Evidence map›Paper›PMID 25569081›Full record

ReviewInternational journal of molecular sciences2015

Potential relationship between inadequate response to DNA damage and development of myelodysplastic syndrome.

Ting Zhou, Peishuai Chen, Jian Gu, Alexander J R Bishop, Linda M Scott, Paul Hasty, Vivienne I Rebel

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2015. 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
1.5field-weighted citation impact, top 18% 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, 26 citations in OpenAlex.

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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

7 authors at 4 institutions in 3 countries.

Ting ZhouGreehey Children's Cancer Research Center, University of Texas Health Science Center San Antonio (UTHSCSA), 8403 Floyd Curl Drive, San Antonio, TX 78229, USA. zhoubaipi@gmail.com.
Peishuai ChenGreehey Children's Cancer Research Center, University of Texas Health Science Center San Antonio (UTHSCSA), 8403 Floyd Curl Drive, San Antonio, TX 78229, USA. ChenP3@uthscsa.edu.
Jian GuDepartment of Hematology, Northern Jiangsu People's Hospital, Yangzhou 225001, China. gujianyz@sina.com.
Alexander J R BishopGreehey Children's Cancer Research Center, University of Texas Health Science Center San Antonio (UTHSCSA), 8403 Floyd Curl Drive, San Antonio, TX 78229, USA. bishopa@uthscsa.edu.
Linda M ScottThe University of Queensland Diamantina Institute, Translational Research Institute, 37 Kent Street, Woolloongabba, QLD 4102, Australia. l.scott3@uq.edu.au.
Paul HastyThe Cancer Therapy Research Center, UTHSCSA, 7979 Wurzbach Road, San Antonio, TX 78229, USA. hastye@uthscsa.edu.
Vivienne I RebelGreehey Children's Cancer Research Center, University of Texas Health Science Center San Antonio (UTHSCSA), 8403 Floyd Curl Drive, San Antonio, TX 78229, USA. rebel@uthscsa.edu.
Cancer Research Center · USThe University of Texas Health Science Center at San Antonio · USNorthern Jiangsu People's Hospital · CNTranslational Research Institute · AU

Funding

Institute for Integration of Medicine & Science: A Partnership to Improve HealthUL1TR001120 · NCATS · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI CLARK, ROBERT A, HARGREAVES, KENNETH M · 2013 to 2017
$16.5M
How does TREX2 maintain and alter chromosomes?R01CA188032 · NCI · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI HASTY, EDWARD PAUL, MONTAGNA, CRISTINA · 2014 to 2018
$1.8M
Study DNA repair in preventing MDS and AML after radiation and benzene exposureR01ES022054 · NIEHS · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI HASTY, EDWARD PAUL · 2012 to 2016
$1.7M
NCATS NIH HHS UL1 TR001120NCI NIH HHS R01 CA188032NIEHS NIH HHS R01 ES022054
6 · The paper itself

Abstract

Hematopoietic stem cells (HSCs) are responsible for the continuous regeneration of all types of blood cells, including themselves. To ensure the functional and genomic integrity of blood tissue, a network of regulatory pathways tightly controls the proliferative status of HSCs. Nevertheless, normal HSC aging is associated with a noticeable decline in regenerative potential and possible changes in other functions. Myelodysplastic syndrome (MDS) is an age-associated hematopoietic malignancy, characterized by abnormal blood cell maturation and a high propensity for leukemic transformation. It is furthermore thought to originate in a HSC and to be associated with the accrual of multiple genetic and epigenetic aberrations. This raises the question whether MDS is, in part, related to an inability to adequately cope with DNA damage. Here we discuss the various components of the cellular response to DNA damage. For each component, we evaluate related studies that may shed light on a potential relationship between MDS development and aberrant DNA damage response/repair.

Indexed as

DNA DamageAgingDNA GlycosylasesDNA RepairEpigenesis, GeneticGenomic InstabilityHematopoietic Stem CellsHumansMyelodysplastic SyndromesDNA Glycosylasesoxoguanine glycosylase 1, human

Identifiers

PMID25569081
PMCPMC4307285
OpenAlexW2011345939

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.