Evidence map›Paper›PMID 24338942›Full record

ReviewThe British journal of radiology2014

Vasculogenesis: a crucial player in the resistance of solid tumours to radiotherapy.

J M Brown

Abstract readReview
In one paragraph

Review in The British journal of radiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

59 citing papers in PubMed, 101 citations in OpenAlex.

  1. Trial
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  3. Macrophage Exclusion after Radiation Therapy (MERT): A First in Human Phase I/II Trial using a CXCR4 Inhibitor in Glioblastoma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2019
    Trial
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  10. TNFSF15 facilitates the differentiation of CD11bCancer biology & medicine · 2023
    Article
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  13. 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

1 author at 1 institution in 1 country.

J M BrownDivision of Radiation and Cancer Biology, Department of Radiation Oncology, Stanford University, Stanford, CA, USA.
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 1R01 CA149318NCI NIH HHS R01 CA128873
6 · The paper itself

Abstract

Tumours have two main ways to develop a vasculature: by angiogenesis, the sprouting of endothelial cells from nearby blood vessels, and vasculogenesis, the formation of blood vessels from circulating cells. Because tumour irradiation abrogates local angiogenesis, the tumour must rely on the vasculogenesis pathway for regrowth after irradiation. Tumour irradiation produces a marked influx of CD11b(+) myeloid cells (macrophages) into the tumours, and these are crucial to the formation of blood vessels in the tumours after irradiation and for the recurrence of the tumours. This process is driven by increased tumour hypoxia, which increases levels of HIF-1 (hypoxia-inducible factor 1), which in turn upregulates SDF-1 (stromal cell-derived factor 1 or CXCL12), the main driver of the vasculogenesis pathway. Inhibition of HIF-1 or of its downstream target SDF-1 prevents the radiation-induced influx of the CD11b(+) myeloid cells and delays or prevents the tumours from recurring following irradiation. Others and we have shown that with a variety of tumours in both mice and rats, the inhibition of the SDF-1/CXCR4 pathway delays or prevents the recurrence of implanted or autochthonous tumours following irradiation or following treatment with vascular disrupting agents or some chemotherapeutic drugs such as paclitaxel. In addition to the recruited macrophages, endothelial progenitor cells (EPCs) are also recruited to the irradiated tumours, a process also driven by SDF-1. Together, the recruited proangiogenic macrophages and the EPCs reform the tumour vasculature and allow the tumour to regrow following irradiation. This is a new paradigm with major implications for the treatment of solid tumours by radiotherapy.

Indexed as

AnimalsChemokine CXCL12FemaleHypoxia-Inducible Factor 1MaleMiceNeoplasmsNeovascularization, PathologicRatsReceptors, CXCR4Signal TransductionStem CellsChemokine CXCL12Hypoxia-Inducible Factor 1Receptors, CXCR4

Identifiers

PMID24338942
PMCPMC4064599
OpenAlexW2141489792

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.