Evidence map›Paper›PMID 16424015›Full record

ArticleCancer research2006

Helicobacter infection is required for inflammation and colon cancer in SMAD3-deficient mice.

Lillian Maggio-Price, Piper Treuting, Weiping Zeng, Mark Tsang, Helle Bielefeldt-Ohmann, Brian M Iritani

Open access · bronzeAbstract read
In one paragraph

Article in Cancer research, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 115 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
115citing papers in PubMed, 2 pooled it
10.7field-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

115 citing papers in PubMed, 2 syntheses or guidelines pooled it, 206 citations in OpenAlex.

  1. Pooled it
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  15. The Interaction Between the Microbiome and Tumors.Frontiers in cellular and infection microbiology · 2021
    Review
  16. Results of endoscopy in 35,525 patients with precancerous diseases of the gastrointestinal tract.International journal of clinical and experimental pathology · 2021
    Article
  17. Article
  18. Article
  19. Role of Inflammation in Pathophysiology of Colonic Disease: An Update.International journal of molecular sciences · 2020
    Review
  20. Article

55 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

6 authors at 2 institutions in 1 country.

Lillian Maggio-PriceDepartment of Comparative Medicine, University of Washington, 1959 Northeast Pacific Avenue, Seattle, WA 98195, USA. lmprice@u.washington.edu
Piper Treuting
Weiping Zeng
Mark Tsang
Helle Bielefeldt-Ohmann
Brian M Iritani
Fred Hutch Cancer Center · USUniversity of Washington · US

Funding

Lymph Node Alterations in CancerR01CA068328 · NCI · UNIVERSITY OF WASHINGTON · PI RUDDELL, M ALANNA · 1996 to 2014
$4.5M
Control of T Lymphopoiesis and Growth by Mad GenesR01AI053568 · NIAID · UNIVERSITY OF WASHINGTON · PI IRITANI, BRIAN M · 2003 to 2007
$1.5M
NCI NIH HHS 2R01 CA 68328NCI NIH HHS R01 CA068328NIAID NIH HHS 1R01 AI 053568-01NIAID NIH HHS R01 AI053568
6 · The paper itself

Abstract

Accumulating evidence suggests that intestinal microbial organisms may play an important role in triggering and sustaining inflammation in individuals afflicted with inflammatory bowel disease (IBD). Moreover, individuals with IBD are at increased risk for developing colorectal cancer, suggesting that chronic inflammation may initiate genetic or epigenetic changes associated with cancer development. We tested the hypothesis that bacteria may contribute to the development of colon cancer by synergizing with defective transforming growth factor-beta (TGF-beta) signaling, a pathway commonly mutated in human colon cancer. Although others have reported that mice deficient in the TGF-beta signaling molecule SMAD3 develop colon cancer, we found that SMAD3-deficient mice maintained free of the Gram-negative enterohepatic bacteria Helicobacter spp. for up to 9 months do not develop colon cancer. Furthermore, infection of SMAD3(-/-) mice with Helicobacter triggers colon cancer in 50% to 66% of the animals. Using real-time PCR, we found that Helicobacter organisms concentrate in the cecum, the preferred site of tumor development. Mucinous adenocarcinomas develop 5 to 30 weeks after infection and are preceded by an early inflammatory phase, consisting of increased proliferation of epithelial cells; increased numbers of cyclooxygenase-2-positive cells, CD4(+) T cells, macrophages; and increased MHC class II expression. Colonic tissue revealed increased transcripts for the oncogene c-myc and the proinflammatory cytokines interleukin-1alpha (IL-1alpha), IL-1beta, IL-6, IFN-gamma, and tumor necrosis factor-alpha, some of which have been implicated in colon cancer. These results suggest that bacteria may be important in triggering colorectal cancer, notably in the context of gene mutations in the TGF-beta signaling pathway, one of the most commonly affected cellular pathways in colorectal cancer in humans.

Indexed as

AnimalsCecumCell ProliferationColonic NeoplasmsCytokinesDNA, BacterialFemaleGenetic Predisposition to DiseaseHelicobacter InfectionsInflammationMaleMicePolymerase Chain ReactionProto-Oncogene Proteins c-mycRisk FactorsSignal TransductionCytokinesDNA, BacterialProto-Oncogene Proteins c-mycSmad3 ProteinSmad3 protein, mouseTransforming Growth Factor beta

Identifiers

PMID16424015
PMCPMC5367923
OpenAlexW2095083228

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.