ReviewBioEssays : news and reviews in molecular, cellular and developmental biology2016
Histone deacetylase inhibitors for cancer therapy: An evolutionarily ancient resistance response may explain their limited success.
Review in BioEssays : news and reviews in molecular, cellular and developmental biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 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
41 citing papers in PubMed, 80 citations in OpenAlex.
- Sirtuin 2 Contributes to Pancreatic Injury and Inflammation by Modulating Immediate Early Response 3-Mediated Ferroptosis in Acute Pancreatitis.Cellular and molecular gastroenterology and hepatology · 2026Article
- Targeted Therapy in Pancreatic Ductal Adenocarcinoma: Current Advances and Challenges.Current oncology (Toronto, Ont.) · 2026Review
- A Model of Butyrate Activity and Resistance in CRC.Journal of cellular and molecular medicine · 2025Review
- Cell-Based Small-Molecule Screening Identifying Proteostasis Regulators Enhancing Factor VIII Missense Mutant Secretion.Biomolecules · 2025Article
- Epigenetic drugs in cancer therapy.Cancer metastasis reviews · 2025Review
- Structural Modifications and Prospects of Histone Deacetylase (HDAC) Inhibitors in Cancer.Current medicinal chemistry · 2025Review
- Searching for Novel HDAC6/Hsp90 Dual Inhibitors with Anti-Prostate Cancer Activity: In Silico Screening and In Vitro Evaluation.Pharmaceuticals (Basel, Switzerland) · 2024Article
- Synthesis and Biological Evaluation of Novel 2-Aroyl Benzofuran-Based Hydroxamic Acids as Antimicrotubule Agents.International journal of molecular sciences · 2024Article
- Epigenetic regulation of cancer-associated fibroblast heterogeneity.Biochimica et biophysica acta. Reviews on cancer · 2023Review
- Differential molecular mechanistic behavior of HDACs in cancer progression.Medical oncology (Northwood, London, England) · 2022Review
- Matrix metalloproteinases, purinergic signaling, and epigenetics: hubs in the spinal neuroglial network following peripheral nerve injury.Histochemistry and cell biology · 2022Article
- Review
- Targeting Histone Deacetylases: Opportunities for Cancer Treatment and Chemoprevention.Pharmaceutics · 2022Review
- Article
- Carbonic Anhydrase IX Inhibitors as Candidates for Combination Therapy of Solid Tumors.International journal of molecular sciences · 2021Review
- Evaluation of histone deacetylase inhibitor substituted zinc and indium phthalocyanines for chemo- and photodynamic therapy.RSC advances · 2021Article
- Epigenomics and immunotherapeutic advances in pediatric brain tumors.NPJ precision oncology · 2021Review
- Histone deacetylase 6 inhibition in urothelial cancer as a potential new strategy for cancer treatment.Oncology letters · 2021Article
- Hypothesis: Sam68 and Pygo2 mediate cell type-specific effects of the modulation of CBP-Wnt and p300-Wnt activities in Colorectal Cancer Cells.Journal of Cancer · 2021Article
- 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 at 1 institution in 1 country.
Funding
Abstract
Histone deacetylase inhibitors (HDACi) are in clinical trials against a variety of cancers. Despite early successes, results against the more common solid tumors have been mixed. How is it that so many cancers, and most normal cells, tolerate the disruption caused by HDACi-induced protein hyperacetylation? And why are a few cancers so sensitive? Here we discuss recent results showing that human cells mount a coordinated transcriptional response to HDACi that mitigates their toxic effects. We present a hypothetical signaling system that could trigger and mediate this response. To account for the existence of such a response, we note that HDACi of various chemical types are made by a variety of organisms to kill or suppress competitors. We suggest that the resistance response in human cells is a necessary evolutionary consequence of exposure to environmental HDACi. We speculate that cancers sensitive to HDACi are those in which the resistance response has been compromised by mutation. Identifying such mutations will allow targeting of HDACi therapy to potentially susceptible cancers. Also see the video abstract here.
Indexed as
Identifiers
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.