Evidence map›Paper›PMID 21245938›Full record

ArticleNeoplasia (New York, N.Y.)2011

Augmented osteolysis in SPARC-deficient mice with bone-residing prostate cancer.

N Patrick McCabe, Bethany A Kerr, Maria Madajka, Amit Vasanji, Tatiana V Byzova

Open access · goldAbstract read
In one paragraph

Article in Neoplasia (New York, N.Y.), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

16 citing papers in PubMed, 26 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Genetic variant ofArchives animal breeding · 2020
    Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Prostate cancer and bone: the elective affinities.BioMed research international · 2014
    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. The interconnectedness of cancer cell signaling.Neoplasia (New York, N.Y.) · 2011
    Article
  16. Matricellular proteins as regulators of cancer metastasis to bone.Matrix biology : journal of the International Society for Matrix Biology
    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

5 authors at 2 institutions in 1 country.

N Patrick McCabeDepartment of Molecular Cardiology, Lerner Research Institute, Cleveland Clinic Foundation, Cleveland, OH 44195, USA.
Bethany A Kerr
Maria Madajka
Amit Vasanji
Tatiana V Byzova
Cleveland Clinic · USJacobs (United States) · US

Funding

Robotics CoreP30AR050953 · NIAMS · CLEVELAND CLINIC LERNER COM-CWRU · PI HASCALL, VINCENT CHARLES · 2004 to 2008
$2.9M
TRAINING PROGRAM IN VASCULAR CELL BIOLOGYT32HL007914 · NHLBI · CLEVELAND CLINIC LERNER COM-CWRU · PI PLOW, EDWARD FRANKLIN · 1999 to 2011
$2.2M
Role of Integrins and bone matrix in prostate cancerR01CA126847 · NCI · CLEVELAND CLINIC LERNER COM-CWRU · PI BYZOVA, TATIANA V · 2007 to 2011
$1.4M
The role of SPARC in prostate cancer growth in boneF32CA117246 · NCI · CLEVELAND CLINIC LERNER COM-CWRU · PI MCCABE, NOEL P · 2005 to 2007
$143k
Molecular Mechanisms of Prostate Cancer Induced Bone RemodelingF32CA142133 · NCI · CLEVELAND CLINIC LERNER COM-CWRU · PI KERR, BETHANY AMBER · 2010 to 2013
$116k
NCI NIH HHS 5F32 CA1172462NCI NIH HHS CA126847NCI NIH HHS F32 CA117246NCI NIH HHS F32 CA142133NCI NIH HHS R01 CA126847NHLBI NIH HHS T32 HL007914NIAMS NIH HHS 1P30 AR050953NIAMS NIH HHS P30 AR050953
6 · The paper itself

Abstract

Prostate cancer preferentially metastasizes to bone, which is rich in structural and matricellular proteins capable of altering prostate cancer progression. This study explores the role of the bone stromal matricellular protein SPARC (osteonectin/BM-40) in the progression of bone metastatic prostate cancer. Quantification of bone destruction analyzed by micro-computed tomography showed augmented osteoclastic resorption, characterized by decreases in several morphometric bone parameters in SPARC knock out (KO) tibiae harboring RM1 murine prostate cancer cells compared with wild type (WT) animals. Tumor progression stimulated osteoclast formation, which was augmented in SPARC KO mice. In vitro differentiation of SPARC KO osteoclasts indicated accelerated progenitor expansion and formation of tartrate-resistant acid phosphatase-positive osteoclast-like cells with increased resorptive capacity, a mechanism resulting in enhanced tumor-induced bone loss in vivo. Whereas altered bone structure due to SPARC KO played a role in increased osteolysis, the enhanced osteolysis was primarily the result of increased resorption by SPARC KO osteoclasts. Our findings indicate that bone stromal SPARC suppresses tumor-induced bone lesion expansion by limiting osteoclast maturation and function.

Indexed as

AnimalsBone NeoplasmsBone ResorptionCell CountCell DifferentiationCell ProliferationCells, CulturedCoculture TechniquesMaleMiceMice, Inbred C57BLMice, KnockoutNeoplasm TransplantationOsteoclastsOsteolysisOsteonectinOsteonectin

Identifiers

PMID21245938
PMCPMC3022426
OpenAlexW1911193638

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.