Evidence map›Paper›PMID 19179545›Full record

ArticleCancer research2009

The role of tumor cell-derived connective tissue growth factor (CTGF/CCN2) in pancreatic tumor growth.

Kevin L Bennewith, Xin Huang, Christine M Ham, Edward E Graves, Janine T Erler, Neeraja Kambham, Jonathan Feazell, George P Yang, Albert Koong, Amato J Giaccia

Open access · bronzeAbstract read
In one paragraph

Article in Cancer research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 96 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
96citing papers in PubMed, 2 pooled it
4.7field-weighted citation impact, top 4% 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

96 citing papers in PubMed, 2 syntheses or guidelines pooled it, 142 citations in OpenAlex.

  1. Pooled it
  2. Loss of HNF6 expression correlates with human pancreatic cancer progression.Laboratory investigation; a journal of technical methods and pathology · 2014
    Pooled it
  3. Article
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  11. Pancreatic cancer: new approaches to drug therapy.International journal of surgery (London, England) · 2024
    Review
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  14. Article
  15. Review
  16. Journal of oncology · 2022
    Article
  17. Article
  18. Review
  19. Review
  20. Article

36 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

10 authors at 2 institutions in 1 country.

Kevin L BennewithDepartment of Radiation Oncology, Stanford University School of Medicine, Stanford, California, USA.
Xin Huang
Christine M Ham
Edward E Graves
Janine T Erler
Neeraja Kambham
Jonathan Feazell
George P Yang
Albert Koong
Amato J Giaccia
Molecular Oncology (United States) · USStanford University · US

Funding

TUMOR BIOLOGYT32CA009151 · NCI · STANFORD UNIVERSITY · PI CLEARY, MICHAEL L · 1985 to 2014
$5.5M
CTGF in Pancreatic Tumor GrowthR01CA116685 · NCI · STANFORD UNIVERSITY · PI GIACCIA, AMATO J. · 2006 to 2010
$1.3M
NCI NIH HHS R01 CA116685NCI NIH HHS T32 CA009151
6 · The paper itself

Abstract

Pancreatic cancer is highly aggressive and refractory to existing therapies. Connective tissue growth factor (CTGF/CCN2) is a fibrosis-related gene that is thought to play a role in pancreatic tumor progression. However, CCN2 can be expressed in a variety of cell types, and the contribution of CCN2 derived from either tumor cells or stromal cells as it affects the growth of pancreatic tumors is unknown. Using genetic inhibition of CCN2, we have discovered that CCN2 derived from tumor cells is a critical regulator of pancreatic tumor growth. Pancreatic tumor cells derived from CCN2 shRNA-expressing clones showed dramatically reduced growth in soft agar and when implanted s.c. We also observed a role for CCN2 in the growth of pancreatic tumors implanted orthotopically, with tumor volume measurements obtained by positron emission tomography imaging. Mechanistically, CCN2 protects cells from hypoxia-mediated apoptosis, providing an in vivo selection for tumor cells that express high levels of CCN2. We found that CCN2 expression and secretion was increased in hypoxic pancreatic tumor cells in vitro, and we observed colocalization of CCN2 and hypoxia in pancreatic tumor xenografts and clinical pancreatic adenocarcinomas. Furthermore, we found increased CCN2 staining in clinical pancreatic tumor tissue relative to stromal cells surrounding the tumor, supporting our assertion that tumor cell-derived CCN2 is important for pancreatic tumor growth. Taken together, these data improve our understanding of the mechanisms responsible for pancreatic tumor growth and progression, and also indicate that CCN2 produced by tumor cells represents a viable therapeutic target for the treatment of pancreatic cancer.

Indexed as

AdenocarcinomaAnimalsCell Growth ProcessesCell HypoxiaConnective Tissue Growth FactorFluorodeoxyglucose F18HumansMaleMiceMice, NudePancreatic NeoplasmsPositron-Emission TomographyRadiopharmaceuticalsRNA, Small InterferingTransfectionTransplantation, HeterologousCCN2 protein, humanConnective Tissue Growth FactorFluorodeoxyglucose F18RadiopharmaceuticalsRNA, Small Interfering

Identifiers

PMID19179545
PMCPMC2747032
OpenAlexW2132445818

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.