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Author Correction: CTLA4 blockade abrogates KEAP1/STK11-related resistance to PD-(L)1 inhibitors

Ferdinandos Skoulidis
Haniel A. Araujo
John V. Heymach
Amendments and CorrectionsOpen Access27 Feb 2025
Nature

Volume: 639, P: E19
CTLA4 blockade abrogates KEAP1/STK11-related resistance to PD-(L)1 inhibitors

Alterations in the tumour suppressor genes STK11 and/or KEAP1 can identify patients with advanced non-small-cell lung cancer who are likely to benefit from combinations of PD-(L)1 and CTLA4 immune checkpoint inhibitors added to chemotherapy.

Ferdinandos Skoulidis
Haniel A. Araujo
John V. Heymach
ResearchOpen Access09 Oct 2024
Nature

Volume: 635, P: 462-471
Aurora kinase A drives the evolution of resistance to third-generation EGFR inhibitors in lung cancer

Nongenetic activation of Aurora kinase A in the majority of patients with non-small-cell lung cancer mediates adaptive resistance to EGFR inhibition and offers an opportunity for combination treatment.

Khyati N. Shah
Roma Bhatt
Sourav Bandyopadhyay
Research26 Nov 2018
Nature Medicine

Volume: 25, P: 111-118
The role of APOBEC3B in lung tumor evolution and targeted cancer therapy resistance

Analyses of in vivo models, cell lines and patient-derived samples show that apolipoprotein B mRNA-editing catalytic subunit 3B (APOBEC3B) not only restrains lung tumor initiation but also that its upregulation is associated with resistance to targeted therapies. This study highlights the complex and context-dependent role of APOBEC3B in lung cancer.

Deborah R. Caswell
Philippe Gui
Charles Swanton
ResearchOpen Access04 Dec 2023
Nature Genetics

Volume: 56, P: 60-73
Focal adhesion kinase-YAP signaling axis drives drug-tolerant persister cells and residual disease in lung cancer

Remaining drug-tolerant persistent (DTP) cancer cells limit the efficacy of targeted therapy in EGFR, ALK and KRAS mutant non-small cell lung cancer (NSCLC). Here, the authors show that focal adhesion kinase (FAK)-YAP signalling supports DTP cells promoting residual disease and targeting this pathway improved tumour response in NSCLC preclinical models.

Franziska Haderk
Yu-Ting Chou
Trever G. Bivona
ResearchOpen Access03 May 2024
Nature Communications

Volume: 15, P: 1-19
Evolution and clinical impact of co-occurring genetic alterations in advanced-stage EGFR-mutant lung cancers

Analysis of a large cohort of EGFR-mutant lung cancer cell-free DNA samples along with longitudinal samples from a patient with EGFR-mutant lung cancer identifies pathways that inhibit EGFR-inhibitor response. Co-occurring genetic alterations influence clinical outcomes and underscore the need for combination therapies.

Collin M Blakely
Thomas B K Watkins
Trever G Bivona
Research06 Nov 2017
Nature Genetics

Volume: 49, P: 1693-1704
Understanding and targeting resistance mechanisms in NSCLC

Despite advances in targeting oncogenic driver mutations, advanced-stage non-small-cell lung cancer (NSCLC) remains largely incurable due to therapeutic resistance. This Review focuses on how understanding the mechanisms of resistance to targeted therapies in NSCLC can inform improved treatment strategies.

Julia Rotow
Trever G. Bivona
Reviews25 Oct 2017
Nature Reviews Cancer

Volume: 17, P: 637-658
Plasma epigenomic profiling reveals treatment-emergent squamous transformation in prostate cancer

Karl Semaan
Rashad Nawfal
Jacob E. Berchuck
ResearchOpen Access09 Jul 2025
npj Precision Oncology

Volume: 9, P: 1-7

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Author Correction: CTLA4 blockade abrogates KEAP1/STK11-related resistance to PD-(L)1 inhibitors

CTLA4 blockade abrogates KEAP1/STK11-related resistance to PD-(L)1 inhibitors

Aurora kinase A drives the evolution of resistance to third-generation EGFR inhibitors in lung cancer

The role of APOBEC3B in lung tumor evolution and targeted cancer therapy resistance

Focal adhesion kinase-YAP signaling axis drives drug-tolerant persister cells and residual disease in lung cancer

Evolution and clinical impact of co-occurring genetic alterations in advanced-stage EGFR-mutant lung cancers

Understanding and targeting resistance mechanisms in NSCLC

Plasma epigenomic profiling reveals treatment-emergent squamous transformation in prostate cancer

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