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Life Sciences · Biochemistry, Genetics and Molecular Biology

Histone Deacetylase Inhibitors Research
Research Guide

What is Histone Deacetylase Inhibitors Research?

Histone Deacetylase Inhibitors Research is the study of compounds that inhibit histone deacetylases (HDACs) to modulate epigenetic regulation, gene expression, cellular functions, and therapeutic applications in cancer and neurodegenerative disorders.

This field encompasses 36,720 papers examining HDACs' roles in acetylation, protein complexes, and enzymatic activity. HDAC inhibitors are investigated for cancer therapy, including glioblastoma and acute myeloid leukemia treatments. Research also addresses impacts on neurodegenerative disorders through epigenetic modifications.

Topic Hierarchy

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graph TD D["Life Sciences"] F["Biochemistry, Genetics and Molecular Biology"] S["Molecular Biology"] T["Histone Deacetylase Inhibitors Research"] D --> F F --> S S --> T style T fill:#DC5238,stroke:#c4452e,stroke-width:2px
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36.7K
Papers
N/A
5yr Growth
844.2K
Total Citations

Research Sub-Topics

Why It Matters

HDAC inhibitors influence cancer therapy by altering epigenetic marks that affect gene expression and tumor progression. In glioblastoma, patients with methylated MGMT promoter benefited from temozolomide, linking epigenetic silencing to treatment outcomes (Hegi et al., 2005). The 2017 ELN recommendations for AML management incorporate advances in epigenetic therapies, reflecting HDAC-related strategies in clinical guidelines (Döhner et al., 2016). Epigenetic alterations, including those targeted by HDAC inhibitors, are ubiquitous in cancers, enabling potential therapeutic reversibility (Esteller, 2008). Lysine acetylation, regulated by HDACs, co-regulates major cellular functions via protein complexes (Choudhary et al., 2009).

Reading Guide

Where to Start

"MGMT Gene Silencing and Benefit from Temozolomide in Glioblastoma" by Hegi et al. (2005), as it provides a clear example of epigenetic modification predicting HDAC inhibitor-related therapy response in a common cancer.

Key Papers Explained

Hegi et al. (2005) "MGMT Gene Silencing and Benefit from Temozolomide in Glioblastoma" establishes epigenetic MGMT silencing's role in temozolomide response, which Stupp et al. (2009) "Effects of radiotherapy with concomitant and adjuvant temozolomide versus radiotherapy alone on survival in glioblastoma" extends to 5-year survival data. Döhner et al. (2016) "Diagnosis and management of AML in adults: 2017 ELN recommendations" builds on epigenetic principles for leukemia guidelines. Jones and Baylin (2007) "The Epigenomics of Cancer" and Esteller (2008) "Epigenetics in Cancer" provide foundational overviews of HDAC-related epigenomics, while Choudhary et al. (2009) "Lysine Acetylation Targets Protein Complexes and Co-Regulates Major Cellular Functions" details molecular mechanisms.

Paper Timeline

100%
graph LR P0["A simple method for clinical ass...
1988 · 4.3K cites"] P1["MGMT Gene Silencing and B...
2005 · 7.1K cites"] P2["Cancer Metastasis: Building a Fr...
2006 · 4.2K cites"] P3["The Epigenomics of Cancer
2007 · 4.4K cites"] P4["Malignant Gliomas in Adults
2008 · 4.2K cites"] P5["Effects of radiotherapy with con...
2009 · 7.6K cites"] P6["Diagnosis and management of AML ...
2016 · 5.7K cites"] P0 --> P1 P1 --> P2 P2 --> P3 P3 --> P4 P4 --> P5 P5 --> P6 style P5 fill:#DC5238,stroke:#c4452e,stroke-width:2px
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Most-cited paper highlighted in red. Papers ordered chronologically.

Advanced Directions

Research continues to explore HDAC inhibitors' integration into glioblastoma protocols post-Stupp et al. (2009) and AML guidelines from Döhner et al. (2016), focusing on combination with temozolomide for MGMT-stratified patients. No recent preprints or news available.

Papers at a Glance

# Paper Year Venue Citations Open Access
1 Effects of radiotherapy with concomitant and adjuvant temozolo... 2009 The Lancet Oncology 7.6K
2 <i>MGMT</i> Gene Silencing and Benefit from Temozolomide in Gl... 2005 New England Journal of... 7.1K
3 Diagnosis and management of AML in adults: 2017 ELN recommenda... 2016 Blood 5.7K
4 The Epigenomics of Cancer 2007 Cell 4.4K
5 A simple method for clinical assay of superoxide dismutase. 1988 Clinical Chemistry 4.3K
6 Cancer Metastasis: Building a Framework 2006 Cell 4.2K
7 Malignant Gliomas in Adults 2008 New England Journal of... 4.2K
8 Selective inhibition of BET bromodomains 2010 Nature 4.2K
9 Lysine Acetylation Targets Protein Complexes and Co-Regulates ... 2009 Science 4.0K
10 Epigenetics in Cancer 2008 New England Journal of... 3.6K

Frequently Asked Questions

What role do HDAC inhibitors play in glioblastoma treatment?

Temozolomide combined with radiotherapy improves survival in glioblastoma, with greater benefit in patients having methylated MGMT promoter, an epigenetic modification influenced by HDAC activity (Stupp et al., 2009; Hegi et al., 2005). MGMT silencing enhances temozolomide efficacy by preventing DNA repair. This underscores HDAC inhibitors' potential in epigenetically sensitized therapies.

How are HDAC inhibitors relevant to acute myeloid leukemia?

The 2017 ELN recommendations for AML diagnosis and management highlight recent advances in epigenetic discoveries, including HDAC inhibition (Döhner et al., 2016). These build on prior guidelines to incorporate targeted therapies. HDAC inhibitors address aberrant gene expression in leukemia cells.

What is the connection between lysine acetylation and HDACs?

Lysine acetylation targets protein complexes and co-regulates cellular functions, with HDACs removing acetyl groups to control activity (Choudhary et al., 2009). This modification is prevalent and dynamically regulates enzymatic processes. HDAC inhibitors disrupt this balance for therapeutic effects.

Why are epigenetic changes significant in cancer?

Epigenetic alterations like those in DNA methylation and histone acetylation are common in cancers and can be reversed by HDAC inhibitors (Jones and Baylin, 2007; Esteller, 2008). These changes affect gene expression without altering DNA sequence. Targeting HDACs offers strategies to restore normal regulation.

What cellular functions do HDACs regulate?

HDACs regulate gene expression, cellular functions, and epigenetic modifications through deacetylation in protein complexes (Choudhary et al., 2009). They impact cancer therapy and neurodegenerative disorders. Inhibitors alter these processes to influence disease states.

Open Research Questions

  • ? How do specific HDAC inhibitors synergize with temozolomide in MGMT-methylated versus unmethylated glioblastomas?
  • ? What are the precise mechanisms by which HDAC inhibition affects AML subtypes beyond current ELN recommendations?
  • ? In which protein complexes does lysine acetylation by HDACs most critically drive metastatic potential in solid tumors?
  • ? Can HDAC inhibitors reverse epigenetic changes in neurodegenerative disorders as effectively as in cancer?
  • ? How do HDAC inhibitors interact with BET bromodomain inhibitors to modulate shared epigenetic targets?

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