Evidence map›Paper›PMID 36284291›Full record

ReviewJournal of biomedical science2022

Biomarkers beyond BRCA: promising combinatorial treatment strategies in overcoming resistance to PARP inhibitors.

Yu-Yi Chu, Clinton Yam, Hirohito Yamaguchi, Mien-Chie Hung

Abstract readReview
In one paragraph

Review in Journal of biomedical science, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 1 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

23 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Review
  8. Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. TAOK1 promotes filament formation in HR repair through phosphorylating USP7.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  14. Review
  15. Leveraging PARP-1/2 to Target Distant Metastasis.International journal of molecular sciences · 2024
    Review
  16. Article
  17. Tumor biomarkers for diagnosis, prognosis and targeted therapy.Signal transduction and targeted therapy · 2024
    Review
  18. Article
  19. Article
  20. 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

4 authors.

Yu-Yi ChuDepartment of Molecular and Cellular Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX, 77030, USA.
Clinton YamDepartment of Breast Medical Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX, 77030, USA.
Hirohito YamaguchiResearch Center for Cancer Biology, and Center for Molecular Medicine, Graduate Institute of Biomedical Sciences, China Medical University, 100, Sec 1, Jingmao Rd., Beitun, Taichung, 40402, Taiwan, ROC.
Mien-Chie HungDepartment of Molecular and Cellular Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX, 77030, USA. mhung@cmu.edu.tw.ORCID http://orcid.org/0000-0003-4317-4740

Funding

Clinical Trial Center, China Medical University Hospital CMU109-YT-06International Breast Cancer Research Foundation BCRF-17-069
6 · The paper itself

Abstract

Poly (ADP-ribose) polymerase (PARP) inhibitors (PARPi) exploit the concept of synthetic lethality and offer great promise in the treatment of tumors with deficiencies in homologous recombination (HR) repair. PARPi exert antitumor activity by blocking Poly(ADP-ribosyl)ation (PARylation) and trapping PARP1 on damaged DNA. To date, the U.S. Food and Drug Administration (FDA) has approved four PARPi for the treatment of several cancer types including ovarian, breast, pancreatic and prostate cancer. Although patients with HR-deficient tumors benefit from PARPi, majority of tumors ultimately develop acquired resistance to PARPi. Furthermore, even though BRCA1/2 mutations are commonly used as markers of PARPi sensitivity in current clinical practice, not all patients with BRCA1/2 mutations have PARPi-sensitive disease. Thus, there is an urgent need to elucidate the molecular mechanisms of PARPi resistance to support the development of rational effective treatment strategies aimed at overcoming resistance to PARPi, as well as reliable biomarkers to accurately identify patients who will most likely benefit from treatment with PARPi, either as monotherapy or in combination with other agents, so called marker-guided effective therapy (Mget). In this review, we summarize the molecular mechanisms driving the efficacy of and resistance to PARPi as well as emerging therapeutic strategies to overcome PARPi resistance. We also highlight the identification of potential markers to predict PARPi resistance and guide promising PARPi-based combination strategies.

Indexed as

NeoplasmsOvarian NeoplasmsAdenosine DiphosphateBiomarkersBRCA1 ProteinDNAFemaleHumansPoly(ADP-ribose) Polymerase InhibitorsRiboseAdenosine DiphosphateBiomarkersBRCA1 ProteinDNAPoly(ADP-ribose) Polymerase InhibitorsRiboseBiomarkersMarker-guided effective therapy (Mget)PARPi-based combination strategiesPARP inhibitorResistance to PARP inhibitor

Identifiers

PMID36284291
PMCPMC9594904

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Registered trials

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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.