Evidence map›Paper›PMID 24605290›Full record

ArticleTranslational cancer research2013

Hematopoietic stem cell senescence and cancer therapy-induced long-term bone marrow injury.

Lijian Shao, Yingying Wang, Jianhui Chang, Yi Luo, Aimin Meng, Daohong Zhou

Open access · greenAbstract read
In one paragraph

Article in Translational cancer research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
1.8field-weighted citation impact, top 16% 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

45 citing papers in PubMed, 73 citations in OpenAlex.

  1. Trial
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  7. Deinoxanthin Recovers HAntioxidants (Basel, Switzerland) · 2025
    Article
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  12. CHIP: a clonal odyssey of the bone marrow niche.The Journal of clinical investigation · 2024
    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

6 authors at 1 institution in 1 country.

Lijian ShaoDivision of Radiation Health, Department of Pharmaceutical Sciences, University of Arkansas for Medical Sciences, Little Rock, Arkansas 72205, USA.
Yingying WangDivision of Radiation Health, Department of Pharmaceutical Sciences, University of Arkansas for Medical Sciences, Little Rock, Arkansas 72205, USA ; Department of Biochemistry and Molecular Biology, Institute of Radiation Medicine, Chinese Academy of Medical Sciences, Tianjin 300192, China.
Jianhui ChangDivision of Radiation Health, Department of Pharmaceutical Sciences, University of Arkansas for Medical Sciences, Little Rock, Arkansas 72205, USA.
Yi LuoDivision of Radiation Health, Department of Pharmaceutical Sciences, University of Arkansas for Medical Sciences, Little Rock, Arkansas 72205, USA.
Aimin MengDepartment of Biochemistry and Molecular Biology, Institute of Radiation Medicine, Chinese Academy of Medical Sciences, Tianjin 300192, China.
Daohong ZhouDivision of Radiation Health, Department of Pharmaceutical Sciences, University of Arkansas for Medical Sciences, Little Rock, Arkansas 72205, USA.
University of Arkansas for Medical Sciences · US

Funding

Cancer Therapy-induced Long-term Bone Marrow InjuryR01CA122023 · NCI · UNIV OF ARKANSAS FOR MED SCIS · PI ZHOU, DAOHONG · 2007 to 2018
$3.1M
Role of p38 MAPK in HSC Self-Renewal and Radiation-Induced Bone Marrow InjuryR01AI080421 · NIAID · UNIV OF ARKANSAS FOR MED SCIS · PI ZHOU, DAOHONG · 2008 to 2012
$1.8M
NCI NIH HHS R01 CA122023NIAID NIH HHS R01 AI080421
6 · The paper itself

Abstract

Due to improvements in early detection and treatment of cancer, the number of long-term cancer survivors is increasing. Unfortunately, these survivors are at increased risk for developing cancer treatment-related late effects, including ionizing radiation (IR)- and chemotherapy-induced long-term bone marrow (LT-BM) injury. Because LT-BM injury can deteriorate over time or after the patients receiving additional cancer treatment or undergoing autologous BM transplantation, it may eventually lead to the development of hypoplastic anemia or myelodysplastic syndrome. This review is to provide a survey of some of these recent findings regarding the underlying mechanisms by which IR and chemotherapy cause LT-BM injury. Particularly, we will highlight the discoveries of the role of reactive oxygen species in regulating HSC self-renewal and the role of oxidative stress in mediating IR- and chemotherapy-induced HSC senescence and LT-BM injury. These discoveries may lead to the development of new therapeutic strategies that have the potential to reduce the late adverse effects of conventional cancer therapy on the hematopoietic system in long-term cancer survivors.

Indexed as

bone marrowchemotherapyHematopoietic stem cellionizing radiationsenescencesuppression

Identifiers

PMID24605290
PMCPMC3941916
OpenAlexW1960445947

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.