Evidence map›Paper›PMID 29644491›Full record

ReviewCurrent treatment options in oncology2018

Update on PARP Inhibitors in Breast Cancer.

Alexandra S Zimmer, Mitchell Gillard, Stanley Lipkowitz, Jung-Min Lee

Abstract readReview
In one paragraph

Review in Current treatment options in oncology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
68citing papers in PubMed, 2 pooled it
–field-weighted citation impact
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

68 citing papers in PubMed, 2 syntheses or guidelines pooled it.

  1. Guideline
  2. Pooled it
  3. Trial
  4. Trial
  5. Article
  6. NADAlzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Review
  7. Review
  8. Article
  9. Review
  10. Review
  11. Article
  12. Article
  13. International journal of oncology · 2025
    Review
  14. Article
  15. Review
  16. Review
  17. Article
  18. Review
  19. Article
  20. Review

8 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

4 authors.

Alexandra S ZimmerWomen's Malignancies Branch, Center for Cancer Research, National Cancer Institute, 10 Center Dr. MSC1906 Building 10, Room 4B54, Bethesda, MD, 20892-1906, USA. alexandra.zimmer@nih.gov.
Mitchell GillardSchool of Medicine, Stony Brook University School of Medicine, 101 Nicolls Road Stony Brook, Bethesda, NY, 11794-8434, USA.
Stanley LipkowitzWomen's Malignancies Branch, Center for Cancer Research, National Cancer Institute, 10 Center Dr. MSC1906 Building 10, Room 4B54, Bethesda, MD, 20892-1906, USA.
Jung-Min LeeWomen's Malignancies Branch, Center for Cancer Research, National Cancer Institute, 10 Center Dr. MSC1906 Building 10, Room 4B54, Bethesda, MD, 20892-1906, USA.

Funding

Targeting DNA damage repair and related pathways in HRD-womens cancersZIABC011525 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI LEE, JUNG-MIN · 2013 to 2025
$14.8M
Intramural NIH HHS ZIA BC011525
6 · The paper itself

Abstract

opinion statementThe single agent activity of PARP inhibitors (PARPi) in germline BRCA mutated (gBRCAm) breast and ovarian cancer suggests untapped potential for this new class of drug in breast cancer. The US Food and Drug Administration has approved three PARPi (olaparib, rucaparib, and niraparib) so far to treat certain ovarian cancers, including those with gBRCAm and olaparib for treatment of gBRCAm breast cancers. Several PARPi are now under clinical development for breast cancer in the various treatment settings. Recently, two phase III trials of olaparib (OlympiaD) and talazoparib (EMBRACA) demonstrated 3-month progression-free survival improvement with PARPi compared to physician's choice single agent chemotherapy in metastatic gBRCAm breast cancer. To date, PARPi seems less efficacious in metastatic breast cancer patients than those with BRCA mutated platinum-sensitive recurrent ovarian cancer, perhaps reflecting the biologic heterogeneity and low somatic BRCA mutation rate in breast cancer. The use of PARPi is gradually evolving, including combination strategies with chemotherapy, targeted agents, radiotherapy, or immunotherapy in women with and without gBRCAm. The role of predictive biomarkers, including molecular signatures and homologous recombination repair deficiency scores based on loss of heterozygosity and other structural genomic aberrations, will be crucial to identify a subgroup of patients who may have benefit from PARPi. An improved understanding of the mechanisms underlying PARPi clinical resistance will also be important to enable the development of new approaches to increase efficacy. This is a field rich in opportunity, and the coming years should see a better understanding of which breast cancer patients we should treat with PARPi and where these agents should come in over the course of treatment.

Indexed as

BRCA1 ProteinBRCA2 ProteinBreast NeoplasmsFemaleHumansIndazolesIndolesNeoplasm Recurrence, LocalPhthalazinesPiperazinesPiperidinesPoly(ADP-ribose) Polymerase InhibitorsPoly(ADP-ribose) PolymerasesProgression-Free SurvivalBRCA1 ProteinBRCA2 ProteinIndazolesIndolesniraparibolaparibPhthalazinesPiperazinesPiperidinesPoly(ADP-ribose) Polymerase InhibitorsPoly(ADP-ribose) PolymerasesrucaparibtalazoparibBRCA mutationsBreast cancerHRR dysfunctionPARP inhibitors

Identifiers

PMID29644491
PMCPMC7430202

What OpenQuestion holds

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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.