Speakers - CIRWC 2024

Abstract

Two of the most prevalent causes of death are cancer and coronary artery disease (CAD), and they commonly coexist, particularly as the world's population ages. CAD can emerge before or after a cancer diagnosis, as well as as a negative side effect of cancer therapy. The leading cause of death in women each year is still invasive ductal carcinoma (IDC), which is fueled by intricate signaling pathways and shares a number of risk factors with coronary artery disease (CAD). Therefore, it's crucial to identify the frequent epigenetic alterations that may cause a disease to advance from CAD to IDC. In both sick situations, we have discovered a number of epigenetic regulators that play a major role in inflammatory pathways. Epitranscriptomic changes such as aberrant m⁶A RNA methylation have been found in CD4⁺T helper cells in both IDC and CAD. By controlling aberrant m⁶A RNA methylation and the tumor suppressor gene P53, CRISPR-Cas9-mediated knockout/overexpression of a specific gene (BRCA1) is a viable therapeutic strategy in sick circumstances.

Additionally, it had an impact on the DNA damage-prone R-loop creation. BRCA1 can also cause CTL-mediated cytotoxicity in breast cancer cells. Understanding how epigenetic pathways can be altered and how they interact could help researchers create newer therapeutic strategies to halt the potential transmission of one disease to another. Understanding the complex link between CAD and IDC should lead to better prevention, quicker detection, and safer treatment methods.