Targeted CML therapy: controlling drug resistance, seeking cure

被引：139

作者：

O'Hare, T ^{[1
]}

Corbin, AS ^{[1
]}

Druker, BJ ^{[1
]}

机构：

[1] Oregon Hlth & Sci Univ, Inst Canc, Howard Hughes Med Inst, Portland, OR 97239 USA

来源：

CURRENT OPINION IN GENETICS & DEVELOPMENT | 2006年 / 16卷 / 01期

关键词：

D O I：

10.1016/j.gde.2005.11.002

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

Targeted cancer therapy with imatinib (Gleevec) has the capability to drive chronic myeloid leukemia (CML) into clinical remission. Some patients, particularly those with advanced disease, develop resistance to imatinib. To counteract this problem, two new BCR-ABL kinase inhibitors for imatinib-refractory disease are currently in clinical trials: the imatinib derivative AMN107 and the dual-specificity SRC/ABL inhibitor dasatinib. Using imatinib to reduce leukemic burden also facilitates the detailed investigation into how the persistence of CML disease depends on BCR-ABL signaling, particularly within the leukemic stem cell compartment. Mathematical models of drug resistance and disease relapse, in addition to experimental systems that recapitulate crucial aspects of advanced disease have deepened our understanding of CML biology. Together, these advances are contributing to a high level of disease control, and might ultimately lead to disease eradication.

引用

页码：92 / 99

页数：8

共 58 条

[31] Lonafarnib reduces the resistance of primitive quiescent CML cells to imatinib mesylate in vitro [J].

Jorgensen, HG ;

Allan, EK ;

Graham, SM ;

Godden, JL ;

Richmond, L ;

Elliott, MA ;

Mountford, JC ;

Eaves, CJ ;

Holyoake, TL .

LEUKEMIA, 2005, 19 (07) :1184-1191

[32]

Kantarjian H, 2005, J CLIN ONCOL, V23, p195S

[33] MDM2 antagonists induce p53-dependent apoptosis in AML: implications for leukemia therapy [J].

Kojima, K ;

Konopleva, M ;

Samudio, IJ ;

Shikami, M ;

Cabreira-Hansen, M ;

McQueen, T ;

Ruvolo, V ;

Tsao, T ;

Zeng, ZH ;

Vassilev, LT ;

Andreeff, M .

BLOOD, 2005, 106 (09) :3150-3159

[34] Drug resistance in cancer: Principles of emergence and prevention [J].

Komarova, NL ;

Wodarz, D .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2005, 102 (27) :9714-9719

[35] Combination of imatinib mesylate with autologous leukocyte-derived heat shock protein and chronic myelogenous leukemia [J].

Li, ZH ;

Qiao, Y ;

Liu, B ;

Laska, EJ ;

Chakravarthi, P ;

Kulko, JM ;

Bona, RD ;

Fang, M ;

Hegde, U ;

Moyo, V ;

Tannenbaum, SH ;

Ménoret, A ;

Gaffney, J ;

Glynn, L ;

Runowicz, CD ;

Srivastava, PK .

CLINICAL CANCER RESEARCH, 2005, 11 (12) :4460-4468

[36] Dynamics of chronic myeloid leukaemia [J].

Michor, F ;

Hughes, TP ;

Iwasa, Y ;

Branford, S ;

Shah, NP ;

Sawyers, CL ;

Nowak, MA .

NATURE, 2005, 435 (7046) :1267-1270

[37]

Nagar B, 2002, CANCER RES, V62, P4236

[38] Structural basis for the autoinhibition of c-Abl tyrosine kinase [J].

Nagar, B ;

Hantschel, O ;

Young, MA ;

Scheffzek, K ;

Veach, D ;

Bornmann, V ;

Clarkson, B ;

Superti-Furga, G ;

Kuriyan, J .

CELL, 2003, 112 (06) :859-871

[39] Mechanisms and implications of imatinib resistance mutations in BCR-ABL [J].

Nardi, V ;

Azam, M ;

Daley, GQ .

CURRENT OPINION IN HEMATOLOGY, 2004, 11 (01) :35-43

[40] Clonal evolution and lack of cytogenetic response are adverse prognostic factors for hematologic relapse of chronic phase CML patients treated with imatinib mesylate [J].

O'Dwyer, ME ;

Mauro, MJ ;

Blasdel, C ;

Farnsworth, M ;

Kurilik, G ;

Hsieh, YC ;

Mori, M ;

Druker, BJ .

BLOOD, 2004, 103 (02) :451-455

← 1 2 3 4 5 6 →