Evidence map›Paper›PMID 32669350›Full record

ArticleCancer research2020

A Novel Mechanism to Induce BRCAness in Cancer Cells.

Changmeng Cai

Open access · bronzeAbstract readComment
In one paragraph

Article in Cancer research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.6field-weighted citation impact, top 31% 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

6 citing papers in PubMed, 10 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. BRCA1 and Breast Cancer: Molecular Mechanisms and Therapeutic Strategies.Frontiers in cell and developmental biology · 2022
    Review
  5. Review
  6. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

1 author at 1 institution in 1 country.

Changmeng CaiCenter for Personalized Cancer Therapy, University of Massachusetts Boston, Boston, Massachusetts. changmeng.cai@umb.edu.
University of Massachusetts Boston · US

Funding

Study the Mechanism of Retinoblastoma Protein Mediated Androgen Receptor Transcriptional Repression Activity on DNA ReplicationR01CA211350 · NCI · UNIVERSITY OF MASSACHUSETTS BOSTON · PI CAI, CHANGMENG · 2017 to 2021
$1.7M
NCI NIH HHS R01 CA211350
6 · The paper itself

Abstract

Cancer cells with germline deleterious mutations of BRCA1 or BRCA2 are deficient in homologous recombination repair and therefore sensitive to PARP inhibitor treatment. However, wild-type BRCA1/2-expressing cells with defects in other DNA damage repair pathway components may also exhibit "BRCAness," which in combination with PARP inhibition can similarly induce synthetic lethality. In this issue of

Indexed as

Breast NeoplasmsPoly(ADP-ribose) Polymerase InhibitorsBRCA1 ProteinBRCA2 ProteinDNA Breaks, Double-StrandedDNA RepairHumansNIMA-Interacting Peptidylprolyl IsomerasePeptidylprolyl IsomeraseBRCA1 ProteinBRCA1 protein, humanBRCA2 ProteinNIMA-Interacting Peptidylprolyl IsomerasePeptidylprolyl IsomerasePIN1 protein, humanPoly(ADP-ribose) Polymerase Inhibitors

Identifiers

PMID32669350
PMCPMC8023356
OpenAlexW3043649838

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.