Evidence map›Paper›PMID 18670646›Full record

ArticleNeoplasia (New York, N.Y.)2008

Thrombospondin 1 and vasoactive agents indirectly alter tumor blood flow.

Jeff S Isenberg, Fuminori Hyodo, Lisa A Ridnour, Caitlin S Shannon, David A Wink, Murali C Krishna, David D Roberts

Open access · goldAbstract read
In one paragraph

Article in Neoplasia (New York, N.Y.), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.1field-weighted citation impact, top 14% 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

25 citing papers in PubMed, 41 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Functions of Thrombospondin-1 in the Tumor Microenvironment.International journal of molecular sciences · 2021
    Review
  5. Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Review
  13. Review
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. The War on Cancer rages on.Neoplasia (New York, N.Y.) · 2009
    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

7 authors at 3 institutions in 1 country.

Jeff S IsenbergLaboratory of Pathology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA.
Fuminori Hyodo
Lisa A Ridnour
Caitlin S Shannon
David A Wink
Murali C Krishna
David D Roberts
National Institutes of Health · USNational Cancer Institute · USCenter for Cancer Research · US

Funding

Cellular Interactions with ThrombospondinZIASC009172 · NCI · DIVISION OF CLINICAL SCIENCES - NCI · PI ROBERTS, DAVID D · 2009 to 2024
$17.9M
Redox Mechanism Process of Nos2 and COX2 in Stroma tumor interactionZIABC010898 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI WINK, DAVID · 2009 to 2025
$8.6M
CELLULAR INTERACTIONS WITH THROMBOSPONDINZ01SC009172 · SC · DIVISION OF CLINICAL SCIENCES - NCI · PI ROBERTS, DAVID D · 1996 to 2008
$1.7M
Redox Mechanism Process of Angiogenesis and Wound HealingZ01BC010898 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI WINK, DAVID · 2008 to 2008
$436k
Intramural NIH HHS
6 · The paper itself

Abstract

Nitric oxide (NO) plays important physiological roles in the vasculature to regulate angiogenesis, blood flow, and hemostasis. In solid tumors, NO is generally acknowledged to mediate angiogenic responses to several growth factors. This contrasts with conflicting evidence that NO can acutely increase tumor perfusion through local vasodilation or diminish perfusion by preferential relaxation of peripheral vascular beds outside the tumor. Because thrombospondin 1 (TSP1) is an important physiological antagonist of NO in vascular cells, we examined whether, in addition to inhibiting tumor angiogenesis, TSP1 can acutely regulate tumor blood flow. We assessed this activity of TSP1 in the context of perfusion responses to NO as a vasodilator and epinephrine as a vasoconstrictor. Nitric oxide treatment of wild type and TSP1 null mice decreased perfusion of a syngeneic melanoma, whereas epinephrine transiently increased tumor perfusion. Acute vasoactive responses were also independent of the level of tumor-expressed TSP1 in a melanoma xenograft, but recovery of basal perfusion was modulated by TSP1 expression. In contrast, overexpression of truncated TSP1 lacking part of its CD47 binding domain lacked this modulating activity. These data indicate that TSP1 primarily regulates long-term vascular responses in tumors, in part, because the tumor vasculature has a limited capacity to acutely respond to vasoactive agents.

Indexed as

AnimalsCell Line, TumorEpinephrineFemaleMelanoma, ExperimentalMiceMice, Inbred C57BLMice, KnockoutNitric OxideRegional Blood FlowThrombospondin 1Time FactorsVasoconstrictor AgentsVasodilator AgentsXenograft Model Antitumor AssaysEpinephrineNitric OxideThrombospondin 1Vasoconstrictor AgentsVasodilator Agents

Identifiers

PMID18670646
PMCPMC2481575
OpenAlexW1550850348

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.