Evidence map›Paper›PMID 32283668›Full record

ReviewInternational journal of molecular sciences2020

The Epigenetic Profile of Tumor Endothelial Cells. Effects of Combined Therapy with Antiangiogenic and Epigenetic Drugs on Cancer Progression.

Oskar Ciesielski, Marta Biesiekierska, Baptiste Panthu, Varvara Vialichka, Luciano Pirola, Aneta Balcerczyk

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing 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

27 citing papers in PubMed, 45 citations in OpenAlex.

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  12. Trained Innate Immunity in Animal Models of Cardiovascular Diseases.International journal of molecular sciences · 2024
    Review
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  19. Pharmacological Activities of Safflower Yellow and Its Clinical Applications.Evidence-based complementary and alternative medicine : eCAM · 2022
    Review
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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

6 authors at 2 institutions in 2 countries.

Oskar CiesielskiDepartment of Molecular Biophysics, Faculty of Biology and Environmental Protection, University of Lodz, Pomorska 141/143, 90-236 Lodz, Poland.ORCID 0000-0002-6375-338X
Marta BiesiekierskaDepartment of Molecular Biophysics, Faculty of Biology and Environmental Protection, University of Lodz, Pomorska 141/143, 90-236 Lodz, Poland.
Baptiste PanthuINSERM Unit 1060, CarMeN Laboratory, Lyon 1 University, 165 Chemin du Grand Revoyet-BP12, F-69495 Pierre Bénite CEDEX, France.
Varvara VialichkaDepartment of Molecular Biophysics, Faculty of Biology and Environmental Protection, University of Lodz, Pomorska 141/143, 90-236 Lodz, Poland.
Luciano PirolaINSERM Unit 1060, CarMeN Laboratory, Lyon 1 University, 165 Chemin du Grand Revoyet-BP12, F-69495 Pierre Bénite CEDEX, France.ORCID 0000-0001-6539-5435
Aneta BalcerczykDepartment of Molecular Biophysics, Faculty of Biology and Environmental Protection, University of Lodz, Pomorska 141/143, 90-236 Lodz, Poland.ORCID 0000-0001-8544-5778
University of Łódź · PLUniversité Claude Bernard Lyon 1 · FR

Funding

Polish Ministry of Science and Higher Education Dimond Grant: DI2018 018948
6 · The paper itself

Abstract

Tumors require a constant supply of nutrients to grow which are provided through tumor blood vessels. To metastasize, tumors need a route to enter circulation, that route is also provided by tumor blood vessels. Thus, angiogenesis is necessary for both tumor progression and metastasis. Angiogenesis is tightly regulated by a balance of angiogenic and antiangiogenic factors. Angiogenic factors of the vascular endothelial growth factor (VEGF) family lead to the activation of endothelial cells, proliferation, and neovascularization. Significant VEGF-A upregulation is commonly observed in cancer cells, also due to hypoxic conditions, and activates endothelial cells (ECs) by paracrine signaling stimulating cell migration and proliferation, resulting in tumor-dependent angiogenesis. Conversely, antiangiogenic factors inhibit angiogenesis by suppressing ECs activation. One of the best-known anti-angiogenic factors is thrombospondin-1 (TSP-1). In pathological angiogenesis, the balance shifts towards the proangiogenic factors and an angiogenic switch that promotes tumor angiogenesis. Here, we review the current literature supporting the notion of the existence of two different endothelial lineages: normal endothelial cells (NECs), representing the physiological form of vascular endothelium, and tumor endothelial cells (TECs), which are strongly promoted by the tumor microenvironment and are biologically different from NECs. The angiogenic switch would be also important for the explanation of the differences between NECs and TECs, as angiogenic factors, cytokines and growth factors secreted into the tumor microenvironment may cause genetic instability. In this review, we focus on the epigenetic differences between the two endothelial lineages, which provide a possible window for pharmacological targeting of TECs.

Indexed as

Epigenesis, GeneticEpigenomeAnimalsBiomarkers, TumorEndothelial CellsEnergy MetabolismGene Expression ProfilingGene Expression Regulation, NeoplasticHumansMolecular Targeted TherapyNeoplasm MetastasisNeoplasmsNeoplasm StagingNeovascularization, PathologicTranscriptomeBiomarkers, Tumorantiangiogenic treatmentcancerepi-drugsepigeneticsmetastasistumor endothelial cells

Identifiers

PMID32283668
PMCPMC7177242
OpenAlexW3015361294

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.