Evidence map›Paper›PMID 19221001›Full record

ArticleCarcinogenesis2009

Novel mechanism for obesity-induced colon cancer progression.

Janette M Birmingham, Julia V Busik, Fay M Hansen-Smith, Jenifer I Fenton

Open access · bronzeAbstract read
In one paragraph

Article in Carcinogenesis, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
5.5field-weighted citation impact, top 3% 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

36 citing papers in PubMed, 85 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Review
  7. Lipedema: A Call to Action!Obesity (Silver Spring, Md.) · 2019
    Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
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  14. Article
  15. Article
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  17. Article
  18. Review
  19. Mechanisms by Which Pleiotropic AmphiphilicCurrent colorectal cancer reports · 2014
    Article
  20. Role of dysregulated expression of leptin and leptin receptors in colorectal carcinogenesis.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014
    Review
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 1 country.

Janette M BirminghamDepartment of Food Science and Human Nutrition, College of Nursing, Michigan State University, East Lansing, MI 48824, USA.
Julia V Busik
Fay M Hansen-Smith
Jenifer I Fenton
Michigan State University · USOakland University · US

Funding

role of adipokines in colon epithelial cell homeostasisR03CA130033 · NCI · MICHIGAN STATE UNIVERSITY · PI FENTON, JENIFER IMIG · 2007 to 2008
$151k
NCI NIH HHS R03CA130033
6 · The paper itself

Abstract

Adipose tissue secretes factors linked to colon cancer risk including leptin. A hallmark of cancer is sustained angiogenesis. While leptin promotes angiogenesis in adipose tissue, it is unknown whether leptin can induce epithelial cells to produce factors that may drive angiogenesis, vascular development and therefore cancer progression. The purpose of this study was to compare the effects of leptin-stimulated colon epithelial cells differing in adenomatous polyposis coli (Apc) genotype (gatekeeper tumor suppressor gene for colon cancer) on angiogenesis. We employed novel colonic epithelial cell lines derived from the Immorto mouse [young adult mouse colon (YAMC)] and the Immorto-Min mouse [Immorto-Min colonic epithelial cell (IMCE)], which carries the Apc Min mutation, to study the effects of leptin-stimulated colon epithelial cells on angiogenesis. We utilized ex vivo rat mesenteric capillary bioassay and human umbilical vein endothelial cell (HUVEC) models to study angiogenesis. IMCE cells stimulated with leptin produced significantly more vascular endothelial growth factor (VEGF) than YAMC (268 +/- 18 versus 124 +/- 8 pg/ml; P < 0.01) cells. Leptin treatment induced dose-dependent increases in VEGF only in IMCE cells. Conditioned media from leptin (50 ng/ml)-treated IMCE cells induced significant capillary formation compared with control, which was blocked by the addition of a neutralizing antibody against VEGF. Conditioned media from leptin-treated IMCE cells also induced HUVEC cell proliferation, chemotaxis, upregulation of adhesion proteins and cell-signaling activation resulting in nuclear factor kappa B nuclear translocation and DNA binding due to VEGF. This is the first study demonstrating that leptin can induce preneoplastic colon epithelial cells to orchestrate VEGF-driven angiogenesis and vascular development, thus providing a specific mechanism and potential target for obesity-associated cancer.

Indexed as

Adenomatous Polyposis Coli ProteinAnimalsBlotting, WesternCell AdhesionCell MovementCell ProliferationCells, CulturedChemotaxisColonic NeoplasmsDisease ProgressionDose-Response Relationship, DrugEndothelium, VascularEnzyme-Linked Immunosorbent AssayHumansLeptinMaleAdenomatous Polyposis Coli ProteinLeptinNF-kappa Bp38 Mitogen-Activated Protein KinasesVascular Endothelial Growth Factor AVEGFA protein, human

Identifiers

PMID19221001
PMCPMC2664456
OpenAlexW2152205622

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.