Evidence map›Paper›PMID 22866200›Full record

ArticleGenes & cancer2011

Molecular mechanisms of tumor angiogenesis.

Safiyyah Ziyad, M Luisa Iruela-Arispe

Open access · bronzeAbstract read
In one paragraph

Article in Genes & cancer, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 108 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
108citing papers in PubMed, 1 pooled it
2.1field-weighted citation impact, top 13% 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

108 citing papers in PubMed, 1 synthesis or guideline pooled it, 215 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Article
  5. Article
  6. Cancer Metastasis: Therapeutic Challenges and Opportunities.Medical oncology (Northwood, London, England) · 2025
    Review
  7. Article
  8. Review
  9. Review
  10. Review
  11. Article
  12. Molecular docking andRSC advances · 2024
    Article
  13. Article
  14. Article
  15. Anti-angiogenic Potential of Trans-chalcone in anCardiovascular & hematological agents in medicinal chemistry · 2024
    Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. Review

48 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

2 authors at 1 institution in 1 country.

Safiyyah ZiyadDepartment of Molecular, Cell and Developmental Biology, University of California, Los Angeles (UCLA), Los Angeles, CA, USA.
M Luisa Iruela-Arispe
University of California, Los Angeles · US

Funding

UCLA NIGMS T32 Program AssessmentT32GM007185 · NIGMS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI TORRES, JORGE · 1985 to 2020
$21.7M
Notch Signaling in Vascular Development and HomeostasisR01HL085618 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI IRUELA-ARISPE, M. LUISA · 2007 to 2011
$1.9M
VEGF Signaling and Tumor MicroenvironmentR01CA126935 · NCI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI IRUELA-ARISPE, M. LUISA · 2007 to 2011
$1.4M
NCI NIH HHS R01 CA126935NHLBI NIH HHS R01 HL085618NIGMS NIH HHS T32 GM007185
6 · The paper itself

Abstract

Tumors have been recently recognized as aberrant organs composed of a complex mixture of highly interactive cells that in addition to the cancer cell include stroma (fibroblasts, adipocytes, and myofibroblasts), inflammatory (innate and adaptive immune cells), and vascular cells (endothelial and mural cells). While initially cancer cells co-opt tissue-resident vessels, the tumor eventually recruits its own vascular supply. The process of tumor neovascularization proceeds through the combined output of inductive signals from the entire cellular constituency of the tumor. During the last two decades, the identification and mechanistic outcome of signaling pathways that mediate tumor angiogenesis have been elucidated. Interestingly, many of the genes and signaling pathways activated in tumor angiogenesis are identical to those operational during developmental vascular growth, but they lack feedback regulatory control and are highly affected by inflammatory cells and hypoxia. Consequently, tumor vessels are abnormal, fragile, and hyperpermeable. The lack of hierarchy and inconsistent investment of mural cells dampen the ability of the vessels to effectively perfuse the tumor, and the resulting hypoxia installs a vicious cycle that continuously perpetuates a state of vascular inefficiency. Pharmacological targeting of blood vessels, mainly through the VEGF signaling pathway, has proven effective in normalizing tumor vessels. This normalization improves perfusion and distribution of chemotherapeutic drugs with resulting tumor suppression and moderate increase in overall survival. However, resistance to antiangiogenic therapy occurs frequently and constitutes a critical barrier in the inhibition of tumor growth. A concrete understanding of the chief signaling pathways that stimulate vascular growth in tumors and their cross-talk will continue to be essential to further refine and effectively abort the angiogenic response in cancer.

Indexed as

angiopoietinsDeltaendothelial cellsEphEphrinJaggedneovascularizationNotchRoboSlitTietumor angiogenesisVEGFVEGFR

Identifiers

PMID22866200
PMCPMC3411131
OpenAlexW2124399329

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.