Evidence map›Paper›PMID 30712876›Full record

ArticleCell2019

Commensal Microbiota Promote Lung Cancer Development via γδ T Cells.

Chengcheng Jin, Georgia K Lagoudas, Chen Zhao, Susan Bullman, Arjun Bhutkar, Bo Hu, Samuel Ameh, Demi Sandel, Xu Sue Liang, Sarah Mazzilli and 6 more

Open access · bronzeAbstract read
In one paragraph

Article in Cell, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 639 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
639citing papers in PubMed, 3 pooled it
35.8field-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

639 citing papers in PubMed, 3 syntheses or guidelines pooled it, 928 citations in OpenAlex.

  1. Pooled it
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  11. γδ T cells in colorectal and liver cancer.Nature reviews. Gastroenterology & hepatology · 2026
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579 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

16 authors at 6 institutions in 1 country.

Chengcheng JinDavid H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, MA 02142, USA.
Georgia K LagoudasDepartment of Biological Engineering, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.
Chen ZhaoLymphocyte Biology Section, Laboratory of Immune System Biology, National Institute of Allergy and Infectious Diseases, NIH, Bethesda, MD 20892, USA.
Susan BullmanBroad Institute of Massachusetts Institute of Technology and Harvard, Cambridge, MA 02142, USA; Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA 02215, USA.
Arjun BhutkarDavid H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, MA 02142, USA.
Bo HuDepartment of Cancer Biology, Dana-Farber Cancer Institute, Boston, MA 02115, USA.
Samuel AmehDavid H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, MA 02142, USA.
Demi SandelDavid H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, MA 02142, USA.
Xu Sue LiangDavid H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, MA 02142, USA.
Sarah MazzilliDepartment of Medicine, Division of Computational Biomedicine, Boston University School of Medicine, Boston, MA 02118, USA.
Mark T WharyDivision of Comparative Medicine, Massachusetts Institute of Technology, Cambridge, MA 02142, USA.
Matthew MeyersonBroad Institute of Massachusetts Institute of Technology and Harvard, Cambridge, MA 02142, USA; Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA 02215, USA.
Ronald GermainLymphocyte Biology Section, Laboratory of Immune System Biology, National Institute of Allergy and Infectious Diseases, NIH, Bethesda, MD 20892, USA.
Paul C BlaineyDavid H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, MA 02142, USA; Department of Biological Engineering, Massachusetts Institute of Technology, Cambridge, MA 02139, USA; Broad Institute of Massachusetts Institute of Technology and Harvard, Cambridge, MA 02142, USA.
James G FoxDepartment of Biological Engineering, Massachusetts Institute of Technology, Cambridge, MA 02139, USA; Division of Comparative Medicine, Massachusetts Institute of Technology, Cambridge, MA 02142, USA.
Tyler JacksDavid H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, MA 02142, USA; Howard Hughes Medical Institute, Massachusetts Institute of Technology, Cambridge, MA 02142, USA. Electronic address: tjacks@mit.edu.
Massachusetts Institute of Technology · USBroad Institute · USNational Institute of Allergy and Infectious Diseases · USBoston University · USDana-Farber Cancer Institute · USHoward Hughes Medical Institute · US

Funding

VIRUS PRODUCTION COREP30CA014051 · NCI · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI MATTHEW G. VANDER HEIDEN · 1985 to 2026
$93.9M
Multiscale Analysis of Immune ResponsesZIAAI000545 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI GERMAIN, RONALD N · 2009 to 2025
$29.4M
TOXICOLOGY CORE UNITP30ES002109 · NIEHS · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI LEVINE, STUART S · 1985 to 2020
$25.6M
(PQB3) Investigating innate immunosurveillance of oncogene-induced danger signalsR01CA185020 · NCI · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI JACKS, TYLER E. · 2014 to 2017
$1.3M
Investigating immune-microbiota interaction in lung cancerR00CA226400 · NCI · UNIVERSITY OF PENNSYLVANIA · PI JIN, CHENGCHENG · 2020 to 2022
$866k
The role of Fusobacterium in colorectal cancer treatment, tumor ecology and chemotherapeutic efficacyR00CA229984 · NCI · FRED HUTCHINSON CANCER RESEARCH CENTER · PI BULLMAN, SUSAN · 2019 to 2021
$718k
Investigating immune-microbiota interaction in lung cancerK99CA226400 · NCI · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI JIN, CHENGCHENG · 2018 to 2019
$252k
The role of Fusobacterium in colorectal cancer treatment, tumor ecology and chemotherapeutic efficacyK99CA229984 · NCI · DANA-FARBER CANCER INST · PI BULLMAN, SUSAN · 2018 to 2018
$129k
Howard Hughes Medical InstituteNCI NIH HHS K99 CA226400NCI NIH HHS K99 CA229984NCI NIH HHS P30 CA014051NCI NIH HHS R00 CA226400NCI NIH HHS R00 CA229984NCI NIH HHS R01 CA185020NIEHS NIH HHS P30 ES002109
6 · The paper itself

Abstract

Lung cancer is closely associated with chronic inflammation, but the causes of inflammation and the specific immune mediators have not been fully elucidated. The lung is a mucosal tissue colonized by a diverse bacterial community, and pulmonary infections commonly present in lung cancer patients are linked to clinical outcomes. Here, we provide evidence that local microbiota provoke inflammation associated with lung adenocarcinoma by activating lung-resident γδ T cells. Germ-free or antibiotic-treated mice were significantly protected from lung cancer development induced by Kras mutation and p53 loss. Mechanistically, commensal bacteria stimulated Myd88-dependent IL-1β and IL-23 production from myeloid cells, inducing proliferation and activation of Vγ6

Indexed as

AnimalsCell ProliferationFemaleHost Microbial InteractionsInterleukin-17Interleukin-1betaInterleukin-23Intraepithelial LymphocytesLungLung NeoplasmsMaleMiceMice, Inbred C57BLMicrobiotaMyeloid Differentiation Factor 88NeutrophilsInterleukin-17Interleukin-1betaInterleukin-23Myd88 protein, mouseMyeloid Differentiation Factor 88Receptors, Antigen, T-Cell, gamma-deltaIL-17inflammationlung adenocarcinomalung cancermicrobiotaneutrophilstumor microenvironmentγδ T cells

Identifiers

PMID30712876
PMCPMC6691977
OpenAlexW2912967789

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.