David P. Carbone, MD, PhD

From the 2014 ASCO Annual Meeting, this internationally renowned lung cancer expert discusses oncogenic driver mutations in lung cancer.

Immune deficiency in cancer patients is well documented, and tumor cells have developed a variety of cellular and molecular mechanisms to avoid antitumor immune responses. These mechanisms include defective presentation of tumor antigens on the cell surface and/or an inability of the host to effectively recognize these cells and target them for destruction. Tumor-induced defects are known to occur in all major branches of the immune system. The continuous administration of vascular endothelial growth factor (VEGF), a factor produced by most solid tumors, inhibits the functional maturation of dendritic cells, significantly decreases T-cell to B-cell ratios in the peripheral lymphoid organs, and induces rapid and dramatic thymic atrophy in tumor-bearing animals. VEGF is abundantly expressed by a large percentage of solid tumors, and defective antigen presentation, T-cell defects, and premature thymic atrophy are known to occur in cancer patients and tumor-bearing animals. This review will encompass the major mechanisms responsible for tumor evasion of immune surveillance and highlight a role for VEGF as a principal contributor to tumor-associated immune deficiencies. [ONCOLOGY 16(Suppl 1):11-18, 2002]

Despite recent advances in the treatment of lung cancer, long-term survival remains rare. As more information pertaining to the biology of lung cancer is understood, it is hoped that improvements in outcome can be realized