Evidence map›Paper›PMID 32747478›Full record

ReviewGenes & development2020

Cells of origin of lung cancers: lessons from mouse studies.

Giustina Ferone, Myung Chang Lee, Julien Sage, Anton Berns

Open access · diamondAbstract readReview
In one paragraph

Review in Genes & development, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 119 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
119citing papers in PubMed, 4 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

119 citing papers in PubMed, 4 syntheses or guidelines pooled it, 199 citations in OpenAlex.

  1. Pooled it
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  5. Article
  6. Review
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  9. Cell-type Specific Alteration ofbioRxiv : the preprint server for biology · 2026
    Article
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  13. Review
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  16. Article
  17. Novel concepts of cell-of origin in neuroendocrine neoplasms.Virchows Archiv : an international journal of pathology · 2026
    Review
  18. Article
  19. Article
  20. Article

59 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.

Giustina FeroneDivision of Molecular Genetics, The Netherlands Cancer Institute, 1066 CX Amsterdam, The Netherlands.
Myung Chang LeeDepartment of Pediatrics, Stanford University School of Medicine, Stanford, California 94305, USA.
Julien SageDepartment of Pediatrics, Stanford University School of Medicine, Stanford, California 94305, USA.
Anton BernsDivision of Molecular Genetics, The Netherlands Cancer Institute, 1066 CX Amsterdam, The Netherlands.
Stanford University · USThe Netherlands Cancer Institute · NL

Funding

Single-Cell Biology and Data Analysis Shared Resource (SCB-DA SR)U54CA217450 · NCI · VANDERBILT UNIVERSITY · PI WEAVER, ALISSA M · 2018 to 2022
$8.5M
Investigating molecular and cellular mechanisms of SCLC development to identify novel therapeutic strategiesR35CA231997 · NCI · STANFORD UNIVERSITY · PI SAGE, JULIEN · 2019 to 2025
$6.2M
Novel therapeutic approaches for enhancing anti-tumor immunity in SCLCU01CA213273 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI BYERS, LAUREN AVERETT, HEYMACH, JOHN V. · 2017 to 2021
$3.0M
Molecular mechanisms of SCLC initiation and detection in mice and humansU01CA231851 · NCI · STANFORD UNIVERSITY · PI KRASNOW, MARK A · 2018 to 2022
$2.9M
European Research Council 319661NCI NIH HHS R35 CA231997NCI NIH HHS U01 CA213273NCI NIH HHS U01 CA231851NCI NIH HHS U54 CA217450
6 · The paper itself

Abstract

As one of the most common forms of cancer, lung cancers present as a collection of different histological subtypes. These subtypes are characterized by distinct sets of driver mutations and phenotypic appearance, and they often show varying degrees of heterogenicity, aggressiveness, and response/resistance to therapy. Intriguingly, lung cancers are also capable of showing features of multiple subtypes or converting from one subtype to another. The intertumoral and intratumoral heterogeneity of lung cancers as well as incidences of subtype transdifferentiation raise the question of to what extent the tumor characteristics are dictated by the cell of origin rather than the acquired driver lesions. We provide here an overview of the studies in experimental mouse models that try to address this question. These studies convincingly show that both the cell of origin and the genetic driver lesions play a critical role in shaping the phenotypes of lung tumors. However, they also illustrate that there is far from a direct one-to-one relationship between the cell of origin and the cancer subtype, as most epithelial cells can be reprogrammed toward diverse lung cancer fates when exposed to the appropriate set of driver mutations.

Indexed as

AdenocarcinomaAnimalsCarcinoma, Squamous CellDisease Models, AnimalEpithelial CellsLung NeoplasmsMiceRespiratory MucosaSmall Cell Lung Carcinomacell of originLuADClung cancerLuSCCmouse modelsNSCLC

Identifiers

PMID32747478
PMCPMC7397855
OpenAlexW3046931490

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.