ReviewCells2022
Role of the Circadian Clock "Death-Loop" in the DNA Damage Response Underpinning Cancer Treatment Resistance.
Review in Cells, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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
18 citing papers in PubMed, 25 citations in OpenAlex.
- Liver progenitor cells perform wound healing in a scratch assay by concerted bistable circuits.NPJ systems biology and applications · 2026Article
- Chromatin Nano-Organization in Peripheral Blood Mononuclear Cells After In-Solution Irradiation with the Beta-Emitter Lu-177.Biomolecules · 2026Article
- Circadian clock and cancer.Military Medical Research · 2026Review
- Article
- Nanomaterial-enabled drug delivery systems for circadian medicine: bridging direct rhythm modulation and chronotherapy.RSC advances · 2025Review
- Circadian rhythms and cancer: implications for timing in therapy.Discover oncology · 2024Review
- Senescence-related signatures predict prognosis and response to immunotherapy in colon cancer.Journal of gastrointestinal oncology · 2024Article
- Modulating DNA damage response in uveal melanoma through embryonic stem cell microenvironment.BMC cancer · 2024Article
- Evening cortisol levels are prognostic for progression-free survival in a prospective pilot study of head and neck cancer patients.Frontiers in oncology · 2024Article
- Long-Term Transcriptomic Changes and Cardiomyocyte Hyperpolyploidy after Lactose Intolerance in Neonatal Rats.International journal of molecular sciences · 2023Article
- The Role of Mitotic Slippage in Creating a "Female Pregnancy-like System" in a Single Polyploid Giant Cancer Cell.International journal of molecular sciences · 2023Article
- Spatial-Temporal Genome Regulation in Stress-Response and Cell-Fate Change.International journal of molecular sciences · 2023Review
- Cdc42 Regulates the Expression of Cytoskeleton and Microtubule Network Proteins to Promote Invasion and Metastasis of Progeny Cells Derived from CoClJournal of Cancer · 2023Article
- Characteristic of Ultrastructure of Mice B16 Melanoma Cells under the Influence of Different Lighting Regimes.Clocks & sleep · 2022Article
- The Transcriptome and Proteome Networks of Malignant Tumours Reveal Atavistic Attractors of Polyploidy-Related Asexual Reproduction.International journal of molecular sciences · 2022Article
- What Are the Reasons for Continuing Failures in Cancer Therapy? Are Misleading/Inappropriate Preclinical Assays to Be Blamed? Might Some Modern Therapies Cause More Harm than Benefit?International journal of molecular sciences · 2022Review
- Polyploidy and Myc Proto-Oncogenes Promote Stress Adaptation via Epigenetic Plasticity and Gene Regulatory Network Rewiring.International journal of molecular sciences · 2022Review
- Life Entrapped in a Network of Atavistic Attractors: How to Find a Rescue.International journal of molecular sciences · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 3 institutions in 3 countries.
Funding
Abstract
Here, we review the role of the circadian clock (CC) in the resistance of cancer cells to genotoxic treatments in relation to whole-genome duplication (WGD) and telomere-length regulation. The CC drives the normal cell cycle, tissue differentiation, and reciprocally regulates telomere elongation. However, it is deregulated in embryonic stem cells (ESCs), the early embryo, and cancer. Here, we review the DNA damage response of cancer cells and a similar impact on the cell cycle to that found in ESCs—overcoming G1/S, adapting DNA damage checkpoints, tolerating DNA damage, coupling telomere erosion to accelerated cell senescence, and favouring transition by mitotic slippage into the ploidy cycle (reversible polyploidy). Polyploidy decelerates the CC. We report an intriguing positive correlation between cancer WGD and the deregulation of the CC assessed by bioinformatics on 11 primary cancer datasets (rho = 0.83; p < 0.01). As previously shown, the cancer cells undergoing mitotic slippage cast off telomere fragments with TERT, restore the telomeres by ALT-recombination, and return their depolyploidised offspring to telomerase-dependent regulation. By reversing this polyploidy and the CC “death loop”, the mitotic cycle and Hayflick limit count are thus again renewed. Our review and proposed mechanism support a life-cycle concept of cancer and highlight the perspective of cancer treatment by differentiation.
Indexed as
Identifiers
What Socratic 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 Socratic graph.