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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
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
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
Mixed responses to targeted therapy driven by chromosomal instability through p53 dysfunction and genome doubling

Mixed responses to targeted therapy within a patient are a clinical challenge. Here the authors show that TP53 loss-of-function cooperates with whole genome doubling which increases chromosomal instability. This leads to greater cellular diversity and multiple routes of resistance, which in turn promotes mixed responses to treatment.

Sebastijan Hobor
Maise Al Bakir
Charles Swanton
ResearchOpen Access13 Jun 2024
Nature Communications

Volume: 15, P: 1-21
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
PERCEPTION predicts patient response and resistance to treatment using single-cell transcriptomics of their tumors

Sinha and colleagues present PERCEPTION, a precision oncology computational pipeline that can predict the response and resistance of patients by analyzing single-cell transcriptomic data from their tumor samples.

Sanju Sinha
Rahulsimham Vegesna
Eytan Ruppin
Research18 Apr 2024
Nature Cancer

Volume: 5, P: 938-952
Inactivation of Capicua drives cancer metastasis

Trever Bivona and colleagues use an in vivo lung cancer metastasis model to show that the transcriptional repressor Capicua (CIC) suppresses invasion and metastasis. CIC inactivation leads to upregulation of ETV4 and MMP24, which is necessary and sufficient for metastasis.

Ross A Okimoto
Frank Breitenbuecher
Trever G Bivona
Research21 Nov 2016
Nature Genetics

Volume: 49, P: 87-96
RAS nucleotide cycling underlies the SHP2 phosphatase dependence of mutant BRAF-, NF1- and RAS-driven cancers

Nichols et al. identify an SHP2 inhibitor that disrupts SOS1-mediated RAS–GTP loading with demonstrated efficacy in various types of tumour driven by mutant BRAF, NF1 or RAS.

Robert J. Nichols
Franziska Haderk
Trever G. Bivona
Research13 Aug 2018
Nature Cell Biology

Volume: 20, P: 1064-1073
RAS-MAPK dependence underlies a rational polytherapy strategy in EML4-ALK–positive lung cancer

Unraveling the signaling dependencies of EMLK4-ALK fusion–driven lung cancer reveals upfront combination therapy strategies.

Gorjan Hrustanovic
Victor Olivas
Trever G Bivona
Research24 Aug 2015
Nature Medicine

Volume: 21, P: 1038-1047
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
Novel computational method for predicting polytherapy switching strategies to overcome tumor heterogeneity and evolution

Vanessa D. Jonsson
Collin M. Blakely
Trever G. Bivona
ResearchOpen Access13 Mar 2017
Scientific Reports

Volume: 7, P: 1-14

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

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

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

Mixed responses to targeted therapy driven by chromosomal instability through p53 dysfunction and genome doubling

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

PERCEPTION predicts patient response and resistance to treatment using single-cell transcriptomics of their tumors

Inactivation of Capicua drives cancer metastasis

RAS nucleotide cycling underlies the SHP2 phosphatase dependence of mutant BRAF-, NF1- and RAS-driven cancers

RAS-MAPK dependence underlies a rational polytherapy strategy in EML4-ALK–positive lung cancer

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

Novel computational method for predicting polytherapy switching strategies to overcome tumor heterogeneity and evolution

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