Evidence map›Paper›PMID 28489818›Full record

ArticleNature2017

A Wnt-producing niche drives proliferative potential and progression in lung adenocarcinoma.

Tuomas Tammela, Francisco J Sanchez-Rivera, Naniye Malli Cetinbas, Katherine Wu, Nikhil S Joshi, Katja Helenius, Yoona Park, Roxana Azimi, Natanya R Kerper, R Alexander Wesselhoeft and 8 more

Abstract read
In one paragraph

Article in Nature, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 227 papers.

0numbers the graph read from it
0cells of the map it votes in
227citing 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

227 citing papers in PubMed.

  1. Article
  2. Genes, fuel, and fate in lung cancer.Biochemical Society transactions · 2026
    Review
  3. Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
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  12. Review
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Review
  20. Article

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

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

18 authors.

Tuomas TammelaDavid H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, Massachusetts 02142, USA.
Francisco J Sanchez-RiveraDavid H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, Massachusetts 02142, USA.
Naniye Malli CetinbasDavid H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, Massachusetts 02142, USA.
Katherine WuDavid H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, Massachusetts 02142, USA.
Nikhil S JoshiDavid H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, Massachusetts 02142, USA.
Katja HeleniusDavid H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, Massachusetts 02142, USA.
Yoona ParkDavid H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, Massachusetts 02142, USA.
Roxana AzimiDavid H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, Massachusetts 02142, USA.
Natanya R KerperDavid H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, Massachusetts 02142, USA.
R Alexander WesselhoeftDavid H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, Massachusetts 02142, USA.
Xin GuDavid H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, Massachusetts 02142, USA.
Leah SchmidtDavid H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, Massachusetts 02142, USA.
Milton Cornwall-BradyDavid H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, Massachusetts 02142, USA.
Ömer H YilmazDavid H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, Massachusetts 02142, USA.
Wen XueDavid H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, Massachusetts 02142, USA.
Pekka KatajistoInstitute of Biotechnology, University of Helsinki, 00014 Helsinki, Finland.
Arjun BhutkarDavid H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, Massachusetts 02142, USA.
Tyler JacksDavid H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, Massachusetts 02142, USA.

Funding

VIRUS PRODUCTION COREP30CA014051 · NCI · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI MATTHEW G. VANDER HEIDEN · 1985 to 2026
$93.9M
USE OF RETROVIRUS PROMOTER TRAP VECTORS TO IDENTIFY ONCOGENES AND ANTI-ONCOGENESP01CA042063 · NCI · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI JACKS, TYLER E. · 1986 to 2021
$30.5M
Investigating Wnt and Lgr5 signaling as regulators of lung cancer heterogeneityK99CA187317 · NCI · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI TAMMELA, TUOMAS · 2014 to 2015
$246k
Howard Hughes Medical InstituteNCI NIH HHS K99 CA187317NCI NIH HHS P01 CA042063NCI NIH HHS P30 CA014051NCI NIH HHS P30-CA14051
6 · The paper itself

Abstract

The heterogeneity of cellular states in cancer has been linked to drug resistance, cancer progression and the presence of cancer cells with properties of normal tissue stem cells. Secreted Wnt signals maintain stem cells in various epithelial tissues, including in lung development and regeneration. Here we show that mouse and human lung adenocarcinomas display hierarchical features with two distinct subpopulations, one with high Wnt signalling activity and another forming a niche that provides the Wnt ligand. The Wnt responder cells showed increased tumour propagation ability, suggesting that these cells have features of normal tissue stem cells. Genetic perturbation of Wnt production or signalling suppressed tumour progression. Small-molecule inhibitors targeting essential posttranslational modification of Wnt reduced tumour growth and markedly decreased the proliferative potential of lung cancer cells, leading to improved survival of tumour-bearing mice. These results indicate that strategies for disrupting pathways that maintain stem-like and niche cell phenotypes can translate into effective anti-cancer therapies.

Indexed as

Disease ProgressionStem Cell NicheWnt Signaling PathwayAdenocarcinomaAdenocarcinoma of LungAnimalsCell ProliferationFemaleHumansLung NeoplasmsMaleMiceNeoplasm TransplantationNeoplastic Stem CellsProtein Processing, Post-TranslationalSmall Molecule LibrariesSmall Molecule LibrariesWnt Proteins

Identifiers

PMID28489818
PMCPMC5903678

What OpenQuestion holds

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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.