Evidence map›Paper›PMID 36639452›Full record

ReviewNature reviews. Clinical oncology2023

At the crossroads of immunotherapy for oncogene-addicted subsets of NSCLC.

Itziar Otano, Alvaro C Ucero, Jon Zugazagoitia, Luis Paz-Ares

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Clinical oncology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 101 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
101citing papers in PubMed, 1 pooled it
40.0field-weighted citation impact, top 1% of its field
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

101 citing papers in PubMed, 1 synthesis or guideline pooled it, 154 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. Article
  6. Targeting the JAK/STAT signalling axis in cancer: chemopreventive potential of natural compounds with emerging focus on retinoids.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
    Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Cancers · 2026
    Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Pan-cancer analysis ofGenes & diseases · 2026
    Article
  17. Article
  18. Article
  19. Article
  20. Review

41 more citing papers are in PubMed but not listed here.

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

4 authors at 2 institutions in 2 countries.

Itziar OtanoH12O-CNIO Lung Cancer Clinical Research Unit, Health Research Institute Hospital 12 de Octubre (i+12)/Spanish National Cancer Research Center (CNIO), Madrid, Spain. iotanoan@alumni.unav.es.ORCID 0000-0002-1433-1711
Alvaro C UceroH12O-CNIO Lung Cancer Clinical Research Unit, Health Research Institute Hospital 12 de Octubre (i+12)/Spanish National Cancer Research Center (CNIO), Madrid, Spain.ORCID 0000-0002-5575-0808
Jon ZugazagoitiaH12O-CNIO Lung Cancer Clinical Research Unit, Health Research Institute Hospital 12 de Octubre (i+12)/Spanish National Cancer Research Center (CNIO), Madrid, Spain.
Luis Paz-AresH12O-CNIO Lung Cancer Clinical Research Unit, Health Research Institute Hospital 12 de Octubre (i+12)/Spanish National Cancer Research Center (CNIO), Madrid, Spain. lpazaresr@seom.org.
Research Institute Hospital 12 de Octubre · ESUniversidad Complutense de Madrid · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Non-small-cell lung cancer (NSCLC) has become a paradigm of precision medicine, with the discovery of numerous disease subtypes defined by specific oncogenic driver mutations leading to the development of a range of molecularly targeted therapies. Over the past decade, rapid progress has also been made in the development of immune-checkpoint inhibitors (ICIs), especially antagonistic antibodies targeting the PD-L1-PD-1 axis, for the treatment of NSCLC. Although many of the major oncogenic drivers of NSCLC are associated with intrinsic resistance to ICIs, patients with certain oncogene-driven subtypes of the disease that are highly responsive to specific targeted therapies might also derive benefit from immunotherapy. However, the development of effective immunotherapy approaches for oncogene-addicted NSCLC has been challenged by a lack of predictive biomarkers for patient selection and limited knowledge of how ICIs and oncogene-directed targeted therapies should be combined. Therefore, whether ICIs alone or with chemotherapy or even in combination with molecularly targeted agents would offer comparable benefit in the context of selected oncogenic driver alterations to that observed in the general unselected NSCLC population remains an open question. In this Review, we discuss the effects of oncogenic driver mutations on the efficacy of ICIs and the immune tumour microenvironment as well as the potential vulnerabilities that could be exploited to overcome the challenges of immunotherapy for oncogene-addicted NSCLC.

Indexed as

Carcinoma, Non-Small-Cell LungImmunotherapyLung NeoplasmsOncogene AddictionAntineoplastic AgentsB7-H1 AntigenHumansOncogenesAntineoplastic AgentsB7-H1 Antigen

Identifiers

PMID36639452
OpenAlexW4315881606

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.