ReviewBioEssays : news and reviews in molecular, cellular and developmental biology2019
Chromatin Stability as a Target for Cancer Treatment.
Review in BioEssays : news and reviews in molecular, cellular and developmental biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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
16 citing papers in PubMed, 33 citations in OpenAlex.
- A novel matrine derivative exerts antitumor effects against hepatocellular carcinoma by inducing oxidative stress and DNA damage.Medical oncology (Northwood, London, England) · 2026Article
- Insights into FACT in Cancers with Targeted Therapeutic Implications.Molecular and cellular biology · 2026Review
- The expression landscape and clinical significance of methyltransferase-like 17 in human cancer and hepatocellular carcinoma: a pan-cancer analysis using multiple databases.Cancer cell international · 2025Article
- Chromatin damage generated by DNA intercalators leads to degradation of RNA Polymerase II.Nucleic acids research · 2024Article
- Comparison of cell response to chromatin and DNA damage.Nucleic acids research · 2023Article
- Aclarubicin stimulates RNA polymerase II elongation at closely spaced divergent promoters.Science advances · 2023Article
- Updates inBiomedicines · 2023Review
- Chromatin and Cancer: Implications of Disrupted Chromatin Organization in Tumorigenesis and Its Diversification.Cancers · 2023Review
- Aclarubicin stimulates RNA polymerase II elongation at closely spaced divergent promoters.bioRxiv : the preprint server for biology · 2023Article
- The Combination of Curaxin CBL0137 and Histone Deacetylase Inhibitor Panobinostat Delays KMT2A-Rearranged Leukemia Progression.Frontiers in oncology · 2022Article
- Dual Targeting of Chromatin Stability By The Curaxin CBL0137 and Histone Deacetylase Inhibitor Panobinostat Shows Significant Preclinical Efficacy in Neuroblastoma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2021Article
- Automated assessment of DNA ploidy, chromatin organization, and stroma fraction to predict prognosis and adjuvant therapy response in patients with stage II colorectal carcinoma.American journal of cancer research · 2021Article
- Prevention of Chromatin Destabilization by FACT Is Crucial for Malignant Transformation.iScience · 2020Article
- Article
- Histone Chaperone FACT and Curaxins: Effects on Genome Structure and Function.Journal of cancer metastasis and treatment · 2019Article
- Article
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
In this essay, I propose that DNA-binding anti-cancer drugs work more via chromatin disruption than DNA damage. Success of long-awaited drugs targeting cancer-specific drivers is limited by the heterogeneity of tumors. Therefore, chemotherapy acting via universal targets (e.g., DNA) is still the mainstream treatment for cancer. Nevertheless, the problem with targeting DNA is insufficient efficacy due to high toxicity. I propose that this problem stems from the presumption that DNA damage is critical for the anti-cancer activity of these drugs. DNA in cells exists as chromatin, and many DNA-targeting drugs alter chromatin structure by destabilizing nucleosomes and inducing histone eviction from chromatin. This effect has been largely ignored because DNA damage is seen as the major reason for anti-cancer activity. I discuss how DNA-binding molecules destabilize chromatin, why this effect is more toxic to tumoral than normal cells, and why cells die as a result of chromatin destabilization.
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What 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.