Evidence map›Paper›PMID 24397478›Full record

ReviewRadiation research2014

DNA damage response genes and the development of cancer metastasis.

Constantinos G Broustas, Howard B Lieberman

Open access · bronzeAbstract readReview
In one paragraph

Review in Radiation research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 147 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
147citing papers in PubMed, 1 pooled it
6.1field-weighted citation impact, top 3% 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

147 citing papers in PubMed, 1 synthesis or guideline pooled it, 265 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Trial
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  7. Article
  8. Telomerase mRNA therapy protects human skin against radiation-induced DNA damage.Molecular therapy : the journal of the American Society of Gene Therapy · 2026
    Article
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  10. Review
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  14. Association of hTERT MNS16A polymorphism with clinical outcomes of North Indian lung cancer patients undergoing platinum-based doublet chemotherapy.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2025
    Article
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  16. Review
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  19. Article
  20. Article

87 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

2 authors at 1 institution in 1 country.

Constantinos G Broustasa Center for Radiological Research, Columbia University College of Physicians and Surgeons, New York, New York 10032.
Howard B Lieberman
Columbia University · US

Funding

THE FUNCTIONAL GENOMICS OF BYSTANDER RESPONSESP01CA049062 · NCI · COLUMBIA UNIV NEW YORK MORNINGSIDE · PI HEI, TOM K. · 1990 to 2014
$21.9M
Mechanisms of Radioresistance and Cell Cycle ProgressionR01CA130536 · NCI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI LIEBERMAN, HOWARD B. · 2007 to 2016
$3.5M
The MRAD9 Radioresistance GeneR01GM079107 · NIGMS · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI LIEBERMAN, HOWARD B. · 2006 to 2013
$2.6M
NCI NIH HHS P01 CA049062NCI NIH HHS P01CA49062NCI NIH HHS R01 CA130536NCI NIH HHS R01CA130536NIGMS NIH HHS R01 GM079107NIGMS NIH HHS R01GM079107
6 · The paper itself

Abstract

DNA damage response genes play vital roles in the maintenance of a healthy genome. Defects in cell cycle checkpoint and DNA repair genes, especially mutation or aberrant downregulation, are associated with a wide spectrum of human disease, including a predisposition to the development of neurodegenerative conditions and cancer. On the other hand, upregulation of DNA damage response and repair genes can also cause cancer, as well as increase resistance of cancer cells to DNA damaging therapy. In recent years, it has become evident that many of the genes involved in DNA damage repair have additional roles in tumorigenesis, most prominently by acting as transcriptional (co-)factors. Although defects in these genes are causally connected to tumor initiation, their role in tumor progression is more controversial and it seems to depend on tumor type. In some tumors like melanoma, cell cycle checkpoint/DNA repair gene upregulation is associated with tumor metastasis, whereas in a number of other cancers the opposite has been observed. Several genes that participate in the DNA damage response, such as RAD9, PARP1, BRCA1, ATM and TP53 have been associated with metastasis by a number of in vitro biochemical and cellular assays, by examining human tumor specimens by immunohistochemistry or by DNA genome-wide gene expression profiling. Many of these genes act as transcriptional effectors to regulate other genes implicated in the pathogenesis of cancer. Furthermore, they are aberrantly expressed in numerous human tumors and are causally related to tumorigenesis. However, whether the DNA damage repair function of these genes is required to promote metastasis or another activity is responsible (e.g., transcription control) has not been determined. Importantly, despite some compelling in vitro evidence, investigations are still needed to demonstrate the role of cell cycle checkpoint and DNA repair genes in regulating metastatic phenotypes in vivo.

Indexed as

AnimalsCarcinogenesisCell Cycle CheckpointsDNA DamageDNA RepairHumansNeoplasm MetastasisNeoplasms

Identifiers

PMID24397478
PMCPMC4064942
OpenAlexW2120211376

What OpenQuestion holds

Textmetadata
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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.