Evidence map›Paper›PMID 8644848›Full record

ArticleThe American journal of pathology1996

Strong expression of kinase insert domain-containing receptor, a vascular permeability factor/vascular endothelial growth factor receptor in AIDS-associated Kaposi's sarcoma and cutaneous angiosarcoma.

L F Brown, K Tognazzi, H F Dvorak, T J Harrist

Abstract read
In one paragraph

Article in The American journal of pathology, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
4.8field-weighted citation impact, top 5% 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

29 citing papers in PubMed, 109 citations in OpenAlex.

  1. Trial
  2. Phase II study of bevacizumab in patients with HIV-associated Kaposi's sarcoma receiving antiretroviral therapy.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2012
    Trial
  3. Trial
  4. Review
  5. Article
  6. Review
  7. Review
  8. Expression of angiopoietin-TIE system components in angiosarcoma.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2013
    Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
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  15. Article
  16. Article
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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 1 institution in 1 country.

L F BrownDepartment of Pathology, Beth Israel Hospital, Boston, Massachusetts 02215, USA.
K Tognazzi
H F Dvorak
T J Harrist
Beth Israel Deaconess Hospital · US

Funding

PERMSELECTIVE PROPERTIES OF TUMOR AND WOUND BLOOD VESSELR01CA050453 · NCI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI DVORAK, HAROLD FISHER · 1989 to 2004
$1.8M
PATHOGENESIS OF TUMOR STROMA GENERATION &WOUND HEALINGR01CA058845 · NCI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI DVORAK, HAROLD FISHER · 1993 to 1997
–
NCI NIH HHS CA50453NCI NIH HHS CA58845
6 · The paper itself

Abstract

Vascular permeability factor (VPF), also known as vascular endothelial growth factor (VEGF), plays an important role in the angiogenesis associated with the growth of many human and animal tumors. VPF/VEGF stimulates endothelial cell growth and increases microvascular permeability by interacting with two endothelial cell tyrosine kinase receptors, KDR and flt-1. We studied 16 cases of AIDS-associated Kaposi's sarcoma (KS), 2 cases of cutaneous angiosarcoma, and 6 cases of capillary hemangioma by in situ hybridization for expression of VPF/VEGF, KDR, and flt-1 mRNAs. We also performed immunohistochemical staining for VPF/VEGF protein in 15 cases. Tumor cells in KS and angiosarcoma strongly expressed KDR but not flt-1 mRNA. Endothelial cells in small stromal vessels in and around these tumors strongly expressed both KDR and flt-1 mRNAs. Tumor cells expressed VPF/VEGF mRNA strongly in only one case of KS, adjacent to an area of necrosis. This was also the only case in which the tumor cells stained substantially for VPF/VEGF protein. VPF/VEGF mRNA and protein were, however, strongly expressed by squamous epithelium in areas of hyperplasia and near areas of ulceration overlying tumors. VPF/VEGF mRNA was also expressed focally at lower levels by infiltrating inflammatory cells, probably macrophages. The strong expression of both KDR and flt-1 in small stromal vessels in and around tumors suggests that VPF/VEGF may be an important regulator of the edema and angiogenesis seen in these tumors. The strong expression of KDR by tumor cells in KS and angiosarcoma implies that VPF/VEGF may also have a direct effect on tumor cells. Tumor cells in four of six capillary hemangiomas strongly expressed both KDR and flt-1 mRNAs in contrast to the high level expression of only KDR observed in the malignant vascular tumors studied. Neither VPF/VEGF mRNA or protein were strongly expressed in capillary hemangiomas. VPF/VEGF and its receptors may play an important but as yet incompletely understood role in the pathogenesis of both benign and malignant vascular tumors.

Indexed as

Acquired Immunodeficiency SyndromeCapillary PermeabilityEndothelial Growth FactorsHemangioma, CapillaryHemangiosarcomaHumansLymphokinesReceptor Protein-Tyrosine KinasesReceptors, Growth FactorReceptors, Vascular Endothelial Growth FactorSarcoma, KaposiSkin NeoplasmsVascular Endothelial Growth Factor AVascular Endothelial Growth FactorsEndothelial Growth FactorsLymphokinesReceptor Protein-Tyrosine KinasesReceptors, Growth FactorReceptors, Vascular Endothelial Growth FactorVascular Endothelial Growth Factor AVascular Endothelial Growth Factors

Identifiers

PMID8644848
PMCPMC1861515
OpenAlexW101219436

What OpenQuestion holds

Textmetadata
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Registered trials

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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.