Evidence map›Paper›PMID 30078354›Full record

ReviewCell cycle (Georgetown, Tex.)2018

Targeting the cell cycle in breast cancer: towards the next phase.

K L Thu, I Soria-Bretones, T W Mak, D W Cescon

Open access · bronzeAbstract readReview
In one paragraph

Review in Cell cycle (Georgetown, Tex.), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 94 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
94citing papers in PubMed, 2 pooled it
13.7field-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.

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

94 citing papers in PubMed, 2 syntheses or guidelines pooled it, 197 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
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  6. Article
  7. Review
  8. Article
  9. Review
  10. Estrogen-like Activity ofBiomedicines · 2025
    Article
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  16. Review
  17. Review
  18. Review
  19. Article
  20. Research Progress with Atractylone as an Antitumor Agent.Molecules (Basel, Switzerland) · 2024
    Review

34 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 at 1 institution in 1 country.

K L Thua Campbell Family Institute for Breast Cancer Research, Princess Margaret Cancer Centre , University Health Network , Toronto , Canada.
I Soria-Bretonesa Campbell Family Institute for Breast Cancer Research, Princess Margaret Cancer Centre , University Health Network , Toronto , Canada.
T W Maka Campbell Family Institute for Breast Cancer Research, Princess Margaret Cancer Centre , University Health Network , Toronto , Canada.
D W Cescona Campbell Family Institute for Breast Cancer Research, Princess Margaret Cancer Centre , University Health Network , Toronto , Canada.ORCID 0000-0002-1080-0998
University Health Network · CA

Funding

CIHR
6 · The paper itself

Abstract

Deregulation of the cell cycle is a hallmark of cancer that enables limitless cell division. To support this malignant phenotype, cells acquire molecular alterations that abrogate or bypass control mechanisms in signaling pathways and cellular checkpoints that normally function to prevent genomic instability and uncontrolled cell proliferation. Consequently, therapeutic targeting of the cell cycle has long been viewed as a promising anti-cancer strategy. Until recently, attempts to target the cell cycle for cancer therapy using selective inhibitors have proven unsuccessful due to intolerable toxicities and a lack of target specificity. However, improvements in our understanding of malignant cell-specific vulnerabilities has revealed a therapeutic window for preferential targeting of the cell cycle in cancer cells, and has led to the development of agents now in the clinic. In this review, we discuss the latest generation of cell cycle targeting anti-cancer agents for breast cancer, including approved CDK4/6 inhibitors, and investigational TTK and PLK4 inhibitors that are currently in clinical trials. In recognition of the emerging population of ER+ breast cancers with acquired resistance to CDK4/6 inhibitors we suggest new therapeutic avenues to treat these patients. We also offer our perspective on the direction of future research to address the problem of drug resistance, and discuss the mechanistic insights required for the successful implementation of these strategies.

Indexed as

AnimalsAntineoplastic AgentsBreast NeoplasmsCell CycleCell Cycle ProteinsCyclin-Dependent KinasesEnzyme InhibitorsFemaleHumansProtein Serine-Threonine KinasesProtein-Tyrosine KinasesAntineoplastic AgentsCell Cycle ProteinsCyclin-Dependent KinasesEnzyme InhibitorsPLK4 protein, humanProtein Serine-Threonine KinasesProtein-Tyrosine KinasesTTK protein, humanbreast cancerCDK4/6 inhibitordrug resistancePLK4TTK

Identifiers

PMID30078354
PMCPMC6152498
OpenAlexW2887054120

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.