Research Projects

Cancer Cachexia (CC) is a metabolic syndrome linked to various cancers, characterized by significant loss of skeletal muscle and adipose tissue. Despite its prevalence, CC is often overlooked due to the focus on treating the tumor itself and lack of approved drug therapy. CC leads to complications such as systemic inflammation, anorexia, insulin resistance, anemia, lipolysis, and fatigue, disrupting cancer treatment regimens. It is most prevalent in patients with advanced cancers, but solid tumors like pancreatic and lung cancer show earlier occurrence. 20-30% of patients die due to CC, rather than tumor burden itself. The disease is triggered by an imbalance in signaling pathways controlling skeletal muscle anabolic and catabolic processes, leading to muscle atrophy. The primary cause of skeletal muscle protein breakdown is the need for higher glucose consumption by tumor cells. Cytokines produced from tumor cells and hosts trigger downstream pathways leading to altered gene expression, including E3 ubiquitin ligases MURF1, Atrogin1, which are central to myofibrilar protein degradation. Understanding the molecular basis of wasting in CC is crucial for developing a viable therapeutic intervention. Research shows that the expression and function of an epigenetic regulator G9a/EHMT2, a SET domain containing methyltransferase, is altered in several cancers. Targeting G9a activity with inhibitors is considered a promising prospect in cancer treatment.