Evidence map›Paper›PMID 12003665›Full record

ReviewJournal of cellular and molecular medicine

Thrombospondin-1 as an endogenous inhibitor of angiogenesis and tumor growth.

Jack Lawler

Open access · bronzeAbstract readReview
In one paragraph

Review in Journal of cellular and molecular medicine. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 232 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
232citing papers in PubMed, 1 pooled it
9.0field-weighted citation impact, top 1% 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

232 citing papers in PubMed, 1 synthesis or guideline pooled it, 543 citations in OpenAlex.

  1. Pooled it
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  5. THBS1: a biomarker for PCOS and its role in pathogenesis via the PI3K/AKT signaling pathway.Mammalian genome : official journal of the International Mammalian Genome Society · 2026
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172 more citing papers are in PubMed but not listed here.

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

1 author at 1 institution in 1 country.

Jack LawlerDepartment of Pathology, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA 02215, USA. jlawler@caregroup.harvard.edu
Beth Israel Deaconess Medical Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Thrombospondin-1 (TSP-1) is a matricellular glycoprotein that influences cellular phenotype and the structure of the extracellular matrix. These effects are important components of the tissue remodeling that is associated with angiogenesis and neoplasia. The genetic mutations in oncogenes and tumor suppressor genes that occur within tumor cells are frequently associated with decreased expression of TSP-1. However, the TSP-1 that is produced by stromal fibroblasts, endothelial cells and immune cells suppresses tumor progression. TSP-1 inhibits angiogenesis through direct effects on endothelial cell migration and survival and through indirect effects on growth factor mobilization. TSP-1 that is present in the tumor microenvironment also acts to suppress tumor cell growth through activation of transforming growth factor beta in those tumor cells that are responsive to TGF beta. In this review, the molecular basis for the role of TSP-1 in the inhibition of tumor growth and angiogenesis is summarized.

Indexed as

Neovascularization, PathologicNeovascularization, PhysiologicAmino Acid SequenceAngiogenesis InhibitorsAnimalsAntineoplastic AgentsCell DivisionDisease ProgressionEnzyme InhibitorsModels, BiologicalMolecular Sequence DataNeoplasmsThrombospondin 1Transforming Growth Factor betaAngiogenesis InhibitorsAntineoplastic AgentsEnzyme InhibitorsThrombospondin 1Transforming Growth Factor beta

Identifiers

PMID12003665
PMCPMC6740251
OpenAlexW2081471836

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.