Evidence map›Paper›PMID 20658650›Full record

ReviewEnvironmental and molecular mutagenesis2010

Initiation of DNA interstrand cross-link repair in mammalian cells.

Erica M Hlavin, Michael B Smeaton, Paul S Miller

Abstract readReview
In one paragraph

Review in Environmental and molecular mutagenesis, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
3.0field-weighted citation impact, top 9% 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

22 citing papers in PubMed, 43 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Involvement of ERCC1 in the pathogenesis of osteoarthritis through the modulation of apoptosis and cellular senescence.Journal of orthopaedic research : official publication of the Orthopaedic Research Society · 2014
    Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. The Fanconi anemia pathway in replication stress and DNA crosslink repair.Cellular and molecular life sciences : CMLS · 2012
    Review
  12. REV1 and DNA polymerase zeta in DNA interstrand crosslink repair.Environmental and molecular mutagenesis · 2012
    Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. Synthesis and molecular modeling of a nitrogen mustard DNA interstrand crosslink.Chemistry (Weinheim an der Bergstrasse, Germany) · 2010
    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

3 authors at 1 institution in 1 country.

Erica M HlavinDepartment of Biochemistry and Molecular Biology, Bloomberg School of Public Health, Johns Hopkins University, Baltimore, Maryland, USA.
Michael B Smeaton
Paul S Miller
Johns Hopkins University · US

Funding

TRAINING IN AREAS FUNDAMENTAL TO CANCER RESEARCHT32CA009110 · NCI · JOHNS HOPKINS UNIVERSITY · PI MATUNIS, MICHAEL J., WEERARATNA, ASHANI T · 1985 to 2025
$13.1M
REPAIR OF INTERSTRAND CROSS LINKED SYNTHETIC DNAR01CA082785 · NCI · JOHNS HOPKINS UNIVERSITY · PI MILLER, PAUL S. · 2000 to 2007
$2.7M
Repair of Interstrand Cross-linked Synthetic DNAR56CA082785 · NCI · JOHNS HOPKINS UNIVERSITY · PI MILLER, PAUL S. · 2009 to 2009
$382k
NCI NIH HHS CA082785NCI NIH HHS R01 CA082785NCI NIH HHS R56 CA082785NCI NIH HHS T32 CA009110NCI NIH HHS T32 CA09110
6 · The paper itself

Abstract

Interstrand cross-links (ICLs) are among the most cytotoxic DNA lesions to cells because they prevent the two DNA strands from separating, thereby precluding replication and transcription. Even though chemotherapeutic cross-linking agents are well established in clinical use, and numerous repair proteins have been implicated in the initial events of mammalian ICL repair, the precise mechanistic details of these events remain to be elucidated. This review will summarize our current understanding of how ICL repair is initiated with an emphasis on the context (replicating, transcribed or quiescent DNA) in which the ICL is recognized, and how the chemical and physical properties of ICLs influence repair. Although most studies have focused on replication-dependent repair because of the relation to highly replicative tumor cells, replication-independent ICL repair is likely to be important in the circumvention of cross-link cytotoxicity in nondividing, terminally differentiated cells that may be challenged with exogenous or endogenous sources of ICLs. Consequently, the ICL repair pathway that should be considered "dominant" appears to depend on the cell type and the DNA context in which the ICL is encountered. The ability to define and inhibit distinct pathways of ICL repair in different cell cycle phases may help in developing methods that increase cytotoxicity to cancer cells while reducing side-effects in nondividing normal cells. This may also lead to a better understanding of pathways that protect against malignancy and aging.

Indexed as

AnimalsCisplatinCodon, InitiatorCross-Linking ReagentsDNA RepairHumansMitomycinTranscription, GeneticCisplatinCodon, InitiatorCross-Linking ReagentsMitomycin

Identifiers

PMID20658650
PMCPMC2911644
OpenAlexW2042308172

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.