Evidence map›Paper›PMID 18167133›Full record

ReviewCancer science2008

Understanding tumor endothelial cell abnormalities to develop ideal anti-angiogenic therapies.

Kyoko Hida, Yasuhiro Hida, Masanobu Shindoh

Open access · greenAbstract readReview
In one paragraph

Review in Cancer science, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
4.4field-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

47 citing papers in PubMed, 129 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Embryonic reprogramming of the tumor vasculature reveals targets for cancer therapy.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  5. Rare Cell Population Analysis in Early-Stage Breast Cancer Patients.Breast cancer : basic and clinical research · 2025
    Article
  6. Article
  7. Turkish journal of haematology : official journal of Turkish Society of Haematology · 2024
    Article
  8. Article
  9. Review
  10. Article
  11. Antiproliferative Effect ofLife (Basel, Switzerland) · 2022
    Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Heparanase and the hallmarks of cancer.Journal of translational medicine · 2020
    Review
  17. Necrosis in the Tumor Microenvironment and Its Role in Cancer Recurrence.Advances in experimental medicine and biology · 2020
    Review
  18. Article
  19. Article
  20. 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

3 authors at 1 institution in 1 country.

Kyoko HidaDepartment of Oral Pathology and Biology, Division of Oral Pathobiological Science, Hokkaido University Graduate School, N13 W7, Kita-ku, Sapporo 060-8586, Japan. khida@den.hokudai.ac.jp
Yasuhiro Hida
Masanobu Shindoh
Hokkaido University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tumor angiogenesis is necessary for solid tumor progression and metastasis. Tumor blood vessels have been shown to differ from their normal counterparts, for example, by changes in morphology. An important concept in tumor angiogenesis is that tumor endothelial cells are assumed to be genetically normal, even though these endothelial cells are structurally and functionally abnormal. To date, many anti-angiogenic drugs have been developed, but, their therapeutic efficacy is not dramatic and they have also been reported to cause toxic side effects. To develop ideal antiangiogenic therapies, understanding tumor endothelial cell abnormalities is important. We have isolated tumor endothelial cells from mouse tumor xenografts and have shown that tumor-associated endothelial cells are abnormal. Tumor-associated endothelial cells upregulate many genes, such as epidermal growth factor receptor (EGFR). Tumor-associated endothelial cells are also more sensitive to EGF. They also have relatively large, heterogeneous nuclei. Unexpectedly, tumor endothelial cells are cytogenetically abnormal. Fluorescence in situ hybridization (FISH) analysis showed that freshly isolated uncultured tumor endothelial cells were aneuploid and had abnormal multiple centrosomes. The degree of aneuploidy was exacerbated by passage in culture. In marked contrast, freshly isolated normal skin and adipose endothelial cells were diploid. They had normal centrosomes and remained cytogenetically stable in culture even up to 20 passages. We conclude that tumor endothelial cells can acquire cytogenetic abnormalities while in the tumor microenvironment. Questions as to whether or not tumor endothelial cells become resistant to antiangiogenic drugs are thus raised. Our preliminary data show that tumor endothelial cells are more resistant to certain chemotherapeutic drugs. Studies to evaluate the mechanism for cytogenetic abnormalities in tumor endothelial cells are underway. It is becoming quite clear that the tumor vasculature is much more complex and unpredictable than initially perceived. Here, we provide an overview of the current studies on tumor endothelial cell abnormalities.

Indexed as

AneuploidyAngiogenesis InhibitorsAnimalsCell DifferentiationEndothelial CellsEndothelium, VascularHumansModels, BiologicalNeoplasmsNeoplastic Stem CellsAngiogenesis Inhibitors

Identifiers

PMID18167133
PMCPMC11159852
OpenAlexW2018009062

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.