Evidence map›Paper›PMID 39186651›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2024

Type I interferon signaling pathway enhances immune-checkpoint inhibition in KRAS mutant lung tumors.

Fernando Fernández-García, Ana Fernández-Rodríguez, Coral Fustero-Torre, Elena Piñeiro-Yáñez, Haiyun Wang, Carmen G Lechuga, Sergio Callejas, Rebeca Álvarez, Alejandra López-García, Laura Esteban-Burgos and 10 more

Abstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 1 pooled it
–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

18 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Trial
  3. Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. MAPK Pathway Mutations Emerge in Mutant IDH1 Inhibitor-Resistant Cholangiocarcinoma and Attenuate the IFN Response.Clinical cancer research : an official journal of the American Association for Cancer Research · 2026
    Article
  9. Review
  10. Review
  11. Distinct molecular subtypes of KRASClinical and translational medicine · 2025
    Article
  12. Interferon Epsilon Loss Is Elusive 9p21 Link to Immune-Cold Tumors, Resistant to Immune Checkpoint Therapy, and Endogenous CXCL9/10 Induction.Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer · 2025
    Review
  13. SystemicProceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Type I interferon signaling pathway enhances immune-checkpoint inhibition in KRAS mutant lung tumors.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
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

20 authors.

Fernando Fernández-GarcíaExperimental Oncology Group, Molecular Oncology Program, Centro Nacional de Investigaciones Oncológicas, Madrid 28029, Spain.ORCID 0000-0001-6011-7452
Ana Fernández-RodríguezExperimental Oncology Group, Molecular Oncology Program, Centro Nacional de Investigaciones Oncológicas, Madrid 28029, Spain.ORCID 0000-0001-5486-6844
Coral Fustero-TorreBioinformatics Unit, Centro Nacional de Investigaciones Oncológicas, Madrid 28029, Spain.
Elena Piñeiro-YáñezBioinformatics Unit, Centro Nacional de Investigaciones Oncológicas, Madrid 28029, Spain.ORCID 0000-0003-2773-2343
Haiyun WangSchool of Life Sciences and Technology, Tongji University, Shanghai 200092, China.
Carmen G LechugaExperimental Oncology Group, Molecular Oncology Program, Centro Nacional de Investigaciones Oncológicas, Madrid 28029, Spain.
Sergio CallejasGenomic Unit, Centro Nacional de Investigaciones Cardiovasculares, Madrid 28029, Spain.ORCID 0000-0003-3351-4940
Rebeca ÁlvarezGenomic Unit, Centro Nacional de Investigaciones Cardiovasculares, Madrid 28029, Spain.ORCID 0000-0002-5286-4500
Alejandra López-GarcíaExperimental Oncology Group, Molecular Oncology Program, Centro Nacional de Investigaciones Oncológicas, Madrid 28029, Spain.
Laura Esteban-BurgosExperimental Oncology Group, Molecular Oncology Program, Centro Nacional de Investigaciones Oncológicas, Madrid 28029, Spain.
Marina SalmónExperimental Oncology Group, Molecular Oncology Program, Centro Nacional de Investigaciones Oncológicas, Madrid 28029, Spain.
Marta San RománExperimental Oncology Group, Molecular Oncology Program, Centro Nacional de Investigaciones Oncológicas, Madrid 28029, Spain.
Carmen GuerraExperimental Oncology Group, Molecular Oncology Program, Centro Nacional de Investigaciones Oncológicas, Madrid 28029, Spain.ORCID 0000-0002-3891-046X
Chiara AmbrogioDepartment of Molecular Biotechnology and Health Sciences, Molecular Biotechnology Center, University of Torino, Torino 10126, Italy.ORCID 0000-0003-4122-701X
Matthias DrostenCentro de Investigación Biomédica en Red de Cáncer, Instituto de Salud Carlos III, Madrid 28029, Spain.
David SantamaríaMolecular Mechanisms of Cancer Program, Centro de Investigación del Cáncer, Consejo Superior de Investigaciones Científicas-Universidad de Salamanca, Salamanca 37007, Spain.
Fátima Al-ShahrourBioinformatics Unit, Centro Nacional de Investigaciones Oncológicas, Madrid 28029, Spain.
Ana DopazoGenomic Unit, Centro Nacional de Investigaciones Cardiovasculares, Madrid 28029, Spain.ORCID 0000-0002-4910-1684
Mariano Barbacid *Experimental Oncology Group, Molecular Oncology Program, Centro Nacional de Investigaciones Oncológicas, Madrid 28029, Spain.ORCID 0000-0002-1480-2624
Monica Musteanu *Centro de Investigación Biomédica en Red de Cáncer, Instituto de Salud Carlos III, Madrid 28029, Spain.ORCID 0000-0002-1753-3765

Funding

Spanish Ministry of Science, Innovation and Universities PID2021-122797OB-I00Spanish Ministry of Science, Innovation and Universities RTI2018-094664-B-I00
6 · The paper itself

Abstract

Lung cancer is the leading cause of cancer mortality worldwide. KRAS oncogenes are responsible for at least a quarter of lung adenocarcinomas, the main subtype of lung cancer. After four decades of intense research, selective inhibitors of KRAS oncoproteins are finally reaching the clinic. Yet, their effect on overall survival is limited due to the rapid appearance of drug resistance, a likely consequence of the high intratumoral heterogeneity characteristic of these tumors. In this study, we have attempted to identify those functional alterations that result from KRAS oncoprotein expression during the earliest stages of tumor development. Such functional changes are likely to be maintained during the entire process of tumor progression regardless of additional co-occurring mutations. Single-cell RNA sequencing analysis of murine alveolar type 2 cells expressing a resident

Indexed as

Immune Checkpoint InhibitorsInterferon Type ILung NeoplasmsMutationProto-Oncogene Proteins p21(ras)Signal TransductionAMP-Activated Protein Kinase KinasesAMP-Activated Protein KinasesAnimalsCell Line, TumorHumansMiceProtein Serine-Threonine KinasesTumor MicroenvironmentTumor Suppressor Protein p53AMP-Activated Protein Kinase KinasesAMP-Activated Protein KinasesHras protein, mouseImmune Checkpoint InhibitorsInterferon Type IKRAS protein, humanProtein Serine-Threonine KinasesProto-Oncogene Proteins p21(ras)STK11 protein, humanStk11 protein, mouseTrp53 protein, mouseTumor Suppressor Protein p53interferon signaling pathwayKRASLKB1lung cancerp53

Identifiers

PMID39186651
PMCPMC11388366

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Registered trials

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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.