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Journal of Parenteral and Enteral Nutrition
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2008 Research Workshop

Myeloid-Derived Suppressor Cells in Cancer Cachexia Syndrome: A New Explanation for an Old Problem

Robert D. Winfield, MD1, Matthew J. Delano, MD1, Kalyan Pande, PhD2, Philip O. Scumpia, PhD1, Drake LaFace, PhD2 and Lyle L. Moldawer, PhD1

From the 1 Department of Surgery, University of Florida College of Medicine, Gainesville, and2 Schering-Plough Biopharma, Inc (Formerly, DNAX Research Inc), Palo Alto, California.

Address correspondence to: Lyle L. Moldawer, PhD, Department of Surgery, University of Florida College of Medicine, Room 6116, Shands Hospital, 1600 SW Archer Road, Gainesville, FL 32610-0286; e-mail: moldawer{at}surgery.ufl.edu.

Cachexia accompanies many chronic inflammatory diseases, including cancer. Lean tissue wasting is only one component of the cancer cachexia response, which also includes anemia, anorexia, a hepatic acute phase protein response, and increased susceptibility to secondary infections. The etiologies of cancer cachexia are multifactorial and include an overproduction of inflammatory mediators, including cytokines produced by inappropriate activation of innate immunity. However, anticytokine therapies have generally not been seriously considered for cancer cachexia, in large part because of the overlapping activities of several inflammatory cytokines and the inability to prospectively identify the contributions of individual mediators. In contrast, recent evidence has focused on an immature myeloid cell population that expands dramatically in the tumors and secondary lymphoid organs of animals with some actively growing tumors. These immature GR-1+CD11b+ cells are metabolically active and secrete large quantities of inflammatory cytokines and chemokines with the potential to produce cachexia. Their expansion is temporally associated with the development of cachexia. Future studies are required to determine whether therapeutic efforts intended to block the expansion of these cells can prevent the lean tissue wasting that accompanies active tumor growth.

Key Words: wasting • sickness syndromes • cytokines • myelopoiesis • t cell • MDSC • malignancy • weight loss • tumor

Journal of Parenteral and Enteral Nutrition, Vol. 32, No. 6, 651-655 (2008)
DOI: 10.1177/0148607108325075
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