Molecular pathogenesis of lung cancer

被引:102
作者
Fong, KM
Sekido, Y
Minna, JD
机构
[1] Univ Texas, SW Med Ctr, Hamon Ctr Therapeut Oncol Res, Dallas, TX 75235 USA
[2] Prince Charles Hosp, Brisbane, Qld 4032, Australia
[3] Nagoya Univ Hosp, Dept Clin Prevent Serv, Nagoya, Aichi, Japan
关键词
D O I
10.1016/S0022-5223(99)70121-2
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Lung cancer is the largest cancer killer of men and women in the United States. In addition to the progress made from antismoking primary prevention measures, new tools to help treat patients with lung cancer are emerging from the rapid advances in knowledge of the molecular pathogenesis of lung cancer. These tools include molecular and cellular biology and are starting to provide an insight into how the tumor cell, by altering oncogenes and tumor suppressor genes, achieves growth advantage, uncontrolled proliferation and metastatic behavior via disruption of key cell-cycle regulators and signal transduction cascades. Moreover, new knowledge is being developed in terms of the molecular definition of individual susceptibility to tobacco smoke carcinogens. These tools are being translated into clinical strategies to complement surgery, radiotherapy, and chemotherapy and also to assist in primary and secondary prevention efforts. This review summarizes current knowledge of the molecular pathogenesis of lung cancer, From this we know that respiratory epithelial cells require many genetic alterations to become invasive and metastatic cancer. We can detect cells with a few such changes in current and former smokers, offering the opportunity to intercede with a biomarker-monitored prevention and early detection effort. This will be coupled with new advances in computed tomography-based screening. Finally, because the molecular alterations are known, new mechanism-based therapies are being developed and brought to the clinic, including new drugs, vaccines, and gene therapy, which also must be integrated with standard therapies.
引用
收藏
页码:1136 / 1152
页数:17
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