In:
Annual Review of Medicine, Annual Reviews, Vol. 54, No. 1 ( 2003-02), p. 73-87
Abstract:
Lung cancer results from multiple changes in the genome of susceptible pulmonary cells caused by exposure to carcinogens found in tobacco smoke, the environment, or the workplace. Recent studies suggest that histologically apparent lung cancer is due to the sequential accumulation of specific genetic and morphologic changes to the normal epithelial cells of the lung. Positive signallers, such as those mediated by the oncogene RAS, and negative signallers, such as those mediated by the tumor suppressor retinoblastoma protein (RB), contribute to unchecked cell growth and proliferation. Other key molecular derangements can also be considered hallmarks of cancer, including evasion of apoptosis and senescence, angiogenesis, tissue invasion, and metastases. Epigenetic inactivation of genes via DNA methylation provides another novel way of evading normal cellular control mechanisms. The new knowledge of the human genome coupled with global methods of detecting genetic abnormalities and profiling gene expression in tumor cells may enable us to understand the signaling pathways of lung cancer cells. These are molecular targets for new cancer therapeutics such as receptor tyrosine kinase inhibitors. This information could advance risk assessment, early detection, prognosis, and therapy for lung cancer.
Type of Medium:
Online Resource
ISSN:
0066-4219
,
1545-326X
DOI:
10.1146/med.2003.54.issue-1
DOI:
10.1146/annurev.med.54.101601.152202
Language:
English
Publisher:
Annual Reviews
Publication Date:
2003
detail.hit.zdb_id:
1481484-5
