Evidence map›Paper›PMID 40032600›Full record

ArticleJournal for immunotherapy of cancer2025

Machine learning identifies clinical tumor mutation landscape pathways of resistance to checkpoint inhibitor therapy in NSCLC.

Vitalay Fomin, WeiQing Venus So, Richard Alex Barbieri, Kenley Hiller-Bittrolff, Elina Koletou, Tiffany Tu, Bruno Gomes, James Cai, Jehad Charo

Abstract read
In one paragraph

Article in Journal for immunotherapy of cancer, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

8 citing papers in PubMed.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors.

Vitalay Fomin *Roche Pharmaceutical Research and Early Development, Data & Analytics, Roche Innovation Center New York, Little Falls, New Jersey, USA.ORCID http://orcid.org/0000-0002-8382-3445
WeiQing Venus So *Roche Pharmaceutical Research and Early Development, Data & Analytics, Roche Innovation Center New York, Little Falls, New Jersey, USA.ORCID http://orcid.org/0000-0002-8416-1455
Richard Alex BarbieriData Science, Capgemini Engineering, Paris, France.
Kenley Hiller-BittrolffData Science, Capgemini Engineering, Paris, France.
Elina KoletouRoche Pharmaceutical Research and Early Development, Data and Analytics, Roche Innovation Center Basel, Basel, Switzerland.ORCID http://orcid.org/0000-0003-4539-5117
Tiffany TuRoche Pharmaceutical Research and Early Development, Data & Analytics, Roche Innovation Center New York, Little Falls, New Jersey, USA.
Bruno GomesRoche Pharmaceutical Research and Early Development Oncology, Roche Innovation Center Basel, Basel, Switzerland.
James CaiRoche Pharmaceutical Research and Early Development, Data & Analytics, Roche Innovation Center New York, Little Falls, New Jersey, USA.
Jehad CharoRoche Pharmaceutical Research and Early Development Oncology, Roche Innovation Center Zurich, Schlieren, Switzerland jehad.charo@roche.com.ORCID http://orcid.org/0000-0002-5409-9160

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundImmune checkpoint inhibitors (CPIs) have revolutionized cancer therapy for several tumor indications. However, a substantial fraction of patients treated with CPIs derive no benefit or have short-lived responses to CPI therapy. Identifying patients who are most likely to benefit from CPIs and deciphering resistance mechanisms is therefore essential for developing adjunct treatments that can abrogate tumor resistance. PATIENTS AND

methodsIn this study, we used a machine learning approach that used the US-based nationwide de-identified Flatiron Health and Foundation Medicine non-small cell lung carcinoma (NSCLC) clinico-genomic database to identify genomic markers that predict clinical responses to CPI therapy. In total, we analyzed data from 4,433 patients with NSCLC.

resultsAnalysis of pretreatment genomic data from 1,511 patients with NSCLC identified. Of the 36 genomic signatures identified, 33 exhibited strong predictive capacity for CPI response (n=1150) compared with chemotherapy response (n=361), while three signatures were prognostic. These 36 genetic signatures had in common a core set of four genes (

conclusionsIn summary, we found several genomic markers and pathways that provide insight into biological mechanisms affecting response to CPI therapy. The analyses identified novel targets and biomarkers that have the potential to provide candidates for combination therapies or patient enrichment strategies, which could increase response rates to CPI therapy in patients with NSCLC.

Indexed as

Carcinoma, Non-Small-Cell LungDrug Resistance, NeoplasmImmune Checkpoint InhibitorsLung NeoplasmsMachine LearningMutationAgedBiomarkers, TumorFemaleHumansMaleMiddle AgedBiomarkers, TumorImmune Checkpoint InhibitorsBiomarkerGenomeImmune Checkpoint InhibitorLung Cancer

Identifiers

PMID40032600
PMCPMC11877243

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.