Breast Cancer as an Epstein-Barr Virus (EBV)-Associated Malignancy

Abstract

The Epstein Barr Virus is among the very first oncogenic viruses to be identified as culprits of human malignancies. Its role as an etiologic agent of breast cancer however remains debated despite mounting molecular evidence. In this chapter we address the challenge of multiple molecular etiologies of breast cancer (BC) with emphasis on the Epstein Barr Virus (EBV) as a potential causative agent within a frame work of gene/environment interaction. We also hope to contribute to a critique of the a concept of universal single agent or gene in cancer etiology. In addition to reviewing further reasons of why EBV should be considered a tumor virus, coupling molecular targets at the initiation stage, we examine evidence for the culpability of EBV as oncogenic virus in relation to the genetic and epigenetic events that leads to carcinogenesis of cancer; and the subsequent downstream interaction including genetic and epigenetic modifiers of signaling and molecular function underlying the cancerous phenotype. The TNF family is taken as an example of how the epigenetic reprogramming process, impacts molecular targets and how these combined interplay of molecular events impinges on pathogenesis and malignancy of breast cancer in humans.

The Role of Epstein-Barr Virus in Modulating Key Tumor Suppressor Genes in Associated Malignancies: Epigenetics, Transcriptional, and Post-Translational Modifications

“…p53 is a DNA-binding protein and a transcription factor that facilitates the activation of several genes in response to stimuli such as DNA damage and oncogene activation [ 81 ]. This protein induces cell-cycle arrest and allows for apoptosis to occur, which is prioritized in the treatment of cancer for killing damaged or cancer cells [ 82 ]. In addition, p53 helps to maintain chromosomal integrity in cell-cycle checkpoints through cell-cycle arrest, which allows for double-stranded break repair [ 83 ].…”