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Targeting CRTC2 reverses mutant NSCLC tumor resistance to immunotherapy.

2/5 보강
Proceedings of the National Academy of Sciences of the United States of America 📖 저널 OA 99.2% 2022: 2/2 OA 2023: 1/1 OA 2024: 8/8 OA 2025: 44/44 OA 2026: 57/58 OA 2022~2026 2026 Vol.123(17) p. e2508762123 OA Lung Cancer Treatments and Mutations
Retraction 확인
출처
PubMed DOI OpenAlex 마지막 보강 2026-04-29

PICO 자동 추출 (휴리스틱, conf 2/4)

유사 논문
P · Population 대상 환자/모집단
환자: tumors harboring mutations are resistant to standard of care anti-PD-1/PD-L1 blockade
I · Intervention 중재 / 시술
추출되지 않음
C · Comparison 대조 / 비교
추출되지 않음
O · Outcome 결과 / 결론
Mechanistically, the abrogation of the binding between CRTC2 and CREB was sufficient to restore sensitivity to immunotherapy. These findings provide critical insights into the central role of CRTC2 in modulating response to ICB and identify the disruption of CRTC2-CREB interaction as a potential therapeutic approach for this patient population.
OpenAlex 토픽 · Lung Cancer Treatments and Mutations Cancer Immunotherapy and Biomarkers Melanoma and MAPK Pathways

Robay D, Ackermann O, Laborde L, Shi X, Oreglia F, Stump R, Ciaghi S, Galli GG, Holzer L, Villemin L, Wagner J, Wu J, Lee LH, Bossen C, Mourikis TP, Gabriel M, Ruddy D, Yu H, Johannessen C, Ferretti S, Costa C

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📝 환자 설명용 한 줄

Non-small cell lung cancer (NSCLC) patients with tumors harboring mutations are resistant to standard of care anti-PD-1/PD-L1 blockade.

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↓ .bib ↓ .ris
APA Dimitri Robay, Ole Ackermann, et al. (2026). Targeting CRTC2 reverses mutant NSCLC tumor resistance to immunotherapy.. Proceedings of the National Academy of Sciences of the United States of America, 123(17), e2508762123. https://doi.org/10.1073/pnas.2508762123
MLA Dimitri Robay, et al.. "Targeting CRTC2 reverses mutant NSCLC tumor resistance to immunotherapy.." Proceedings of the National Academy of Sciences of the United States of America, vol. 123, no. 17, 2026, pp. e2508762123.
PMID 42018410 ↗

Abstract

Non-small cell lung cancer (NSCLC) patients with tumors harboring mutations are resistant to standard of care anti-PD-1/PD-L1 blockade. For this patient population there are no currently available tailored treatments, underlying the critical need to discover effective therapeutic strategies. In this study, we dissected the molecular mechanisms responsible for -mediated resistance to immune checkpoint blockade (ICB) and identified CRTC2, a coactivator of the transcription factor cAMP response element-binding protein (CREB), as a key signaling node regulating -dependent cell-extrinsic functions. CRTC2 deletion remodeled the immune profiles of -KO tumors and resensitized them to anti-PD-1 treatment, comparably to -proficient tumors. Mechanistically, the abrogation of the binding between CRTC2 and CREB was sufficient to restore sensitivity to immunotherapy. These findings provide critical insights into the central role of CRTC2 in modulating response to ICB and identify the disruption of CRTC2-CREB interaction as a potential therapeutic approach for this patient population.

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