ABSTRACT
It becomes more and more important to understand the biology of lung cancer as new therapeutic agents are emerging in the field of clinical oncology. These agents are often referred to as targeted therapy or biologic therapy. New advances in molecular technologies are providing insight into the pathobiology of lung cancer development. It is now known that clinical lung cancers have accumulated numerous clonal genetic and epigenetic alterations as a multistep process. 1 In many research laboratories molecular studies are these days performed in an integrated approach with clinical investigators to find new ways for early diagnosis, risk assessment, prevention, and treatment for this frequent and deadly disease. In the following, the spectrum of molecular alterations in lung cancer are described as hallmarks of cancer, subdivided as suggested by Hanahan and Weinberg: 2
abnormalities in self-sufficiency of growth • signals; evading apoptosis; • insensitivity to anti-growth signals; • limitless replicative potential; • sustained angiogenesis; • tissue invasion and metastasis. •
GROWTH SIGNALS AND LUNG CANCER
In tumor cells, activated (proto)oncogenes often encode molecules involved in aberrant growth factor signaling, either by directly promoting cell growth, by mimicking other growth factors, or by neutralizing growth inhibitory signals. Growth factors are proteins that bind to receptors (usually on the cell surface) and trigger activation of cellular proliferation and/or differentiation.
