Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học 'Respiratory Research cung cấp cho các bạn kiến thức về ngành y đề tài: "The molecular basis of lung cancer: molecular abnormalities and therapeutic implications. | Respiratory Research BioMed Central Review Open Access The molecular basis of lung cancer molecular abnormalities and therapeutic implications Pierre P Massion and David P Carbone Address Vanderbilt-Ingram Comprehensive Cancer Center Vanderbilt University Medical Center Nashville Tennessee . 37232-6838 Email Pierre P Massion - David P Carbone - Corresponding author Published 07 October 2003 Received 17 July 2003 Accepted 07 October 2003 Respiratory Research 2003 4 12 This article is available from http content 4 1 12 2003 Massion and Carbone licensee BioMed Central Ltd. This is an Open Access article verbatim copying and redistribution of this article are permitted in all media for any purpose provided this notice is preserved along with the article s original URL. Abstract Lung cancer is the number one cause of cancer-related death in the western world. Its incidence is highly correlated with cigarette smoking and about 10 of long-term smokers will eventually be diagnosed with lung cancer underscoring the need for strengthened anti-tobacco policies. Among the 10 of patients who develop lung cancer without a smoking history the environmental or inherited causes of lung cancer are usually unclear. There is no validated screening method for lung cancer even in high-risk populations and the overall five-year survival has not changed significantly in the last 20 years. However major progress has been made in the understanding of the disease and we are beginning to see this knowledge translated into the clinic. In this review we will summarize the current state of knowledge regarding the cascade of events associated with lung cancer development. From subclinical DNA damage to overt invasive disease the mechanisms leading to clinically and molecularly heterogeneous tumors are being unraveled. These lesions allow cells to escape the normal regulation of cell division apoptosis and .
