Evidence map›Paper›PMID 16114062›Full record

ArticleThe Prostate2006

Integrin-dependent amplification of the G2 arrest induced by ionizing radiation.

Celeste L Kremer, Monika Schmelz, Anne E Cress

Open access · greenAbstract read
In one paragraph

Article in The Prostate, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
2.4field-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

12 citing papers in PubMed, 20 citations in OpenAlex.

  1. Beyond DNA damage: 3D tumor models and the integrin mechanobiology of radioresistance.Journal of experimental & clinical cancer research : CR · 2026
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  11. The tumor microenvironment is a dominant force in multidrug resistance.Drug resistance updates : reviews and commentaries in antimicrobial and anticancer chemotherapy
    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

3 authors at 1 institution in 1 country.

Celeste L KremerArizona Cancer Center, University of Arizona, Tucson, Arizona 85724, USA.
Monika Schmelz
Anne E Cress
University of Arizona · US

Funding

VITAMIN AP30CA023074 · NCI · UNIVERSITY OF ARIZONA · PI Dan Theodorescu · 1985 to 2026
$110.2M
Integrative Cancer Scholars Training GrantT32CA009213 · NCI · UNIVERSITY OF ARIZONA · PI CAREW, JENNIFER S, CURIEL-LEWANDROWSKI, CLARA · 1985 to 2024
$8.6M
Cancer Prevention and Control Translational ResearchR25CA078447 · NCI · UNIVERSITY OF ARIZONA · PI ALBERTS, DAVID SAMUEL · 1998 to 2014
$7.6M
RADIATION SIGNALING THROUGH THE ALPHA6 BETA4 INTEGRINR01CA075152 · NCI · UNIVERSITY OF ARIZONA · PI CRESS, ANNE ELIZABETH · 1998 to 2005
$1.5M
Cancer Prevention and Control Health Disparities Training ProgramT32CA078447 · NCI · UNIVERSITY OF ARIZONA · PI ALBERTS, DAVID SAMUEL, HARRIS, ROBIN B · 2016 to 2020
$1.2M
NCI NIH HHS CA23074NCI NIH HHS CA75152NCI NIH HHS CA78447NCI NIH HHS P30 CA023074NCI NIH HHS R01 CA075152NCI NIH HHS R25 CA078447NCI NIH HHS T32 CA009213NCI NIH HHS T32 CA078447NCI NIH HHS T32CA09213
6 · The paper itself

Abstract

The progressive loss of laminin 5 and the alpha6beta4 integrin is a characteristic of the transition of prostatic intraepithelial neoplasia (PIN) to invasive human prostate cancer. Our objective was to determine if the loss of the interaction with laminin 5 would influence the ability of human epithelial cells to respond to DNA damage. Three cellular damage responses to ionizing radiation (IR) were analyzed including G2 progression, cdc2 phosphorylation, and cell survival. The adhesion of normal human prostate epithelial cells to laminin 5 amplified the G2 arrest induced by IR, and depends on a known cell binding domain of laminin 5. The alteration of G2 arrest was confirmed by an inhibition of phospho-cdc2 nuclear translocation. In contrast, a prostate epithelial cancer cell line blocked in G2 independent of adhesion to laminin 5. The survival of these cell lines in response to IR was unaffected by adhesion to laminin 5. These results suggest that cell adhesion to laminin 5 in normal cells will amplify the IR induced G2 cell cycle progression block without altering cell survival. The loss of laminin 5 and the alpha6beta4 integrin in PIN lesions may contribute to the selection and progression of genetically unstable cell types via attenuation of a DNA damage induced G2 arrest.

Indexed as

Cell AdhesionCell LineDNA DamageDose-Response Relationship, RadiationEpithelial CellsG2 PhaseHumansIntegrin alpha6beta4IntegrinsMaleProstateRadiation, IonizingIntegrin alpha6beta4Integrins

Identifiers

PMID16114062
PMCPMC2732347
OpenAlexW2077216855

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.