Because cancer cachexia differs significantly from starvation, nutritional supplementation must be used in conjunction with other anti-cachexia agents to reverse the chronic systemic inflammatory state and the effects of circulating tumor-derived factors seen in cachexia. Careful identification of patients at risk and those suffering from this syndrome will lead to better outcomes and treatments. Ultimately, more research is needed to better treat this devastating condition.

Background. Animal models suggest that cyclooxygenase-2 (COX-2) inhibitors may be beneficial in suppressing cancer cachexia. We investigated the effect of short-course celecoxib on body composition, inflammation, and quality of life (QOL) in patients with cancer cachexia in a phase II clinical pilot trial.Methods. Eleven cachectic patients with head and neck or gastrointestinal cancer were randomly assigned to receive placebo or celecoxib for 21 days while awaiting the initiation of cancer therapy. Body composition, resting energy expenditure, QOL, physical function, and inflammatory markers were measured on days 1 and 21.Results. Patients receiving celecoxib experienced statistically significant increases in weight and body mass index (BMI), while patients receiving placebo experienced weight loss and a decline in BMI. Patients receiving celecoxib also had increases in QOL scores.Conclusions. This syndrome is distinct from starvation in that it involves preferential wasting of lean body mass (LBM) while visceral proteins are preserved; elevated systemic inflammation, including increased levels of acute phase proteins and inflammatory cytokines; and elaboration of tumor-derived catabolic factors.2 Cachexia remains difficult to treat, with few U.S. Food and Drug Administrationapproved therapeutic options other than megestrol acetate, dronabinol, and oxandrolone.2 These

Cancer cachexia is a morbid wasting syndrome common among patients with head and neck cancer. While its clinical manifestations have been well characterized, its pathophysiology remains complex. A comprehensive literature search on cancer cachexia was performed using the National Library of Medicine's PubMed. The Cochrane Library and Google search engine were also used. Recent evidence and new concepts on the pathophysiology of cancer cachexia are summarized. Targeted therapies are presented, and new concepts are highlighted. Cancer cachexia is characterized by complex, multilevel pathogenesis. It involves up-regulated tissue catabolism and impaired anabolism, release of tumor-derived catabolic factors and inflammatory cytokines, and neuroendocrine dysfunction. These culminate to create an energy-inefficient state characterized by wasting, chronic inflammation, neuroendocrine dysfunction, and anorexia.

To determine whether mice unable to mount an intact inflammatory response because of a Toll-like receptor (TLR) pathway defect will develop less severe cancer cachexia.

In patients 25 years of age or younger, NPC is more common in African Americans. This may represent a genetic and racial predisposition of this unusual disease in the United States. Late-stage presentations and distant recurrences are common. Platinum-based combination chemoradiotherapy and aggressive management of metastatic disease, however, is associated with good long-term survival. Further study of the possibly changing epidemiology and racial genetics of this unusual tumor is warranted.