Evidence map›Paper›PMID 33553154›Full record

ReviewFrontiers in cell and developmental biology2020

Role of Base Excision Repair Pathway in the Processing of Complex DNA Damage Generated by Oxidative Stress and Anticancer Drugs.

Yeldar Baiken, Damira Kanayeva, Sabira Taipakova, Regina Groisman, Alexander A Ishchenko, Dinara Begimbetova, Bakhyt Matkarimov, Murat Saparbaev

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in cell and developmental biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 1 pooled it
2.0field-weighted citation impact, top 13% 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

16 citing papers in PubMed, 1 synthesis or guideline pooled it, 27 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Dynamic changes of DNA methylation induced by benzo(a)pyrene in cancer.Genes and environment : the official journal of the Japanese Environmental Mutagen Society · 2023
    Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. 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

8 authors at 5 institutions in 2 countries.

Yeldar BaikenSchool of Sciences and Humanities, Nazarbayev University, Nur-Sultan, Kazakhstan.
Damira KanayevaSchool of Sciences and Humanities, Nazarbayev University, Nur-Sultan, Kazakhstan.
Sabira TaipakovaDepartment of Molecular Biology and Genetics, Faculty of Biology and Biotechnology, al-Farabi Kazakh National University, Almaty, Kazakhstan.
Regina GroismanGroupe ≪Mechanisms of DNA Repair and Carcinogenesis≫, Equipe Labellisée LIGUE 2016, CNRS UMR9019, Université Paris-Saclay, Gustave Roussy Cancer Campus, Villejuif, France.
Alexander A IshchenkoGroupe ≪Mechanisms of DNA Repair and Carcinogenesis≫, Equipe Labellisée LIGUE 2016, CNRS UMR9019, Université Paris-Saclay, Gustave Roussy Cancer Campus, Villejuif, France.
Dinara BegimbetovaNational Laboratory Astana, Nazarbayev University, Nur-Sultan, Kazakhstan.
Bakhyt MatkarimovNational Laboratory Astana, Nazarbayev University, Nur-Sultan, Kazakhstan.
Murat SaparbaevDepartment of Molecular Biology and Genetics, Faculty of Biology and Biotechnology, al-Farabi Kazakh National University, Almaty, Kazakhstan.
Nazarbayev University · KZAl-Farabi Kazakh National University · KZCentre National de la Recherche Scientifique · FRInstitut Gustave Roussy · FRUniversité Paris-Saclay · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chemical alterations in DNA induced by genotoxic factors can have a complex nature such as bulky DNA adducts, interstrand DNA cross-links (ICLs), and clustered DNA lesions (including double-strand breaks, DSB). Complex DNA damage (CDD) has a complex character/structure as compared to singular lesions like randomly distributed abasic sites, deaminated, alkylated, and oxidized DNA bases. CDD is thought to be critical since they are more challenging to repair than singular lesions. Although CDD naturally constitutes a relatively minor fraction of the overall DNA damage induced by free radicals, DNA cross-linking agents, and ionizing radiation, if left unrepaired, these lesions cause a number of serious consequences, such as gross chromosomal rearrangements and genome instability. If not tightly controlled, the repair of ICLs and clustered bi-stranded oxidized bases via DNA excision repair will either inhibit initial steps of repair or produce persistent chromosomal breaks and consequently be lethal for the cells. Biochemical and genetic evidences indicate that the removal of CDD requires concurrent involvement of a number of distinct DNA repair pathways including poly(ADP-ribose) polymerase (PARP)-mediated DNA strand break repair, base excision repair (BER), nucleotide incision repair (NIR), global genome and transcription coupled nucleotide excision repair (GG-NER and TC-NER, respectively), mismatch repair (MMR), homologous recombination (HR), non-homologous end joining (NHEJ), and translesion DNA synthesis (TLS) pathways. In this review, we describe the role of DNA glycosylase-mediated BER pathway in the removal of complex DNA lesions.

Indexed as

base excision repairbulky DNA adductDNA glycosylaseFanconi anemiainter-strand DNA crosslinknucleotide excision repair

Identifiers

PMID33553154
PMCPMC7862338
OpenAlexW3124203833

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.