Evidence map›Paper›PMID 24634660›Full record

ReviewFrontiers in physiology2014

Role of tumor associated macrophages in tumor angiogenesis and lymphangiogenesis.

Vladimir Riabov, Alexandru Gudima, Nan Wang, Amanda Mickley, Alexander Orekhov, Julia Kzhyshkowska

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 357 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
357citing papers in PubMed, 1 pooled it
18.2field-weighted citation impact, top 1% 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

357 citing papers in PubMed, 1 synthesis or guideline pooled it, 615 citations in OpenAlex.

  1. Pooled it
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  8. Therapeutic potential of targeting macrophage polarization in metastatic gastric cancer: a review on core mechanisms and clinical progress.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
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  20. Immunity and Beyond: Emerging Roles of Monocytes and Macrophages in Cancer.Advances in experimental medicine and biology · 2026
    Review

297 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

6 authors at 3 institutions in 2 countries.

Vladimir RiabovDepartment of Dermatology, University Medical Center and Medical Faculty Mannheim, Ruprecht-Karls University of Heidelberg Mannheim, Germany ; Department of Nanopathology, Institute of General Pathology and Pathophysiology, Russian Academy of Medical Sciences Moscow, Russia.
Alexandru GudimaDepartment of Dermatology, University Medical Center and Medical Faculty Mannheim, Ruprecht-Karls University of Heidelberg Mannheim, Germany ; Department of Innate Immunity and Tolerance, University Medical Center and Medical Faculty Mannheim, Institute of Transfusion Medicine and Immunology, Ruprecht-Karls University of Heidelberg Mannheim, Germany.
Nan WangDepartment of Dermatology, University Medical Center and Medical Faculty Mannheim, Ruprecht-Karls University of Heidelberg Mannheim, Germany.
Amanda MickleyDepartment of Dermatology, University Medical Center and Medical Faculty Mannheim, Ruprecht-Karls University of Heidelberg Mannheim, Germany ; Department of Innate Immunity and Tolerance, University Medical Center and Medical Faculty Mannheim, Institute of Transfusion Medicine and Immunology, Ruprecht-Karls University of Heidelberg Mannheim, Germany.
Alexander OrekhovDepartment of Nanopathology, Institute of General Pathology and Pathophysiology, Russian Academy of Medical Sciences Moscow, Russia.
Julia KzhyshkowskaDepartment of Dermatology, University Medical Center and Medical Faculty Mannheim, Ruprecht-Karls University of Heidelberg Mannheim, Germany ; Department of Nanopathology, Institute of General Pathology and Pathophysiology, Russian Academy of Medical Sciences Moscow, Russia ; Department of Innate Immunity and Tolerance, University Medical Center and Medical Faculty Mannheim, Institute of Transfusion Medicine and Immunology, Ruprecht-Karls University of Heidelberg Mannheim, Germany.
Research Institute of General Pathology and Pathophysiology, the Russian Academy of Medical Sciences · RUUniversity Hospital Heidelberg · DEUniversity Medical Centre Mannheim · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tumor angiogenesis is an essential process for supplying rapidly growing malignant tissues with essential nutrients and oxygen. An angiogenic switch allows tumor cells to survive and grow, and provides them access to vasculature resulting in metastatic disease. Monocyte-derived macrophages recruited and reprogrammed by tumor cells serve as a major source of angiogenic factors boosting the angiogenic switch. Tumor endothelium releases angiopoietin-2 and further facilitates recruitment of TIE2 receptor expressing monocytes (TEM) into tumor sites. Tumor-associated macrophages (TAM) sense hypoxia in avascular areas of tumors, and react by production of angiogenic factors such as VEGFA. VEGFA stimulates chemotaxis of endothelial cells (EC) and macrophages. In some tumors, TAM appeared to be a major source of MMP9. Elevated expression of MMP9 by TAM mediates extracellular matrix (ECM) degradation and the release of bioactive VEGFA. Other angiogenic factors released by TAM include basic fibroblast growth factor (bFGF), thymidine phosphorylase (TP), urokinase-type plasminogen activator (uPA), and adrenomedullin (ADM). The same factors used by macrophages for the induction of angiogenesis [like vascular endothelial growth factor A (VEGF-A) and MMP9] support lymphangiogenesis. TAM can express LYVE-1, one of the established markers of lymphatic endothelium. TAM support tumor lymphangiogenesis not only by secretion of pro-lymphangiogenic factors but also by trans-differentiation into lymphatic EC. New pro-angiogenic factor YKL-40 belongs to a family of mammalian chitinase-like proteins (CLP) that act as cytokines or growth factors. Human CLP family comprises YKL-40, YKL-39, and SI-CLP. Production of all three CLP in macrophages is antagonistically regulated by cytokines. It was recently established that YKL-40 induces angiogenesis in vitro and in animal tumor models. YKL-40-neutralizing monoclonal antibody blocks tumor angiogenesis and progression. The role of YKL-39 and SI-CLP in tumor angiogenesis and lymphangiogenesis remains to be investigated.

Indexed as

chitinase-like proteinLYVE-1stabilin-1TIE2 receptortumor-associated macrophagesVEGF

Identifiers

PMID24634660
PMCPMC3942647
OpenAlexW2106102605

What OpenQuestion holds

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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.