Evidence map›Paper›PMID 35785170›Full record

ReviewFrontiers in oncology2022

Homologous Recombination Deficiency in Ovarian, Breast, Colorectal, Pancreatic, Non-Small Cell Lung and Prostate Cancers, and the Mechanisms of Resistance to PARP Inhibitors.

Negesse Mekonnen, Hobin Yang, Young Kee Shin

Registry-linked trialOpen access · goldAbstract readReview
In one paragraph

Review in Frontiers in oncology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT07303218 (The HER Project), which is not on this map. Cited by 66 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
66citing papers in PubMed, 2 pooled it
8.8field-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.

NCT07303218 active not recruitingnot on this mapstarted 2025, after this paper: background citation

The HER Project: Homologous Recombination Deficiency in EGFR-Mutated NSCLC, a Retrospective and Prospective Translational Single-center Study

TypeobservationalSponsorIRCCS San RaffaeleRan2025 to 2032Enrolled100ConditionsEGFR, Non Small Cell Lung Cancer, Homologous Recombination Deficiency, PARP InhibitorArmsNo Intervention: Observational Cohort
3 · Its place in the literature

Who cites it

66 citing papers in PubMed, 2 syntheses or guidelines pooled it, 104 citations in OpenAlex.

  1. Pooled it
  2. Pathogenic variants inJournal of medicine and life · 2025
    Pooled it
  3. Article
  4. Review
  5. Genomic Alterations in Quadruple-Negative Breast Cancer Tumors.International journal of molecular sciences · 2026
    Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Double jeopardy: howFrontiers in cell and developmental biology · 2026
    Review
  12. Oncology research · 2026
    Article
  13. Review
  14. Review
  15. Article
  16. Review
  17. Review
  18. Article
  19. Article
  20. Article

6 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 2 institutions in 2 countries.

Negesse MekonnenDepartment of Pharmacy, Research Institute of Pharmaceutical Science, Seoul National University College of Pharmacy, Seoul, South Korea.
Hobin YangDepartment of Pharmacy, Research Institute of Pharmaceutical Science, Seoul National University College of Pharmacy, Seoul, South Korea.
Young Kee ShinDepartment of Pharmacy, Research Institute of Pharmaceutical Science, Seoul National University College of Pharmacy, Seoul, South Korea.
Seoul National University · KRBahir Dar University · ET

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Homologous recombination (HR) is a highly conserved DNA repair mechanism that protects cells from exogenous and endogenous DNA damage. Breast cancer 1 (BRCA1) and breast cancer 2 (BRCA2) play an important role in the HR repair pathway by interacting with other DNA repair proteins such as Fanconi anemia (FA) proteins, ATM, RAD51, PALB2, MRE11A, RAD50, and NBN. These pathways are frequently aberrant in cancer, leading to the accumulation of DNA damage and genomic instability known as homologous recombination deficiency (HRD). HRD can be caused by chromosomal and subchromosomal aberrations, as well as by epigenetic inactivation of tumor suppressor gene promoters. Deficiency in one or more HR genes increases the risk of many malignancies. Another conserved mechanism involved in the repair of DNA single-strand breaks (SSBs) is base excision repair, in which poly (ADP-ribose) polymerase (PARP) enzymes play an important role. PARP inhibitors (PARPIs) convert SSBs to more cytotoxic double-strand breaks, which are repaired in HR-proficient cells, but remain unrepaired in HRD. The blockade of both HR and base excision repair pathways is the basis of PARPI therapy. The use of PARPIs can be expanded to sporadic cancers displaying the "BRCAness" phenotype. Although PARPIs are effective in many cancers, their efficacy is limited by the development of resistance. In this review, we summarize the prevalence of HRD due to mutation, loss of heterozygosity, and promoter hypermethylation of 35 DNA repair genes in ovarian, breast, colorectal, pancreatic, non-small cell lung cancer, and prostate cancer. The underlying mechanisms and strategies to overcome PARPI resistance are also discussed.

Indexed as

base excision repairDNA repair geneshereditary and familial cancerloss of heterozygosityPARP inhibitorpathogenic mutationpromoter hypermethylation

Identifiers

PMID35785170
PMCPMC9247200
OpenAlexW4283014430

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

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 Socratic graph.