Evidence map›Paper›PMID 23684797›Full record

ReviewDNA repair2013

DNA damage response in peripheral nervous system: coping with cancer therapy-induced DNA lesions.

Ella W Englander

Open access · greenAbstract readReview
In one paragraph

Review in DNA repair, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

25 citing papers in PubMed, 50 citations in OpenAlex.

  1. Exercise alleviates cisplatin-induced toxicity in the hippocampus of mice by inhibiting neuroinflammation and improving synaptic plasticity.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2024
    Article
  2. Article
  3. Article
  4. Review
  5. Protective effects ofVeterinary research forum : an international quarterly journal · 2022
    Article
  6. Review
  7. Review
  8. Article
  9. Effect of Bortezomib on Global Gene Expression in PC12-Derived Nerve Cells.International journal of molecular sciences · 2020
    Article
  10. Article
  11. p38/TF/HIF-BioMed research international · 2019
    Article
  12. Mitigation of cisplatin-induced peripheral neuropathy by canagliflozin in rats.Naunyn-Schmiedeberg's archives of pharmacology · 2018
    Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. Article
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

1 author at 1 institution in 1 country.

Ella W EnglanderDepartment of Surgery, University of Texas Medical Branch, 301 University Boulevard, Galveston, TX 77555, USA. elenglan@utmb.edu
The University of Texas Medical Branch at Galveston · US

Funding

HYPOXIA-INDUCED DNA DAMAGE AND REPAIR IN THE RAT BRAINR01NS039449 · NINDS · UNIVERSITY OF TEXAS MEDICAL BR GALVESTON · PI ENGLANDER, ELLA W · 2000 to 2010
$2.9M
Mechanisms of Neurotoxicity of Combustion-smoke Inhalation to the BrainR01ES014613 · NIEHS · UNIVERSITY OF TEXAS MED BR GALVESTON · PI ENGLANDER, ELLA W · 2007 to 2012
$1.7M
NIEHS NIH HHS ES014613NIEHS NIH HHS R01 ES014613NINDS NIH HHS NS039449NINDS NIH HHS R01 NS039449
6 · The paper itself

Abstract

In the absence of blood brain barrier (BBB) the DNA of peripheral nervous system (PNS) neurons is exposed to a broader spectrum of endogenous and exogenous threats compared to that of the central nervous system (CNS). Hence, while CNS and PNS neurons cope with many similar challenges inherent to their high oxygen consumption and vigorous metabolism, PNS neurons are also exposed to circulating toxins and inflammatory mediators due to relative permeability of PNS blood nerve barrier (BNB). Consequently, genomes of PNS neurons incur greater damage and the question awaiting investigation is whether specialized repair mechanisms for maintenance of DNA integrity have evolved to meet the additional needs of PNS neurons. Here, I review data showing how PNS neurons manage collateral DNA damage incurred in the course of different anti-cancer treatments designed to block DNA replication in proliferating tumor cells. Importantly, while PNS neurotoxicity and concomitant chemotherapy-induced peripheral neuropathy (CIPN) are among major dose limiting barriers in achieving therapy goals, CIPN is partially reversible during post-treatment nerve recovery. Clearly, cell recovery necessitates mobilization of the DNA damage response and underscores the need for systematic investigation of the scope of DNA repair capacities in the PNS to help predict post-treatment risks to recovering neurons.

Indexed as

AnimalsAntimitotic AgentsAntineoplastic AgentsBlood-Brain BarrierCentral Nervous SystemDisease Models, AnimalDNADNA DamageDNA RepairHumansNeoplasmsNeuronsPeripheral Nervous SystemPeripheral Nervous System DiseasesAntimitotic AgentsAntineoplastic AgentsDNABase excision repair (BER)Blood brain barrier (BBB)Blood nerve barrier (BNB)Chemotherapy-induced peripheral neuropathy (CIPN)Cisplatin cross-linksCytosine arabinoside (ara-C)Dorsal root ganglion (DRG)Ionizing radiation (IR)Nucleotide excision repair (NER)Peripheral nervous system (PNS)

Identifiers

PMID23684797
PMCPMC3733271
OpenAlexW2026709638

What OpenQuestion holds

Textmetadata
LicenceTDM
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.