Evidence map›Paper›PMID 2786890›Full record

ArticleThe Journal of clinical investigation1989

Stimulation of human prostatic carcinoma cell growth by factors present in human bone marrow.

M Chackal-Roy, C Niemeyer, M Moore, B R Zetter

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 1989. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
5.4field-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

24 citing papers in PubMed, 133 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Synergistic effect of SCF and G-CSF on stem-like properties in prostate cancer cell lines.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2012
    Article
  6. Review
  7. Cancer to bone: a fatal attraction.Nature reviews. Cancer · 2011
    Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Spinal cord compression in prostate cancer.Journal of neuro-oncology · 1995
    Review
  18. Inhibition of tumor growth by elimination of granulocytes.The Journal of experimental medicine · 1995
    Article
  19. Prostate cancer progression. Implications of histopathology.The American journal of pathology · 1994
    Review
  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 at 3 institutions in 1 country.

M Chackal-RoyDepartment of Applied Biology, Massachusetts Institute of Technology Cambridge 02139.
C Niemeyer
M Moore
B R Zetter
Boston Children's Hospital · USDana-Farber Cancer Institute · USHarvard University · US

Funding

TUMOR INTERACTIONS WITH THE VASCULATURER37CA037393 · NCI · CHILDREN'S HOSPITAL BOSTON · PI ZETTER, BRUCE R · 1988 to 2010
$4.5M
Modulators of Prostate Cancer MetastasisR01CA037393 · NCI · CHILDREN'S HOSPITAL BOSTON · PI ZETTER, BRUCE R · 1985 to 2015
$2.6M
NCI NIH HHS CA-37393
6 · The paper itself

Abstract

Malignant prostatic carcinoma, a major cause of cancer mortality in males, most often metastasizes to secondary sites in bone. Frequently, the growth rate of the secondary tumor in bone marrow is considerably greater than that of the slowly growing primary prostatic tumor. We now report that two lines of human prostatic carcinoma cells proliferate in response to conditioned media from unstimulated human, rat, or bovine bone marrow. Nonprostatic tumor cell lines showed little or no growth response to the same medium. The proliferative activity found in bone marrow was not duplicated by any of a variety of purified growth factors including epidermal growth factor (EGF), acidic or basic fibroblast growth factor (FGF), platelet-derived growth factor (PDGF), transforming growth factor (TGF) alpha or beta, interleukins 1, 2, 3, 4 or 6, granulocyte (G), macrophage (M) or granulocyte-macrophage (GM) colony stimulating factor (CSF). Whereas a mixture of G-CSF, M-CSF, and IL 3 produced a mitogenic response in the prostatic carcinoma cells, these three factors were not present in our bone marrow samples in sufficient quantities to promote the observed proliferative response. To further identify the cellular source of the proliferative activity present in bone marrow-conditioned medium, we tested conditioned media made from human bone marrow stromal cells. The stromal cell conditioned medium stimulated increased growth of the prostatic carcinoma cells to levels equivalent to those observed with the bone marrow conditioned medium. These results suggest that novel mitogenic factors that are produced by bone marrow stromal cells and remain in the bone marrow cavity may account, in part, for the preferential growth of prostatic metastases in bone.

Indexed as

AdenocarcinomaAnimalsBone MarrowBone Marrow CellsBone NeoplasmsCattleCell LineColony-Stimulating FactorsCulture MediaEpidermal Growth FactorFibroblast Growth FactorsHumansMalePlatelet-Derived Growth FactorProstatic NeoplasmsRatsColony-Stimulating FactorsCulture MediaEpidermal Growth FactorFibroblast Growth FactorsPlatelet-Derived Growth FactorTransforming Growth Factors

Identifiers

PMID2786890
PMCPMC303950
OpenAlexW2153189056

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.