Evidence map›Paper›PMID 16990761›Full record

ReviewLeukemia2007

The history of the angiogenic switch concept.

D Ribatti, B Nico, E Crivellato, A M Roccaro, A Vacca

Abstract readReview
PubMed Publisher
In one paragraph

Review in Leukemia, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 99 papers.

0numbers the graph read from it
0cells of the map it votes in
99citing papers in PubMed
5.2field-weighted citation impact, top 4% 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

99 citing papers in PubMed, 250 citations in OpenAlex.

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  11. Tryptase and tumor angiogenesis.Frontiers in oncology · 2024
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39 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

5 authors at 2 institutions in 1 country.

D RibattiDepartment of Human Anatomy and Histology, University of Bari Medical School, Bari, Italy. ribatti@anatomia.uniba.it
B Nico
E Crivellato
A M Roccaro
A Vacca
University of Bari Aldo Moro · ITUniversity of Udine · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Spontaneously arising tumor cells are not usually angiogenic at first. The phenotypic switch to angiogenesis is usually accomplished by a substet that induces new capillaries that then converge toward the tumor. The switch clearly involves more than simple upregulation of angiogenic activity and is thought to be the result of a net balance of positive and negative regulators. Tumor growth is although to require disruption of this balance and hence this switch must turned on for cancer progression. Progenitor endothelial cells, the crosstalk between angiogenic factors and their receptors and the interaction between vasculogenesis and lymphangiogenesis are all factors that may contribute to the switch. Its promotion is also the outcome of genetic instability resulting in the emergence of tumor cell lines. This review describes the history of the angiogenic switch illustrated in the literature and with particular reference to the three transgenic mouse models, namely RIP1-TAG2, keratin-14 (K14) (human papilloma virus) HPV16 and papilloma virus, used for stage-specific assessment of the effects of antiangiogenic and antitumorigenic agents.

Indexed as

Neovascularization, PathologicAnimalsAntigens, Viral, TumorBone Marrow CellsCell Transformation, NeoplasticDisease Models, AnimalHuman papillomavirus 16HumansKeratin-14MiceMice, TransgenicNeoplasmsSignal TransductionStem CellsVascular Endothelial Growth FactorsAntigens, Viral, TumorKeratin-14Vascular Endothelial Growth Factors

Identifiers

PMID16990761
OpenAlexW2089030718

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.