Evidence map›Paper›PMID 21822499›Full record

ArticleAmerican journal of cancer research2011

Direct evidence for lineage-dependent effects of bone marrow stromal cells on tumor progression.

Michelle R Dawson, Sung-Suk Chae, Rakesh K Jain, Dan G Duda

Abstract read
In one paragraph

Article in American journal of cancer research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
–field-weighted citation impact
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

22 citing papers in PubMed.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. Multiple myeloma in the marrow: pathogenesis and treatments.Annals of the New York Academy of Sciences · 2016
    Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Could cancer initiate from bone marrow progenitors?Iranian journal of cancer prevention · 2013
    Review
  18. Article
  19. Article
  20. 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.

Michelle R DawsonSteele Laboratory for Tumor Biology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
Sung-Suk Chae
Rakesh K Jain
Dan G Duda

Funding

Vascular Normalization: Rolse of Perivascular CellsP01CA080124 · NCI · MASSACHUSETTS GENERAL HOSPITAL · PI JAIN, RAKESH K. · 2000 to 2016
$35.0M
Integrative Biology of Tumor MetastasisR01CA085140 · NCI · MASSACHUSETTS GENERAL HOSPITAL · PI JAIN, RAKESH K. · 2005 to 2009
$8.6M
Probing Tumor Microenvironment Using NanotechnologyR01CA126642 · NCI · MASSACHUSETTS GENERAL HOSPITAL · PI JAIN, RAKESH K. · 2008 to 2012
$8.3M
Training Program in Pathophysiology of Solid TumorsT32CA073479 · NCI · MASSACHUSETTS GENERAL HOSPITAL · PI JAIN, RAKESH K. · 1998 to 2012
$3.0M
Role of BMDCs in Solid Tumor Growth and RelapseR01CA115767 · NCI · MASSACHUSETTS GENERAL HOSPITAL · PI JAIN, RAKESH K. · 2006 to 2010
$2.2M
Role of SDF1a pathway in prostate cancer relapse and metastasis post-radiotherapyR01CA159258 · NCI · MASSACHUSETTS GENERAL HOSPITAL · PI DUDA, DAN GABRIEL · 2011 to 2015
$1.6M
Visualizing Immune Responses in vivo: a systems biology approachR21CA139168 · NCI · MASSACHUSETTS GENERAL HOSPITAL · PI DUDA, DAN GABRIEL · 2009 to 2010
$412k
NCI NIH HHS P01 CA080124NCI NIH HHS R01 CA085140NCI NIH HHS R01 CA115767NCI NIH HHS R01 CA126642NCI NIH HHS R01 CA159258NCI NIH HHS R21 CA139168NCI NIH HHS T32 CA073479
6 · The paper itself

Abstract

We sought to characterize the function of bone marrow stromal cell (BMSC) populations in tumor progression. Because this function may depend on the cell-lineage and mouse strain heterogeneity, we first characterized ex vivo the BMSCs harvested from C57BL/6 versus FVB mice and established their in vivo function in tumor growth and metastasis experiments. All plastic-adherent BMSCs expressed platelet-derived growth factor receptor beta (PDGFRβ) and stem cell antigen 1 (Sca1), consistent with a mesenchymal precursor phenotype, as well as CD80. Moreover, these BMSCs were capable of differentiation along mesenchymal lineage into adipocytes, osteoblasts, chondrocytes or myofibroblasts. However, further phenotypic analysis detected a distinct populations of myeloid (CD11b(+)) precursor cells amongst the ex vivo expanded BMSCs -with specific surface marker phenotypes and gene expression pattern. When co-implanted with metastatic cancer cells, all the BMSCs persisted and integrated into tumor stroma, but only myeloid BMSCs significantly promoted tumor growth and metastasis. These data demonstrate the differential effect of BMSCs sub-populations on tumor progression. These results may have important implications for anti-tumor therapy and for the use of mesenchymal BMSCs as cell-based therapies.

Indexed as

bone marrow-derived cellsmesenchymalmetastasisMyeloidtumor

Identifiers

PMID21822499
PMCPMC3150110

What OpenQuestion holds

Textmetadata
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.