Lung carcinoma is the leading cause of carcinoma death in the world. Despite recent advances in understanding the molecular biology of lung cancer and the introduction of new therapeutic agents for its treatment, its dismal 5-year survival rate has not changed substantially. Clinical approaches have not significantly improved the survival of patients with advanced lung cancer. However, recent discoveries about the molecular mechanisms responsible for lung cancer initiation and proliferation have unveiled new targets for therapy. One of the hallmark features of cancer cells is their ability to evade programmed cell death or apoptosis. Alterations in pro- and anti-apoptotic pathways are common in cancer cells and defects in regulation of apoptosis have been implicated in both lung tumorigenesis and drug resistance. Thus, targeting apoptosis through the direct or indirect manipulation of the pro-apoptotic machinery offers a novel strategy for treatment. This mini review summaries the molecular events that contribute to drug-induced apoptosis and how lung tumors evade apoptotic death followed by an analysis of the implications for treatment.
Current Cancer Drug Targets aims to cover all the latest and outstanding developments on the medicinal chemistry, pharmacology, molecular biology, genomics and biochemistry of contemporary molecular drug targets involved in cancer, e.g. disease specific proteins, receptors, enzymes, genes. Each issue of the journal contains a series of timely in-depth reviews written by leaders in the field covering a range of current topics on drug targets involved in cancer. As the discovery, identification, characterization and validation of novel human drug targets for anti-cancer drug discovery continues to grow; this journal has become essential reading for all pharmaceutical scientists involved in drug discovery and development.