Evidence map›Paper›PMID 27320729›Full record

ReviewGene2016

POLD1: Central mediator of DNA replication and repair, and implication in cancer and other pathologies.

Emmanuelle Nicolas, Erica A Golemis, Sanjeevani Arora

Open access · greenAbstract readReview
In one paragraph

Review in Gene, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 96 papers.

0numbers the graph read from it
0cells of the map it votes in
96citing papers in PubMed
7.3field-weighted citation impact, top 2% 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

96 citing papers in PubMed, 138 citations in OpenAlex.

  1. Trial
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  4. Article
  5. A dominant mutation in tomato DNA POLYMERASE DELTA 1 causes geminivirus DNA replication catastrophe.Proceedings of the National Academy of Sciences of the United States of America · 2026
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  13. Gut microbes · 2025
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  17. The DREAM complex links somatic mutation, lifespan, and disease.bioRxiv : the preprint server for biology · 2025
    Article
  18. Article
  19. Synergic anti-tumor effects of photodynamic therapy and resveratrol on triple-negative breast cancer cells.Photochemical & photobiological sciences : Official journal of the European Photochemistry Association and the European Society for Photobiology · 2025
    Article
  20. Article

36 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

3 authors at 1 institution in 1 country.

Emmanuelle NicolasProgram in Molecular Therapeutics, Fox Chase Cancer Center, Philadelphia, PA 19111, USA.
Erica A GolemisProgram in Molecular Therapeutics, Fox Chase Cancer Center, Philadelphia, PA 19111, USA.
Sanjeevani AroraProgram in Molecular Therapeutics, Fox Chase Cancer Center, Philadelphia, PA 19111, USA. Electronic address: sanjeevani.arora@fccc.edu.
Fox Chase Cancer Center · US

Funding

WORD PROCESSING CENTER--COREP30CA006927 · NCI · RESEARCH INST OF FOX CHASE CAN CTR · PI Dietmar J Kappes · 1985 to 2026
$138.8M
TRAINING PROGRAM IN CANCER RESEARCHT32CA009035 · NCI · RESEARCH INST OF FOX CHASE CAN CTR · PI CHERNOFF, JONATHAN · 1985 to 2020
$10.5M
BioGPS: Extensible Web 2.0 gene portal for structured and unstructured annotationR01GM083924 · NIGMS · SCRIPPS RESEARCH INSTITUTE, THE · PI SU, ANDREW I, WU, CHUNLEI · 2008 to 2021
$5.6M
Msi2 regulates the aggressiveness of Non-Small Cell Lung Cancer (NSCLC)R21CA191425 · NCI · RESEARCH INST OF FOX CHASE CAN CTR · PI GOLEMIS, ERICA A. · 2016 to 2017
$427k
NCI NIH HHS P30 CA006927NCI NIH HHS R21 CA191425NCI NIH HHS T32 CA009035NIGMS NIH HHS R01 GM083924
6 · The paper itself

Abstract

The evolutionarily conserved human polymerase delta (POLD1) gene encodes the large p125 subunit which provides the essential catalytic activities of polymerase δ (Polδ), mediated by 5'-3' DNA polymerase and 3'-5' exonuclease moieties. POLD1 associates with three smaller subunits (POLD2, POLD3, POLD4), which together with Replication Factor C and Proliferating Nuclear Cell Antigen constitute the polymerase holoenzyme. Polδ function is essential for replication, with a primary role as the replicase for the lagging strand. Polδ also has an important proofreading ability conferred by the exonuclease activity, which is critical for ensuring replicative fidelity, but also serves to repair DNA lesions arising as a result of exposure to mutagens. Polδ has been shown to be important for multiple forms of DNA repair, including nucleotide excision repair, double strand break repair, base excision repair, and mismatch repair. A growing number of studies in the past decade have linked germline and sporadic mutations in POLD1 and the other subunits of Polδ with human pathologies. Mutations in Polδ in mice and humans lead to genomic instability, mutator phenotype and tumorigenesis. The advent of genome sequencing techniques has identified damaging mutations in the proofreading domain of POLD1 as the underlying cause of some inherited cancers, and suggested that mutations in POLD1 may influence therapeutic management. In addition, mutations in POLD1 have been identified in the developmental disorders of mandibular hypoplasia, deafness, progeroid features and lipodystrophy and atypical Werner syndrome, while changes in expression or activity of POLD1 have been linked to senescence and aging. Intriguingly, some recent evidence suggests that POLD1 function may also be altered in diabetes. We provide an overview of critical Polδ activities in the context of these pathologic conditions.

Indexed as

DNA RepairDNA ReplicationAgingAnimalsCarcinogenesisDNA Polymerase IIIGene Expression RegulationHumansMiceMutationNeoplasmsProliferating Cell Nuclear AntigenProtein SubunitsReplication Protein CSignal TransductionWerner SyndromeDNA Polymerase IIIPOLD1 protein, humanProliferating Cell Nuclear AntigenProtein SubunitsReplication Protein CDNA damage responseHypermutationMDPL syndromep125POLD1Polymerase deltaReplication

Identifiers

PMID27320729
PMCPMC4969162
OpenAlexW2433046934

What OpenQuestion holds

Textmetadata
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.