Evidence map›Paper›PMID 9777955›Full record

ArticleThe American journal of pathology1998

Host microvasculature influence on tumor vascular morphology and endothelial gene expression.

W G Roberts, J Delaat, M Nagane, S Huang, W K Cavenee, G E Palade

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

39 citing papers in PubMed, 106 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. The role of PLVAP in endothelial cells.Cell and tissue research · 2023
    Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Review
  10. Host tissue determinants of tumour immunity.Nature reviews. Cancer · 2019
    Review
  11. Review
  12. Review
  13. Glioma: experimental models and reality.Acta neuropathologica · 2017
    Review
  14. Immunotherapeutic Targeting of Tumor-Associated Blood Vessels.Advances in experimental medicine and biology · 2017
    Review
  15. Review
  16. Review
  17. Liposomes as nanomedical devices.International journal of nanomedicine · 2015
    Review
  18. Brain tumor-targeted drug delivery strategies.Acta pharmaceutica Sinica. B · 2014
    Review
  19. 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

6 authors at 2 institutions in 1 country.

W G RobertsDepartment of Cellular and Molecular Medicine, University of California-San Diego, La Jolla, USA.
J Delaat
M Nagane
S Huang
W K Cavenee
G E Palade
University of California, San Diego · USLudwig Cancer Research · US

Funding

LOCATION OF PORE SYSTEMS IN CAPILLARY WALLSR37HL017080 · NHLBI · YALE UNIVERSITY · PI PALADE, GEORGE E · 1987 to 1996
–
NHLBI NIH HHS R37 HL17080-22
6 · The paper itself

Abstract

We have previously demonstrated that vascular endothelial growth factor-165 (VEGF), a tumor-secreted angiogenic factor, can acutely and chronically induce fenestrations in microvascular endothelium (Cancer Res 1997, 57:765-772). Because the morphology and function of microvascular endothelium differs from tissue to tissue, we undertook studies to examine whether the neovasculature in tumors also differed depending upon tumor location. Four tumor types implanted in the brain or subcutis in nude mice were studied: a murine rhabdomyosarcoma (M1S), a murine mammary carcinoma (EMT), and two human glioblastomas (U87 and U251). In addition, we studied Chinese hamster ovary cells stably transfected with human VEGF165. As previously reported, tumors grown in the subcutaneous space had a microvasculature that was fenestrated and had open endothelial gaps. The identical tumors when grown in the brain also had fenestrated endothelium and vessels with open endothelial gaps, but they were drastically reduced in occurrence. Open endothelial gaps were not seen in all tumors implanted in the brain (EMT and M1S), although fenestrated endothelium was always seen. VEGF and VEGF receptors were measured in tumors from both locations by immunoblotting and competitive polymerase chain reaction, respectively. VEGF amount was not significantly different between the tumor locations. Interestingly, total tumor vascular mRNA expression of both Flk-1 and Flt-1 was greater in tumor vessels derived from the brain compared with tumor vessels derived from subcutaneous tissues. These results demonstrate that the host microvascular environment determines the morphology and function of the tumor vasculature and that endothelia from different tissues vary in their ability to express the VEGF receptors given identical stimuli.

Indexed as

AnimalsBrain NeoplasmsCHO CellsCricetinaeDNA, NeoplasmDNA PrimersEndothelial Growth FactorsEndothelium, VascularGene ExpressionGlioblastomaHumansLymphokinesMaleMammary Neoplasms, ExperimentalMiceMice, Inbred BALB CDNA, NeoplasmDNA PrimersEndothelial Growth FactorsLymphokinesProto-Oncogene ProteinsReceptor Protein-Tyrosine KinasesReceptors, Growth FactorReceptors, Vascular Endothelial Growth FactorRNA, MessengerVascular Endothelial Growth Factor AVascular Endothelial Growth Factor Receptor-1Vascular Endothelial Growth FactorsVEGFA protein, human

Identifiers

PMID9777955
PMCPMC1853053
OpenAlexW1969222099

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.