Insulin-like growth factor receptor 1 (IGFR-1) is significantly associated with longer survival in non-small-cell lung cancer patients treated with gefitinib

被引:85
作者
Cappuzzo, F.
Toschi, L.
Tallini, G.
Ceresoli, G. L.
Domenichini, I.
Bartolini, S.
Finocchiaro, G.
Magrini, E.
Metro, G.
Cancellieri, A.
Trisolini, R.
Crino, L.
Bunn, P. A., Jr.
Santoro, A.
Franklin, W. A.
Varella-Garcia, M.
Hirsch, F. R.
机构
[1] Univ Colorado, Ctr Canc, Dept Med Med Oncol & Pathol, Aurora, CO USA
[2] Bellaria Maggiore Hosp, Dept Med Oncol, Bologna, Italy
[3] Ist Clin Humanitas, Dept Med Oncol, Rozzano, Italy
[4] CINECA Interuniv Consortium, Bologna, Italy
关键词
IGFR-1; PTEN; EGFR; tyrosine kinase inhibitor; gefitinib; non-small-cell lung cancer;
D O I
10.1093/annonc/mdl077
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Background: The aim of the study was to assess whether loss of PTEN and expression of insulin-like growth factor receptor 1 (IGFR-1) could be responsible for intrinsic resistance to the tyrosine kinase inhibitor (TKI) gefitinib. Patients and methods: One hundred and twenty-four gefitinib-treated patients with advanced non-small-cell lung cancer (NSCLC) were analyzed for PTEN and IGFR-1 expression by immunohistochemistry. Results: IGFR-1 was evaluated in 77 patients and resulted positive in 30 (39.0%). IGFR-1 expression was not significantly associated with clinical or biological characteristics. No difference in response to gefitinib treatment (16.7% versus 12.8%, P = 0.74) and time to progression (2.6 versus 3.06 months, P = 0.83) was observed between IGFR-1+ and IGFR-1-. Median survival was significantly longer in IGFR-1+ patients (17.8 versus 7.3 months, P = 0.013). PTEN expression was successfully evaluated in 93 cases. Loss of PTEN was detected in 19 tumors (20.4%) and was not associated with any clinical or biological characteristic. No difference in terms of response, time to progression and survival was observed between PTEN+ and PTEN- patients. In multivariable analysis IGFR-1 negative status was significantly associated with higher risk of death (hazard ratio 2.21, P = 0.012). Conclusions: IGFR-1 expression and loss of PTEN are not associated with intrinsic resistance to gefitinib. Clinical relevance of these two biomarkers as determinant for acquired resistance, and the prognostic role of IGFR-1 expression in patients not exposed to TKIs should be evaluated further.
引用
收藏
页码:1120 / 1127
页数:8
相关论文
共 59 条
[31]   Efficacy of gefitinib, an inhibitor of the epidermal growth factor receptor tyrosine kinase, in symptomatic patients with non-small cell lung cancer - A randomized trial [J].
Kris, MG ;
Natale, RB ;
Herbst, RS ;
Lynch, TJ ;
Prager, D ;
Belani, CP ;
Schiller, JH ;
Kelly, K ;
Spiridonidis, H ;
Sandler, A ;
Albain, KS ;
Cella, D ;
Wolf, MK ;
Averbuch, SD ;
Ochs, JJ ;
Kay, AC .
JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION, 2003, 290 (16) :2149-2158
[32]   MOLECULAR AND CELLULAR ASPECTS OF THE INSULIN-LIKE GROWTH-FACTOR-I RECEPTOR [J].
LEROITH, D ;
WERNER, H ;
BEITNERJOHNSON, D ;
ROBERTS, CT .
ENDOCRINE REVIEWS, 1995, 16 (02) :143-163
[33]  
Li DM, 1997, CANCER RES, V57, P2124
[34]   PTEN, a putative protein tyrosine phosphatase gene mutated in human brain, breast, and prostate cancer [J].
Li, J ;
Yen, C ;
Liaw, D ;
Podsypanina, K ;
Bose, S ;
Wang, SI ;
Puc, J ;
Miliaresis, C ;
Rodgers, L ;
McCombie, R ;
Bigner, SH ;
Giovanella, BC ;
Ittmann, M ;
Tycko, B ;
Hibshoosh, H ;
Wigler, MH ;
Parsons, R .
SCIENCE, 1997, 275 (5308) :1943-1947
[35]   Insulin-like growth factor-I receptor signaling and resistance to trastuzumab (Herceptin) [J].
Lu, YH ;
Zi, XL ;
Zhao, YH ;
Mascarenhas, D ;
Pollak, M .
JNCI-JOURNAL OF THE NATIONAL CANCER INSTITUTE, 2001, 93 (24) :1852-1857
[36]   Activating mutations in the epidermal growth factor receptor underlying responsiveness of non-small-cell lung cancer to gefitinib [J].
Lynch, TJ ;
Bell, DW ;
Sordella, R ;
Gurubhagavatula, S ;
Okimoto, RA ;
Brannigan, BW ;
Harris, PL ;
Haserlat, SM ;
Supko, JG ;
Haluska, FG ;
Louis, DN ;
Christiani, DC ;
Settleman, J ;
Haber, DA .
NEW ENGLAND JOURNAL OF MEDICINE, 2004, 350 (21) :2129-2139
[37]  
Olaussen KA, 2003, ANTICANCER RES, V23, P4885
[38]   EGFR mutations in lung cancer:: Correlation with clinical response to gefitinib therapy [J].
Paez, JG ;
Jänne, PA ;
Lee, JC ;
Tracy, S ;
Greulich, H ;
Gabriel, S ;
Herman, P ;
Kaye, FJ ;
Lindeman, N ;
Boggon, TJ ;
Naoki, K ;
Sasaki, H ;
Fujii, Y ;
Eck, MJ ;
Sellers, WR ;
Johnson, BE ;
Meyerson, M .
SCIENCE, 2004, 304 (5676) :1497-1500
[39]   KRAS mutations and primary resistance of lung adenocarcinomas to gefitinib or erlotinib [J].
Pao, W ;
Wang, TY ;
Riely, GJ ;
Miller, VA ;
Pan, QL ;
Ladanyi, M ;
Zakowski, MF ;
Heelan, RT ;
Kris, MG ;
Varmus, HE .
PLOS MEDICINE, 2005, 2 (01) :57-61
[40]   Acquired resistance of lung adenocarcinomas to gefitinib or erlotinib is associated with a second mutation in the EGFR kinase domain [J].
Pao, W ;
Miller, VA ;
Politi, KA ;
Riely, GJ ;
Somwar, R ;
Zakowski, MF ;
Kris, MG ;
Varmus, H .
PLOS MEDICINE, 2005, 2 (03) :225-235