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Updated: Jul 3, 2026

Studying Cell Cycle-regulated Gene Expression by Two Complementary Cell Synchronization Protocols
12:02

Studying Cell Cycle-regulated Gene Expression by Two Complementary Cell Synchronization Protocols

Published on: June 6, 2017

PKMYT1 in Cancer: Beyond Cell Cycle Checkpoints to Context-Dependent Therapeutic Vulnerability

Lingxi Li1, Binfan He1, Mengmeng Hao1

  • 1Department of General Surgery, Translational Medicine Institute, the Affiliated Chenzhou Hospital, Hengyang Medical School, University of South China, Chenzhou, China.

Genes, Chromosomes & Cancer
|July 2, 2026
PubMed

Insights

PKMYT1 is a promising cancer target, crucial for cancer cells managing DNA damage but not normal cells. Inhibiting PKMYT1 shows therapeutic potential, especially in specific genetic contexts like CCNE1 amplification.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Therapeutics

Background:

  • PKMYT1 exhibits tumor-selective expression and is vital for cancer cell replication stress management.
  • It's dispensable in normal cells but critical for cancer cells facing DNA damage, offering a therapeutic window.

Purpose of the Study:

  • To review PKMYT1's mechanistic roles in cancer.
  • To evaluate its clinical landscape and potential as a therapeutic target.
  • To discuss biomarker strategies for precision targeting.

Main Methods:

  • Literature review and critical evaluation of existing research on PKMYT1.
  • Analysis of PKMYT1's role in cell cycle regulation, signaling, metabolism, and immune evasion.
  • Examination of clinical trial data and preclinical studies involving PKMYT1 inhibitors.

Main Results:

  • PKMYT1 inhibition leads to synthetic lethality in CCNE1-amplified and TP53-deficient cancers.
  • PKMYT1 acts as an oncoprotein, influencing signaling, metabolism, and immune evasion (cGAS-STING).
  • Selective inhibitors like lunresertib are in clinical trials, often in combination therapies.

Conclusions:

  • PKMYT1 is a key target for replication stress-high malignancies.
  • Precision targeting based on genetic signatures (CCNE1, TP53, ER) is crucial for efficacy.
  • Understanding context-dependent roles and resistance mechanisms is essential for optimizing PKMYT1-targeted therapies.
Keywords:
CCNE1 amplificationLunresertib (RP‐6306)PKMYT1Precision oncologyReplication stressRynthetic lethality

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