Evidence map›Paper›PMID 31898156›Full record

ReviewBreast cancer (Tokyo, Japan)2020

DNA damage repair functions and targeted treatment in breast cancer.

Chenfeng He, Kosuke Kawaguchi, Masakazu Toi

Abstract readReview
PubMed Publisher
In one paragraph

Review in Breast cancer (Tokyo, Japan), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
–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

14 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Emerging Roles of RNF168 in Tumor Progression.Molecules (Basel, Switzerland) · 2023
    Review
  6. Article
  7. Advances in Anti-Cancer Activities of Flavonoids inInternational journal of molecular sciences · 2022
    Review
  8. Article
  9. The Development ofRadiology. Imaging cancer · 2022
    Review
  10. Review
  11. Article
  12. Review
  13. Article
  14. Review
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.

Chenfeng HeDepartment of Breast Surgery, Graduate School of Medicine, Kyoto University, 54 Shogoin-kawaharacho, Sakyo-ku, Kyoto, 606-8507, Japan.
Kosuke KawaguchiDepartment of Breast Surgery, Graduate School of Medicine, Kyoto University, 54 Shogoin-kawaharacho, Sakyo-ku, Kyoto, 606-8507, Japan. kkosuke@kuhp.kyoto-u.ac.jp.
Masakazu ToiDepartment of Breast Surgery, Graduate School of Medicine, Kyoto University, 54 Shogoin-kawaharacho, Sakyo-ku, Kyoto, 606-8507, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cell DNA is continuously attacked by endogenous and exogenous agents, which causes DNA damage. During long-term evolution, complex defense systems for DNA damage repair are formed by cells to maintain genome stability. Defects in the DNA damage repair process may lead to various diseases, including tumors. Therefore, DNA damage repair systems have become a new anti-tumor drug target. To date, a number of inhibitors related to DNA damage repair systems have been developed, particularly for tumors with BRCA1 and BRCA2 mutations. Poly (ADP-ribose) polymerase inhibitors developed by synthetic lethality are widely used in individualized tumor therapy. In this review, we briefly introduce the mechanisms underlying DNA damage repair, particularly in breast cancer, and mainly focus on new treatments targeting the DNA damage repair pathway in breast cancer.

Indexed as

DNA DamageDNA RepairMolecular Targeted TherapyAntineoplastic AgentsBiomarkers, TumorBreast NeoplasmsFemaleHumansAntineoplastic AgentsBiomarkers, TumorBRCA1/2DNA damage repairPARP inhibitorSynthetic lethality

Identifiers

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.