Biological and clinical significance of KRAS mutations in lung cancer: an oncogenic driver that contrasts with EGFR mutation

被引:175
作者
Suda, Kenichi [1 ]
Tomizawa, Kenji [1 ]
Mitsudomi, Tetsuya [1 ]
机构
[1] Aichi Canc Ctr Hosp, Dept Thorac Surg, Chikusa Ku, Nagoya, Aichi 4648681, Japan
基金
日本学术振兴会;
关键词
Lung cancer; Oncogene addiction; Targeted therapy; Personalized medicine; GROWTH-FACTOR-RECEPTOR; K-RAS ONCOGENE; EML4-ALK FUSION GENE; TRANSFORMING GENES; CELL-LINES; PHASE-III; SOMATIC MUTATIONS; TYROSINE KINASE; NEVER SMOKERS; JAPANESE PATIENTS;
D O I
10.1007/s10555-010-9209-4
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
KRAS and epidermal growth factor receptor (EGFR) are the two most frequently mutated proto-oncogenes in adenocarcinoma of the lung. The occurrence of these two oncogenic mutations is mutually exclusive, and they exhibit many contrasting characteristics such as clinical background, pathological features of patients harboring each mutation, and prognostic or predictive implications. Lung cancers harboring the EGFR mutations are remarkably sensitive to EGFR tyrosine kinase inhibitors such as gefitinib or erlotinib. This discovery has dramatically changed the clinical treatment of lung cancer in that it almost doubled the duration of survival for lung cancer patients with an EGFR mutation. In this review, we describe the features of KRAS mutations in lung cancer and contrast these with the features of EGFR mutations. Recent strategies to combat lung cancer harboring KRAS mutations are also reviewed.
引用
收藏
页码:49 / 60
页数:12
相关论文
共 105 条
[1]  
[Anonymous], J CLIN ONCOL S
[2]  
[Anonymous], J CLIN ONCOL
[3]   Systematic RNA interference reveals that oncogenic KRAS-driven cancers require TBK1 [J].
Barbie, David A. ;
Tamayo, Pablo ;
Boehm, Jesse S. ;
Kim, So Young ;
Moody, Susan E. ;
Dunn, Ian F. ;
Schinzel, Anna C. ;
Sandy, Peter ;
Meylan, Etienne ;
Scholl, Claudia ;
Froehling, Stefan ;
Chan, Edmond M. ;
Sos, Martin L. ;
Michel, Kathrin ;
Mermel, Craig ;
Silver, Serena J. ;
Weir, Barbara A. ;
Reiling, Jan H. ;
Sheng, Qing ;
Gupta, Piyush B. ;
Wadlow, Raymond C. ;
Le, Hanh ;
Hoersch, Sebastian ;
Wittner, Ben S. ;
Ramaswamy, Sridhar ;
Livingston, David M. ;
Sabatini, David M. ;
Meyerson, Matthew ;
Thomas, Roman K. ;
Lander, Eric S. ;
Mesirov, Jill P. ;
Root, David E. ;
Gilliland, D. Gary ;
Jacks, Tyler ;
Hahn, William C. .
NATURE, 2009, 462 (7269) :108-U122
[4]   GENETIC MECHANISMS IN TUMOR INITIATION AND PROGRESSION .10. THE RAS GENE FAMILY AND HUMAN CARCINOGENESIS [J].
BOS, JL .
MUTATION RESEARCH, 1988, 195 (03) :255-271
[5]  
BOS JL, 1989, CANCER RES, V49, P4682
[6]   Epidermal growth factor receptor gene and protein and gefitinib sensitivity in non-small-cell lung cancer [J].
Cappuzzo, F ;
Hirsch, FR ;
Rossi, E ;
Bartolini, S ;
Ceresoli, GL ;
Bemis, L ;
Haney, J ;
Witta, S ;
Danenberg, K ;
Domenichini, I ;
Ludovini, V ;
Magrini, E ;
Gregorc, V ;
Doglioni, C ;
Sidoni, A ;
Tonato, M ;
Franklin, WA ;
Crino, L ;
Bunn, PA ;
Varella-Garcia, M .
JNCI-JOURNAL OF THE NATIONAL CANCER INSTITUTE, 2005, 97 (09) :643-655
[7]   P21RAS IS MODIFIED BY A FARNESYL ISOPRENOID [J].
CASEY, PJ ;
SOLSKI, PA ;
DER, CJ ;
BUSS, JE .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1989, 86 (21) :8323-8327
[8]   RaIB GTPase-mediated activation of the IκB family kinase TBK1 couples innate immune signaling to tumor cell survival [J].
Chien, Yuchen ;
Kim, Sungchan ;
Bumeister, Ron ;
Loo, Yueh-Ming ;
Kwon, Sung Won ;
Johnson, Cynthia L. ;
Balakireva, Mirey G. ;
Romeo, Yves ;
Kopelovich, Levy ;
Gale, Michael, Jr. ;
Yeaman, Charles ;
Camonis, Jacques H. ;
Zhao, Yingming ;
White, Michael A. .
CELL, 2006, 127 (01) :157-170
[9]   Tumour biology -: Senescence in premalignant tumours [J].
Collado, M ;
Gil, J ;
Efeyan, A ;
Guerra, C ;
Schuhmacher, AJ ;
Barradas, M ;
Benguría, A ;
Zaballos, A ;
Flores, JM ;
Barbacid, M ;
Beach, D ;
Serrano, M .
NATURE, 2005, 436 (7051) :642-642
[10]  
CUTSEM EV, 2008, J CLIN ONCOLOGY, V26