摘要: Thoracic oncologists traditionally have made treatment decisions based upon tumor histology, distinguishing non-small cell lung cancer (NSCLC) from small (SCLC). However, recent data has revealed that at least one histological subtype of NSCLC, adenocarcinoma comprises multiple molecularly distinct diseases. Lung subsets now can be defined by specific ‘driver’ mutations in genes encoding components the EGFR signaling pathway. Importantly, these implications regarding targeted therapy. Here, we focus on mutant NSCLC—a prime example a clinically relevant molecular subset cancer, with mechanisms drug sensitivity, primary resistance, and acquired resistance to tyrosine kinase inhibitors. Efforts are being overcome resistance. These findings illustrate how knowledge about genetic drivers tumors lead rational therapy for individual patients.
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Shinichi Toyooka, Katsuyuki Kiura, Tetsuya Mitsudomi, None, EGFR mutation and response of lung cancer to gefitinib. The New England Journal of Medicine. ,vol. 352, pp. 2136- ,(2005) , 10.1056/NEJM200505193522019
Sarah Sherlock, Zhuang Liu, Qizhen Cao, Hongjie Dai, Xiaoyuan Chen, Corrine Davis, Kai Chen, Drug delivery with carbon nanotubes for in vivo cancer treatment arXiv: Materials Science. ,(2008) , 10.1158/0008-5472
Jim R Woodburn, Susan E Ashton, Simon P Guy, Keith H Gibson, Brenda J Curry, Andrew J Barker, Alan E Wakeling, ZD1839 (Iressa): an orally active inhibitor of epidermal growth factor signaling with potential for cancer therapy. Cancer Research. ,vol. 62, pp. 5749- 5754 ,(2002)
Vincent A. Pollack, Catherine DiOrio, April Theleman, Elsa G. Barbacci, Leslie R. Pustilnik, Mark Neveu, Mikel P. Moyer, Kenneth K. Iwata, Lee Arnold, Michael J. Morin, James D. Moyer, Bruce Boman, Penny Miller, Ann Cunningham, Margaret M. Reynolds, Don Sloan, Jonathan Doty, Induction of Apoptosis and Cell Cycle Arrest by CP-358,774, an Inhibitor of Epidermal Growth Factor Receptor Tyrosine Kinase Cancer Research. ,vol. 57, pp. 4838- 4848 ,(1997)
V. A. Miller, H. A. Wakelee, P. N. Lara, J. Cho, N. M. Chowhan, D. Costa, N. Vrindavanam, R. Yanagihara, N. Pennell, T. J. Lynch, Activity and tolerance of XL647 in NSCLC patients with acquired resistance to EGFR-TKIs: Preliminary results of a phase II trial Journal of Clinical Oncology. ,vol. 26, pp. 8028- 8028 ,(2008) , 10.1200/JCO.2008.26.15_SUPPL.8028
Elena Tamborini, Lorena Bonadiman, Angela Greco, Veronica Albertini, Tiziana Negri, Alessandro Gronchi, Rossella Bertulli, Maurizio Colecchia, Paolo G. Casali, Marco A. Pierotti, Silvana Pilotti, A new mutation in the KIT ATP pocket causes acquired resistance to imatinib in a gastrointestinal stromal tumor patient. Gastroenterology. ,vol. 127, pp. 294- 299 ,(2004) , 10.1053/J.GASTRO.2004.02.021
Daniel B. Costa, Susan T. Schumer, Daniel G. Tenen, Susumu Kobayashi, Differential Responses to Erlotinib in Epidermal Growth Factor Receptor (EGFR)-Mutated Lung Cancers With Acquired Resistance to Gefitinib Carrying the L747S or T790M Secondary Mutations Journal of Clinical Oncology. ,vol. 26, pp. 1182- 1184 ,(2008) , 10.1200/JCO.2007.14.9039
Sreenath V. Sharma, Daphne W. Bell, Jeffrey Settleman, Daniel A. Haber, Epidermal growth factor receptor mutations in lung cancer Nature Reviews Cancer. ,vol. 7, pp. 169- 181 ,(2007) , 10.1038/NRC2088
Susan Branford, Zbigniew Rudzki, Sonya Walsh, Andrew Grigg, Chris Arthur, Kerry Taylor, Richard Herrmann, Kevin P. Lynch, Timothy P. Hughes, High frequency of point mutations clustered within the adenosine triphosphate-binding region of BCR/ABL in patients with chronic myeloid leukemia or Ph-positive acute lymphoblastic leukemia who develop imatinib (STI571) resistance. Blood. ,vol. 99, pp. 3472- 3475 ,(2002) , 10.1182/BLOOD.V99.9.3472
Nancy E. Hynes, Heidi A. Lane, ERBB receptors and cancer: the complexity of targeted inhibitors. Nature Reviews Cancer. ,vol. 5, pp. 341- 354 ,(2005) , 10.1038/NRC1609