Cambridge University School of Medicine, UK
Posters & Accepted Abstracts: J Cancer Sci Ther
Human cancer develops as a localized focus of uncontrolled cell growth and subsequently progresses into systemic disease. Cancer research primarily focuses on the agents, events, and genetic alterations underlying tumor initiation, progression and metastasis. However, many cancer patients die because of cachexia, a systemic wasting disease caused by the tumor, but manifested by alterations in distant organs resulting in weight loss, fatigue, anemia, progressive atrophy of the white adipose tissue (WAT) and skeletal muscle. Systemic inflammation and metabolic dysfunction have been proposed as the major culprits in cachexia pathophysiology, but their chronological appearance and regulation remain elusive. We have recently shown that during the clinical progression of cancer, inflammatory mediators trigger a phenotypic switch from WAT to brown adipose tissue (BAT), a phenomenon termed WAT-browning, which is functionally responsible for increased lipid mobilization and energy consumption. WAT-browning contributes to the metabolic dysfunction observed in cancer and leads to the wasting syndrome. Current investigation focuses on the cellular players and molecular events that drive the inflammatory response during cachexia.
Cancer Science & Therapy received 3644 citations as per Google Scholar report