Evidence map›Paper›PMID 26896565›Full record

ReviewPharmacology & therapeutics2016

DNA repair targeted therapy: The past or future of cancer treatment?

Navnath S Gavande, Pamela S VanderVere-Carozza, Hilary D Hinshaw, Shadia I Jalal, Catherine R Sears, Katherine S Pawelczak, John J Turchi

Open access · hybridAbstract readReview
In one paragraph

Review in Pharmacology & therapeutics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 202 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
202citing papers in PubMed, 1 pooled it
23.5field-weighted citation impact, top 1% 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

202 citing papers in PubMed, 1 synthesis or guideline pooled it, 379 citations in OpenAlex.

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142 more citing papers are in PubMed but not listed here.

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 3 institutions in 1 country.

Navnath S GavandeDepartment of Medicine, Indiana University School of Medicine, Indianapolis, IN 46202, United States.
Pamela S VanderVere-CarozzaDepartment of Medicine, Indiana University School of Medicine, Indianapolis, IN 46202, United States.
Hilary D HinshawDepartment of Obstetrics and Gynecology, Indiana University School of Medicine, Indianapolis, IN 46202, United States.
Shadia I JalalDepartment of Medicine, Indiana University School of Medicine, Indianapolis, IN 46202, United States.
Catherine R SearsDepartment of Medicine, Indiana University School of Medicine, Indianapolis, IN 46202, United States.
Katherine S PawelczakNERx Biosciences, Indianapolis, IN 46202, United States.
John J TurchiDepartment of Medicine, Indiana University School of Medicine, Indianapolis, IN 46202, United States; NERx Biosciences, Indianapolis, IN 46202, United States; Department of Biochemistry & Molecular Biology, Indiana University School of Medicine, Indianapolis, IN 46202, United States. Electronic address: jturchi@iu.edu.
Indiana University School of MedicineIndiana University – Purdue University Indianapolis · USNĒRx BioSciences (United States) · US

Funding

Targeting nucleotide excision repair in combination cancer therapyR01CA180710 · NCI · INDIANA UNIVERSITY INDIANAPOLIS · PI TURCHI, JOHN J. · 2013 to 2017
$1.6M
Development of Novel Agents Targeting Genome Stability and Maintenance for TreatiR41CA162648 · NCI · NERX BIOSCIENCES, INC. · PI TURCHI, JOHN J. · 2012 to 2013
$361k
Development of novel lung cancer therapeutics targeting the DNA damage responseR41CA195926 · NCI · NERX BIOSCIENCES, INC. · PI PAWELCZAK, KATHERINE, TURCHI, JOHN J. · 2015 to 2017
$299k
NCI NIH HHS R01 CA180710NCI NIH HHS R01-CA180710NCI NIH HHS R41 CA162648NCI NIH HHS R41-CA162648NCI NIH HHS R41 CA195926
6 · The paper itself

Abstract

The repair of DNA damage is a complex process that relies on particular pathways to remedy specific types of damage to DNA. The range of insults to DNA includes small, modest changes in structure including mismatched bases and simple methylation events to oxidized bases, intra- and interstrand DNA crosslinks, DNA double strand breaks and protein-DNA adducts. Pathways required for the repair of these lesions include mismatch repair, base excision repair, nucleotide excision repair, and the homology directed repair/Fanconi anemia pathway. Each of these pathways contributes to genetic stability, and mutations in genes encoding proteins involved in these pathways have been demonstrated to promote genetic instability and cancer. In fact, it has been suggested that all cancers display defects in DNA repair. It has also been demonstrated that the ability of cancer cells to repair therapeutically induced DNA damage impacts therapeutic efficacy. This has led to targeting DNA repair pathways and proteins to develop anti-cancer agents that will increase sensitivity to traditional chemotherapeutics. While initial studies languished and were plagued by a lack of specificity and a defined mechanism of action, more recent approaches to exploit synthetic lethal interaction and develop high affinity chemical inhibitors have proven considerably more effective. In this review we will highlight recent advances and discuss previous failures in targeting DNA repair to pave the way for future DNA repair targeted agents and their use in cancer therapy.

Indexed as

AnimalsAntineoplastic AgentsDNADNA AdductsDNA Breaks, Double-StrandedDNA RepairNeoplasmsAntineoplastic AgentsDNADNA AdductsCancerDNA damageDNA repairRadiationReplication protein A

Identifiers

PMID26896565
PMCPMC4811676
OpenAlexW2281629727

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.