ReviewAmerican journal of cancer research2025
Exploiting replication stress for synthetic lethality in MYC-driven cancers.
Review in American journal of cancer research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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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
6 citing papers in PubMed.
- ERCC6 at the Transcription-Replication Interface: Integration of Transcription-Coupled Repair with Replication Stress Responses.International journal of molecular sciences · 2026Review
- CDK12/13 Inhibition Induces DNA Hypomethylation and Sensitizes Cancer Cells to Compounds Targeting DNA-PK.Journal of cellular and molecular medicine · 2026Article
- METTL3-YTHDF1-driven mMolecular and cellular biochemistry · 2026Article
- c-Medical sciences (Basel, Switzerland) · 2026Review
- Ubiquitin System-Driven Proteostasis in DNA Damage Response.International journal of molecular sciences · 2026Review
- Synthetic lethality and DNA damage response targeting in cancer stem cells: a comprehensive review.Discover oncology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The oncoprotein MYC, overexpressed in more than 70% of human cancers, plays a pivotal role in regulating gene transcription and has long been recognized as a promising target for cancer therapy. However, no MYC-targeted drug has been approved for clinical use, largely due to the lack of a well-defined druggable domain and its nuclear localization. MYC-overexpressing cancer cells exhibit increased replication stress, driven by factors such as elevated replication origin firing, nucleotide depletion, replication-transcription conflicts, and heightened reactive oxygen species (ROS) production. Simultaneously, MYC activates compensatory mechanisms, including enhanced DNA repair, checkpoint-mediated cell cycle regulation, and metabolic reprogramming, to mitigate this stress and support cell survival. Interfering with these compensatory pathways exacerbates replication stress, leading to synthetic lethality in MYC-driven cancer cells. In this review, we summarize recent advances in leveraging replication stress to achieve synthetic lethality in MYC-driven cancers. Furthermore, we discuss current strategies targeting replication stress, highlighting new opportunities for the development of therapies against MYC-driven malignancies.
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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.