Evidence map›Paper›PMID 30228179›Full record

ArticleCancer discovery2018

Intertumoral Heterogeneity in SCLC Is Influenced by the Cell Type of Origin.

Dian Yang, Sarah K Denny, Peyton G Greenside, Andrea C Chaikovsky, Jennifer J Brady, Youcef Ouadah, Jeffrey M Granja, Nadine S Jahchan, Jing Shan Lim, Shirley Kwok and 10 more

Open access · bronzeAbstract read
In one paragraph

Article in Cancer discovery, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 113 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
113citing papers in PubMed, 1 pooled it
6.3field-weighted citation impact, top 2% 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

113 citing papers in PubMed, 1 synthesis or guideline pooled it, 174 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Molecular mechanisms and therapeutic targets in lung cancer-nerve crosstalk.Chinese medical journal pulmonary and critical care medicine · 2026
    Review
  4. Review
  5. Novel concepts of cell-of origin in neuroendocrine neoplasms.Virchows Archiv : an international journal of pathology · 2026
    Review
  6. Review
  7. Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Current and future therapies for small cell lung carcinoma.Journal of hematology & oncology · 2025
    Review
  20. Article

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

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

20 authors at 6 institutions in 3 countries.

Dian YangCancer Biology Program, Stanford University, Stanford, California.
Sarah K DennyDepartment of Genetics, Stanford University, Stanford, California.
Peyton G GreensideProgram in Biomedical Informatics, Stanford University, Stanford, California.
Andrea C ChaikovskyCancer Biology Program, Stanford University, Stanford, California.
Jennifer J BradyDepartment of Genetics, Stanford University, Stanford, California.
Youcef OuadahCancer Biology Program, Stanford University, Stanford, California.
Jeffrey M GranjaDepartment of Genetics, Stanford University, Stanford, California.
Nadine S JahchanDepartment of Genetics, Stanford University, Stanford, California.
Jing Shan LimCancer Biology Program, Stanford University, Stanford, California.
Shirley KwokDepartment of Pathology, Stanford University, Stanford, California.
Christina S KongDepartment of Pathology, Stanford University, Stanford, California.
Anna S BerghoffInstitute of Neurology, Medical University of Vienna, Vienna, Austria.
Anna SchmittDepartment of Internal Medicine I, University Hospital of Cologne, Cologne, Germany.
H Christian ReinhardtDepartment of Internal Medicine I, University Hospital of Cologne, Cologne, Germany.
Kwon-Sik ParkDepartment of Microbiology, Immunology, and Cancer Biology, University of Virginia School of Medicine, Charlottesville, Virginia.
Matthias PreusserDepartment of Medicine I, Medical University of Vienna, Vienna, Austria.ORCID 0000-0003-3541-2315
Anshul KundajeDepartment of Genetics, Stanford University, Stanford, California.ORCID 0000-0003-3084-2287
William J GreenleafDepartment of Genetics, Stanford University, Stanford, California.
Julien SageCancer Biology Program, Stanford University, Stanford, California. mwinslow@stanford.edu julsage@stanford.edu.
Monte M WinslowCancer Biology Program, Stanford University, Stanford, California. mwinslow@stanford.edu julsage@stanford.edu.
Stanford University · USStanford Medicine · USComprehensive Cancer Center Vienna · ATUniversity Hospital Cologne · DEUniversity of Cologne · DEUniversity of Virginia · US

Funding

Leveraging innovative technologies in basic and clinical cancer researchT32CA009302 · NCI · STANFORD UNIVERSITY · PI LAURA D ATTARDI, Aaron M Newman · 1985 to 2026
$19.1M
Molecular Biophysics Training Program at StanfordT32GM008294 · NIGMS · STANFORD UNIVERSITY · PI HUANG, KERWYN C. · 1989 to 2019
$7.4M
Molecular mechanisms of SCLC initiation and detection in mice and humansU01CA231851 · NCI · STANFORD UNIVERSITY · PI KRASNOW, MARK A · 2018 to 2022
$2.9M
Deep learning frameworks for regulatory genomics.DP2GM123485 · NIGMS · STANFORD UNIVERSITY · PI KUNDAJE, ANSHUL · 2016 to 2016
$2.4M
Molecular and cellular mechanisms of SCLC metastasisR01CA206540 · NCI · STANFORD UNIVERSITY · PI SAGE, JULIEN · 2016 to 2019
$1.7M
(PQ4A) Metabolic Plasticity of Pre-Malignant Cells During Tumor ProgressionR01CA194461 · NCI · UNIVERSITY OF VIRGINIA · PI PARK, KWON-SIK · 2015 to 2018
$1.6M
NCI NIH HHS R01 CA194461NCI NIH HHS R01 CA206540NCI NIH HHS T32 CA009302NCI NIH HHS U01 CA231851NIGMS NIH HHS DP2 GM123485NIGMS NIH HHS T32 GM008294
6 · The paper itself

Abstract

The extent to which early events shape tumor evolution is largely uncharacterized, even though a better understanding of these early events may help identify key vulnerabilities in advanced tumors. Here, using genetically defined mouse models of small cell lung cancer (SCLC), we uncovered distinct metastatic programs attributable to the cell type of origin. In one model, tumors gain metastatic ability through amplification of the transcription factor NFIB and a widespread increase in chromatin accessibility, whereas in the other model, tumors become metastatic in the absence of NFIB-driven chromatin alterations. Gene-expression and chromatin accessibility analyses identify distinct mechanisms as well as markers predictive of metastatic progression in both groups. Underlying the difference between the two programs was the cell type of origin of the tumors, with NFIB-independent metastases arising from mature neuroendocrine cells. Our findings underscore the importance of the identity of cell type of origin in influencing tumor evolution and metastatic mechanisms.

Indexed as

AnimalsCell Line, TumorDisease Models, AnimalHumansLung NeoplasmsMiceSmall Cell Lung Carcinoma

Identifiers

PMID30228179
PMCPMC6195211
OpenAlexW2892249755

What OpenQuestion holds

Textmetadata
LicenceTDM
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.