ReviewCancer metastasis reviews2025
Role of PLK4 inhibition in cancer therapy.
Review in Cancer metastasis reviews, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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.
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.
Who cites it
3 citing papers in PubMed.
- Design, Synthesis, and Biological Activity Evaluation of Quinazoline-Based PLK4 Inhibitors.Biomedicines · 2026Article
- Migrasome-mediated clearance of PLK4: a novel mechanism for centrosome homeostasis and tumor targeting.EBioMedicine · 2026Article
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Genomic instability is a hallmark of cancer and is associated with tumor progression and therapeutic resistance. Centrioles and centrosomes are a critical determinant of genomic stability. Polo-like kinase 4 (PLK4) is a serine-threonine kinase that plays a critical role in the regulation of centrosome duplication. PLK4 overexpression drives tumorigenesis and has been shown to be overexpressed in a wide variety of human tumors, where it is associated with more advanced disease and worse clinical outcomes. As such, there has been significant interest in pharmacologically targeting PLK4 using small-molecule inhibitors for therapeutic gain in multiple cancer types. In this review, we will discuss the functions of PLK4 in normal and oncogenic processes. We will further discuss the current state of PLK4 as a therapeutic target in cancer by reviewing the current literature on PLK4 inhibitors in both the preclinical and clinical space. Finally, we will discuss the emerging data exploring rational combinations of PLK4 inhibitors with DNA-damaging agents and immunotherapies as a means to unlock the potential of these agents in cancer therapy.
Indexed as
Identifiers
40512236What OpenQuestion holds
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 OpenQuestion graph.