Evidence map›Paper›PMID 25328138›Full record

ReviewOncogene2015

Topoisomerase IIα in chromosome instability and personalized cancer therapy.

T Chen, Y Sun, P Ji, S Kopetz, W Zhang

Open access · greenAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Oncogene, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 127 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
127citing papers in PubMed, 2 pooled it
5.3field-weighted citation impact, top 4% 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

127 citing papers in PubMed, 2 syntheses or guidelines pooled it, 210 citations in OpenAlex.

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67 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

5 authors at 2 institutions in 2 countries.

T Chen1] Department of Pathology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA [2] Department of Endoscopy Center, Zhongshan Hospital, Fudan University, Shanghai, China.
Y SunDepartment of Pathology, Tianjin Medical University Cancer Institute and Hospital, Tianjin, China.
P JiDepartment of Pathology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
S KopetzDepartment of Gastrointestinal Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
W ZhangDepartment of Pathology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
The University of Texas MD Anderson Cancer Center · USTianjin Medical University Cancer Institute and Hospital · CN

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Fabien Delerue · 1985 to 2026
$290.8M
NCI NIH HHS CA16672NCI NIH HHS P30 CA016672
6 · The paper itself

Abstract

Genome instability is a hallmark of cancer cells. Chromosome instability (CIN), which is often mutually exclusive from hypermutation genotypes, represents a distinct subtype of genome instability. Hypermutations in cancer cells are due to defects in DNA repair genes, but the cause of CIN is still elusive. However, because of the extensive chromosomal abnormalities associated with CIN, its cause is likely a defect in a network of genes that regulate mitotic checkpoints and chromosomal organization and segregation. Emerging evidence has shown that the chromosomal decatenation checkpoint, which is critical for chromatin untangling and packing during genetic material duplication, is defective in cancer cells with CIN. The decatenation checkpoint is known to be regulated by a family of enzymes called topoisomerases. Among them, the gene encoding topoisomerase IIα (TOP2A) is commonly altered at both gene copy number and gene expression level in cancer cells. Thus, abnormal alterations of TOP2A, its interacting proteins, and its modifications may have a critical role in CIN in human cancers. Clinically, a large arsenal of topoisomerase inhibitors has been used to suppress DNA replication in cancer. However, they often lead to the secondary development of leukemia because of their effect on the chromosomal decatenation checkpoint. Therefore, topoisomerase drugs must be used judiciously and administered on an individual basis. In this review, we highlight the biological function of TOP2A in chromosome segregation and the mechanisms that regulate this enzyme's expression and activity. We also review the roles of TOP2A and related proteins in human cancers, and raise a perspective for how to target TOP2A in personalized cancer therapy.

Indexed as

Chromosomal InstabilityAnimalsAntigens, NeoplasmChromosome SegregationDisease ProgressionDNA-Binding ProteinsDNA Topoisomerases, Type IIHumansNeoplasmsPoly-ADP-Ribose Binding ProteinsPrecision MedicineTopoisomerase II InhibitorsAntigens, NeoplasmDNA-Binding ProteinsDNA Topoisomerases, Type IIPoly-ADP-Ribose Binding ProteinsTOP2A protein, humanTopoisomerase II Inhibitors

Identifiers

PMID25328138
PMCPMC4404185
OpenAlexW2006226275

What OpenQuestion holds

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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.