Evidence map›Paper›PMID 24012342›Full record

ReviewSeminars in radiation oncology2013

Inhibiting vasculogenesis after radiation: a new paradigm to improve local control by radiotherapy.

Brown J Martin

Abstract readReview
In one paragraph

Review in Seminars in radiation oncology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
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

21 citing papers in PubMed, 32 citations in OpenAlex.

  1. The Role ofMedicina (Kaunas, Lithuania) · 2020
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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

1 author at 1 institution in 1 country.

Brown J MartinDepartment of Radiation Oncology, Stanford University, Stanford, CA. Electronic address: mbrown@stanford.edu.
Stanford University · US

Funding

Effect of Bone Marrow Cells on the Radiosensitivity of Brain and Mouth CancersR01CA128873 · NCI · STANFORD UNIVERSITY · PI BROWN, JOHN MARTIN · 2008 to 2012
$2.5M
Development of Clinical Strategies to Prevent GBM Recurrences After RadiotherapyR01CA149318 · NCI · STANFORD UNIVERSITY · PI BROWN, JOHN MARTIN · 2011 to 2015
$2.4M
NCI NIH HHS R01 CA128873NCI NIH HHS R01 CA149318
6 · The paper itself

Abstract

Tumors are supported by blood vessels, and it has long been debated whether their response to irradiation is affected by radiation damage to the vasculature. We have shown in preclinical models that, indeed, radiation is damaging to the tumor vasculature and strongly inhibits tumor angiogenesis. However, the vasculature can recover by colonization from circulating cells, primarily proangiogenenic CD11b+ monocytes or macrophages from the bone marrow. This secondary pathway of blood vessel formation, known as vasculogenesis, thus acts to restore the tumor vasculature and allows the tumor to recur following radiation. The stimulus for the influx of these CD11b+ cells into tumors following irradiation is the increased levels of hypoxia-inducible factor-1 in the tumor due to induced tumor hypoxia secondary to blood vessel loss. This increases tumor levels of the chemokine stromal cell-derived factor-1, which has chemokine receptors CXCR4 and CXCR7 on monocytes and endothelial cells thereby capturing these cells in the tumors. The increase in CD11b+ monocytes in tumors following irradiation can be prevented using antibodies or small molecules that inhibit hypoxia-inducible factor-1 or the interaction of stromal cell-derived factor-1 with its receptors. We show that the effect of inhibiting these chemokine-chemokine receptor interactions is a marked increase in the radiation response of transplanted or chemically induced tumors in mice and rats. This strategy of inhibiting vasculogenesis following tumor irradiation is a new paradigm in radiotherapy and suggests that higher levels of local control of tumors in several sites would be achievable with this strategy.

Indexed as

AnimalsBone Marrow CellsCD11b AntigenCell HypoxiaChemokine CXCL12ChemokinesHumansHypoxia-Inducible Factor 1MacrophagesMonocytesNeoplasmsNeovascularization, PathologicCD11b AntigenChemokine CXCL12ChemokinesHypoxia-Inducible Factor 1

Identifiers

PMID24012342
PMCPMC3768004
OpenAlexW2095491230

What OpenQuestion holds

Textmetadata
LicenceTDM
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.