Targeting epigenetic mediators of gene expression in thoracic malignancies

David S Schrump1

  • 1Thoracic Oncology Section, Surgery Branch, Center for Cancer Research, National Cancer Institute, Rm. 4-3940, 10 Center Drive, MSC 1201, Bethesda, MD 20892-1201, USA. david_schrump@nih.gov

Insights

Epigenomic alterations, including DNA methylation and histone modifications, are crucial in thoracic cancers. Targeting these epigenetic changes offers promising new treatment strategies for lung and esophageal cancers.

Area of Science:

  • Oncology
  • Epigenetics
  • Molecular Biology

Background:

  • Lung, esophageal cancers, and malignant pleural mesotheliomas are highly lethal neoplasms.
  • Limited understanding exists regarding the epigenetic mechanisms driving these thoracic malignancies.
  • Epigenetic dysregulation plays a critical role in cancer initiation and progression.

Purpose of the Study:

  • To review the clinical relevance of epigenomic alterations in thoracic malignancies.
  • To discuss the roles of DNA methylation, histone code perturbations, and polycomb group proteins.
  • To highlight translational efforts targeting epigenetic regulators for cancer treatment.

Main Methods:

  • Review of current literature on epigenomic alterations in thoracic cancers.
  • Focus on DNA methylation patterns.
  • Analysis of histone modifications and polycomb group protein involvement.
  • Examination of therapeutic strategies targeting epigenetic regulators.

Main Results:

  • Epigenomic alterations, including DNA methylation and histone modifications, are frequently observed in thoracic neoplasms.
  • These alterations impact gene expression critical for cancer development.
  • Targeting epigenetic regulators shows potential in preclinical and clinical settings.

Conclusions:

  • Epigenomic alterations are key drivers in thoracic malignancies.
  • Therapeutic strategies targeting epigenetic mechanisms offer a promising avenue for novel cancer treatments.
  • Further research is needed to fully elucidate and exploit these epigenetic targets.

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