: Generalizable AI separates TROP-2 and cMET phenotypes.." Clinical cancer research : an official journal of the American Association for Cancer Research, 2026.
PMID 41945491

Abstract

[BACKGROUND] Antibody drug conjugates (ADCs) targeting TROP-2 and cMET are entering clinical trials in NSCLC. Their translation depends on reliable biomarker assessment, a task still dominated by subjective visual scoring and inconsistent reproducibility.

[METHODS] We built a modular AI pipeline that detects cells, classifies carcinoma cells, and quantifies membranous and cytoplasmic expression. A membranous scorer trained on TROP-2 was applied zero-shot to cMET, HER2, and PD-L1. The analysis covered 1,142 resected NSCLCs, integrating expression maps with clinicopathologic, molecular, and tumor microenvironment (TME) features.

[RESULTS] The AI scorer recapitulated pathologist annotations with near-perfect correlation (r = 0.98-0.99, ρ = 97-98, τ = 0.88-0.89, CCC = 0.97-0.98) for TROP-2 and generalized to other markers (cMET r = 0.99, ρ = 0.96, τ = 0.91, CCC = 0.96; HER2 r = 0.93, ρ = 0.72, τ = 0.60, CCC = 0.92; and PD-L1 [TPS] r = 0.85, ρ = 0.84, τ = 0.68, CCC = 0.82 / [H-score] r = 0.87, ρ = 0.86, τ = 0.70, CCC = 0.85). Its agreement with six pathologists matched interobserver variability (0.86-0.96). Expression maps revealed contrasting spatial and cellular patterns: TROP-2 dominated LUSC (mean H-Scores 141.3/103.2 vs. 74.5/45.7 in LUAD for membrane/cytoplasm) and marked immune-deserted tumors. cMET prevailed in LUAD (mean 50.4 vs. 20.6 in LUSC), co-localized with fibroblast-rich, immune-active TME and KRAS mutations.

[CONCLUSIONS] Foundation model-based scoring produces expert-level, scalable biomarker quantification. The resulting TME phenotypes - TROP-2-high immune-deserted vs cMET-high, immune-active - reveal therapeutic implications for combining ADCs with immunotherapies or kinase inhibitors.