Evidence map›Paper›PMID 16098182›Full record

ReviewCell proliferation2005

Cytometric assessment of DNA damage in relation to cell cycle phase and apoptosis.

Xuan Huang, H Dorota Halicka, Frank Traganos, Toshiki Tanaka, Akira Kurose, Zbigniew Darzynkiewicz

Open access · bronzeAbstract readReview
In one paragraph

Review in Cell proliferation, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.

0numbers the graph read from it
0cells of the map it votes in
66citing papers in PubMed
5.7field-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

66 citing papers in PubMed, 193 citations in OpenAlex.

  1. Trial
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  6. Tumor selective Ru(III) Schiff bases complexes with strong in vitro activity toward cisplatin-resistant MDA-MB-231 breast cancer cells.Journal of biological inorganic chemistry : JBIC : a publication of the Society of Biological Inorganic Chemistry · 2023
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6 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 2 institutions in 2 countries.

Xuan HuangBrander Cancer Research Institute, New York Medical College, Valhalla, NY 10532, USA.
H Dorota Halicka
Frank Traganos
Toshiki Tanaka
Akira Kurose
Zbigniew Darzynkiewicz
New York Medical College · USYamaguchi University · JP

Funding

PROBES FOR FLOW CYTOMETRYR01CA028704 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI DARZYNKIEWICZ, ZBIGNIEW · 1985 to 2014
$6.0M
NCI NIH HHS CA 28 704NCI NIH HHS R01 CA028704
6 · The paper itself

Abstract

Reviewed are the methods aimed to detect DNA damage in individual cells, estimate its extent and relate it to cell cycle phase and induction of apoptosis. They include the assays that reveal DNA fragmentation during apoptosis, as well as DNA damage induced by genotoxic agents. DNA fragmentation that occurs in the course of apoptosis is detected by selective extraction of degraded DNA. DNA in chromatin of apoptotic cells shows also increased propensity to undergo denaturation. The most common assay of DNA fragmentation relies on labelling DNA strand breaks with fluorochrome-tagged deoxynucleotides. The induction of double-strand DNA breaks (DSBs) by genotoxic agents provides a signal for histone H2AX phosphorylation on Ser139; the phosphorylated H2AX is named gammaH2AX. Also, ATM-kinase is activated through its autophosphorylation on Ser1981. Immunocytochemical detection of gammaH2AX and/or ATM-Ser1981(P) are sensitive probes to reveal induction of DSBs. When used concurrently with analysis of cellular DNA content and caspase-3 activation, they allow one to correlate the extent of DNA damage with the cell cycle phase and with activation of the apoptotic pathway. The presented data reveal cell cycle phase-specific patterns of H2AX phosphorylation and ATM autophosphorylation in response to induction of DSBs by ionizing radiation, topoisomerase I and II inhibitors and carcinogens. Detection of DNA damage in tumour cells during radio- or chemotherapy may provide an early marker predictive of response to treatment.

Indexed as

DNA DamageAnimalsApoptosisAtaxia Telangiectasia Mutated ProteinsCell CycleCell Cycle ProteinsCytophotometryDNA AdductsDNA-Binding ProteinsHistonesHumansPhosphorylationProtein Serine-Threonine KinasesTumor Suppressor ProteinsAtaxia Telangiectasia Mutated ProteinsATM protein, humanCell Cycle ProteinsDNA AdductsDNA-Binding ProteinsH2AX protein, humanHistonesProtein Serine-Threonine KinasesTumor Suppressor Proteins

Identifiers

PMID16098182
PMCPMC1360473
OpenAlexW2114487246

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.