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Related Concept Videos

Epigenetic Regulation01:37

Epigenetic Regulation

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Epigenetic changes alter the physical structure of the DNA without changing the genetic sequence and often regulate whether genes are turned on or off. This regulation ensures that each cell produces only proteins necessary for its function. For example, proteins that promote bone growth are not produced in muscle cells. Epigenetic mechanisms play an essential role in healthy development. Conversely, precisely regulated epigenetic mechanisms are disrupted in diseases like cancer.
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Cancer is the second leading cause of death in the United States. A cancer cell is genetically unstable and hence can mutate faster. They can also modify their microenvironment and escape immune surveillance. The difficulties in treating cancer are further compounded by the emergence of rapid resistance to anticancer drugs. The most common ways to attain resistance in cancer cells include alteration in drug transport and metabolism, modification of drug target, elevated DNA damage response, or...
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Inheritance of Chromatin Structures03:17

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Epigenetics is the study of inherited changes in a cell's phenotype without changing the DNA sequences. It provides a form of memory for the differential gene expression pattern to maintain cell lineage, position-effect variegation, dosage compensation, and maintenance of chromatin structures such as telomeres and centromeres. For example, the structure and location of the centromere on chromosomes are epigenetically inherited. Its functionality is not dictated or ensured by the underlying...
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The histone proteins in the nucleosomes are post-translationally modified (PTM) to increase or decrease access to DNA. The commonly observed PTMs are methylation, acetylation, phosphorylation, and ubiquitination of lysine amino acids in the histone H3 tail region. These histone modifications have specific meaning for the cell. Hence, they are called "histone code". The protein complex involved in histone modification is termed as "reader-writer" complex.
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The targeted cancer therapies, also known as “molecular targeted therapies,” take advantage of the molecular and genetic differences between the cancer cells and the normal cells. It needs a thorough understanding of the cancer cells to develop drugs that can target specific molecular aspects that drive the growth, progression, and spread of cancer cells without affecting the growth and survival of other normal cells in the body.
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Related Experiment Video

Updated: Jun 6, 2025

An Integrated Platform for Genome-wide Mapping of Chromatin States Using High-throughput ChIP-sequencing in Tumor Tissues
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HDAC-driven mechanisms in anticancer resistance: epigenetics and beyond.

Martina Minisini1, Martina Mascaro1, Claudio Brancolini1

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Cancer Drug Resistance (Alhambra, Calif.)
|December 3, 2024
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Summary

Histone deacetylases (HDACs) contribute to cancer drug resistance by altering gene expression through epigenetic modifications. Understanding these HDAC mechanisms is crucial for overcoming treatment challenges and preventing cancer recurrence.

Keywords:
DNA damageHDACsPARPacetylationchemotherapyhormone deprivationpalbociclib

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Author Spotlight: Epigenetic Modifications and Metabolic Rewiring as Targets for Cancer Therapy
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Author Spotlight: Epigenetic Modifications and Metabolic Rewiring as Targets for Cancer Therapy

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Area of Science:

  • Oncology
  • Epigenetics
  • Molecular Biology

Background:

  • Cancer drug resistance and recurrence pose significant clinical challenges.
  • Epigenetic alterations, particularly changes in histone acetylation, are implicated in treatment failure.
  • Histone deacetylases (HDACs) are key regulators of chromatin structure and gene expression.

Purpose of the Study:

  • To review the role of HDACs in the development of cancer drug resistance.
  • To elucidate the epigenetic mechanisms by which HDACs contribute to treatment failure.
  • To highlight potential therapeutic strategies targeting HDACs to overcome resistance.

Main Methods:

  • Literature review of studies investigating HDACs and cancer drug resistance.
  • Analysis of epigenetic mechanisms involving histone acetylation and HDAC targets.
  • Examination of HDAC's influence on gene expression, including promoters and enhancers.

Main Results:

  • HDACs regulate gene expression by controlling histone acetylation and DNA accessibility.
  • Dysregulation of HDACs can lead to altered expression of genes involved in drug sensitivity.
  • Non-histone targets of HDACs also contribute to the development of drug resistance.

Conclusions:

  • HDACs are critical mediators of epigenetic changes that drive cancer drug resistance.
  • Targeting HDACs offers a promising strategy to re-sensitize tumors to chemotherapy and other cancer treatments.
  • Further research into HDAC functions and non-histone targets is needed to optimize therapeutic interventions.