Evidence map›Paper›PMID 18058030›Full record

ArticleClinical & experimental metastasis2008

Analyses of the role of endogenous SPARC in mouse models of prostate and breast cancer.

Sunny Y Wong, Denise Crowley, Roderick T Bronson, Richard O Hynes

Abstract read
In one paragraph

Article in Clinical & experimental metastasis, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed, 1 pooled it
2.6field-weighted citation impact, top 12% 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

24 citing papers in PubMed, 1 synthesis or guideline pooled it, 66 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Secretome profiling ofFrontiers in oncology · 2023
    Article
  4. Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Bone matrix osteonectin limits prostate cancer cell growth and survival.Matrix biology : journal of the International Society for Matrix Biology · 2012
    Article
  14. Article
  15. Integrin β4 regulates SPARC protein to promote invasion.The Journal of biological chemistry · 2012
    Article
  16. Review
  17. Article
  18. Review
  19. Review
  20. Lymphangiogenesis and lymphatic metastasis in breast cancer.Pathophysiology : the official journal of the International Society for Pathophysiology · 2010
    Article
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.

Sunny Y WongHoward Hughes Medical Institute, Center for Cancer Research, Massachusetts Institute of Technology, 77 Massachusetts Avenue, Cambridge, MA 02139, USA.
Denise Crowley
Roderick T Bronson
Richard O Hynes
Massachusetts Institute of Technology · USTufts University · US

Funding

Tumor Cell Networks CenterU54CA112967 · NCI · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI LAUFFENBURGER, DOUGLAS A · 2004 to 2015
$26.2M
CELL-SURFACE STRUCTURE AND TRANSFORMATIONSR01CA017007 · NCI · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI HYNES, RICHARD O · 1985 to 2005
$2.9M
Howard Hughes Medical InstituteNCI NIH HHS R01 CA017007NCI NIH HHS R01CA17007NCI NIH HHS U54 CA112967NCI NIH HHS U54-CA112967
6 · The paper itself

Abstract

Secreted protein, acidic and rich in cysteine (SPARC, also known as osteonectin or BM-40) is a glycoprotein component of the extracellular matrix that has been reported to be involved with a variety of cellular processes. Although SPARC expression levels are frequently altered in a variety of tumor types, the exact implications of deregulated SPARC expression--whether it promotes, inhibits or has no effect on tumor progression--have remained unclear. Our recent gene expression analyses have shown that SPARC is significantly downregulated in highly metastatic human prostate cancer cells. To test the role of endogenous SPARC in tumorigenesis directly, we examined cancer progression and metastasis in SPARC(+/-) and SPARC(-/-) mice using two separate transgenic mouse tumor models: transgenic adenocarcinoma of the mouse prostate (TRAMP) and murine mammary tumor virus-polyoma middle T (MMTV-PyMT). Surprisingly, in both instances, we found that loss of SPARC had no significant effects on tumor initiation, progression or metastasis. Tumor angiogenesis and collagen deposition were also largely unaffected. Our results indicate that, although differential SPARC expression may be a useful marker of aggressive, metastasis-prone tumors, loss of SPARC is not sufficient either to promote or to inhibit cancer progression in two spontaneous mouse tumor models.

Indexed as

AdenocarcinomaAnimalsAntigens, Polyomavirus TransformingBreast NeoplasmsCell Line, TumorCollagenCrosses, GeneticFemaleHumansMaleMammary Tumor Virus, MouseMiceMice, TransgenicNeoplasm MetastasisNeovascularization, PathologicOsteonectinAntigens, Polyomavirus TransformingCollagenOsteonectin

Identifiers

PMID18058030
PMCPMC3252392
OpenAlexW1982822262

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.