Esophageal Cancers: Leveraging Alterations in Mitochondrial Biology to Improve Patient Outcomes

Mohammad Faujul Kabir, Mary Grace Murray, Reshu Saxena, Alena Klochkova, Jasmine Cruz, Kelly A. Whelan

Research output: Chapter in Book/Report/Conference proceedingChapterpeer-review

Abstract

Esophageal cancer is one of the most aggressive forms of human malignancy. Esophageal squamous cell carcinoma (ESCC) and esophageal adenocarcinoma (EAC) are the predominant histological subtypes of esophageal cancer. Although ESCC and EAC differ with regard to pathophysiology, histology, geographical distribution, risk factors, and clinical characteristics, both have 5-year survival rates of less than 20%, underscoring the need for a better understanding of esophageal cancer biology in order to improve patient outcomes in this disease. Mitochondria are dynamic organelles that play essential roles in various cellular processes, including metabolism, redox homeostasis, calcium signaling, and apoptosis. As such, it is not surprising that alterations in mitochondrial biology have been associated with carcinogenesis across tissue types. Here, we will review the current literature implicating mitochondria in the development and progression of esophageal cancer, both ESCC and EAC, as well as how mitochondrial biology may intersect with therapeutic response in these deadly malignancies. Given the urgent need for effective strategies to improve patient outcomes in esophageal cancer, critical examination of mitochondrial biology in the context of ESCC and EAC has great potential to provide insights that will guide development of novel approaches to diagnosis, monitoring, and therapy for these deadly disease entities.

Original languageEnglish
Title of host publicationComprehensive Pharmacology
PublisherElsevier
Pages96-111
Number of pages16
Volume6
ISBN (Electronic)9780128204726
DOIs
StatePublished - Jan 1 2022
Externally publishedYes

Keywords

  • Cancer therapy
  • Esophageal cancer
  • Mitochondria

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