Evidence map›Paper›PMID 29660759›Full record

ReviewCancer2018

PARP inhibitors in breast cancer: Bringing synthetic lethality to the bedside.

Anita A Turk, Kari B Wisinski

Open access · bronzeAbstract readReview
In one paragraph

Review in Cancer, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 90 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
90citing papers in PubMed, 1 pooled it
5.1field-weighted citation impact, top 3% 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

90 citing papers in PubMed, 1 synthesis or guideline pooled it, 155 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. A Pyrone Glucoside fromBiomolecules · 2026
    Article
  6. Article
  7. Review
  8. Cancer-associated TRF1 mutations alter PARP1 interaction dynamics: an in silico study.Mammalian genome : official journal of the International Mammalian Genome Society · 2026
    Article
  9. Article
  10. Article
  11. Review
  12. Review
  13. Therapeutic Potential of Plant Phenolic Acids Combating Cancer Drug Resistance.Recent advances in food, nutrition & agriculture · 2026
    Review
  14. Review
  15. Article
  16. Article
  17. Review
  18. Review
  19. Article
  20. Review

30 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

2 authors at 1 institution in 1 country.

Anita A TurkUniversity of Wisconsin Carbone Cancer Center, Madison, Wisconsin.
Kari B WisinskiUniversity of Wisconsin Carbone Cancer Center, Madison, Wisconsin.ORCID 0000-0003-3535-0652
University of Wisconsin Carbone Cancer Center · US

Funding

UW COMPREHENSIVE CANCER CENTER SUPPORTP30CA014520 · NCI · UNIVERSITY OF WISCONSIN-MADISON · PI AMY TRENTHAM-DIETZ · 1985 to 2026
$142.6M
NCI NIH HHS P30 CA014520
6 · The paper itself

Abstract

Individuals with breast and ovarian cancer susceptibility gene 1 (BRCA1) or BRCA2 germline mutations have a significantly increased lifetime risk for breast and ovarian cancers. BRCA-mutant cancer cells have abnormal homologous recombination (HR) repair of DNA. In these tumors, the base excision repair (BER) pathway is important for cell survival. The poly(adenosine diphosphate-ribose) polymerase (PARP) enzymes play a key role in BER, and PARP inhibitors are effective in causing cell death in BRCA-mutant cells while sparing normal cells-a concept called synthetic lethality. PARP inhibitors are the first cancer therapeutics designed to exploit synthetic lethality. Recent clinical trials in BRCA-mutant, metastatic breast cancer demonstrated improved outcomes with single-agent PARP inhibitors (olaparib and talazoparib) over chemotherapy. However, resistance to PARP inhibitors remains a challenge. Primarily due to myelosuppression, the combination of PARP inhibitors with chemotherapy has been difficult. Novel combinations with chemotherapy, immunotherapy, and other targeted therapies are being pursued. In this review, the authors discuss current knowledge of PARP inhibitors in BRCA-mutant breast cancer and potential future directions for these agents. Cancer 2018;124:2498-506. © 2018 American Cancer Society.

Indexed as

Antineoplastic Agents, ImmunologicalAntineoplastic Combined Chemotherapy ProtocolsBRCA1 ProteinBRCA2 ProteinBreast NeoplasmsCell SurvivalClinical Trials as TopicDNA RepairDrug Resistance, NeoplasmFemaleHumansMolecular Targeted TherapyPatient SelectionPoly(ADP-ribose) Polymerase InhibitorsPoly(ADP-ribose) PolymerasesSynthetic Lethal MutationsAntineoplastic Agents, ImmunologicalBRCA1 ProteinBRCA1 protein, humanBRCA2 ProteinBRCA2 protein, humanPoly(ADP-ribose) Polymerase InhibitorsPoly(ADP-ribose) Polymerasesbreast and ovarian cancer susceptibility gene (BRCA)-mutantbreast cancerDNA repairhereditarypoly(adenosine diphosphate-ribose) polymerase (PARP)

Identifiers

PMID29660759
PMCPMC5990439
OpenAlexW2802157782

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.