Opinion - Switching on kinases: oncogenic activation of BRAF and the PDGFR family

被引：153

作者：

Dibb, NJ

Dilworth, SM

Mol, CD

机构：

[1] Univ London Imperial Coll Sci Technol & Med, Inst Reprod & Dev Biol, London W12 ONN, England

[2] Univ London Imperial Coll Sci Technol & Med, Div Invest Sci, London W12 ONN, England

[3] Syrrx Inc, San Diego, CA 92121 USA

来源：

NATURE REVIEWS CANCER | 2004年 / 4卷 / 09期

基金：

英国生物技术与生命科学研究理事会;

关键词：

D O I：

10.1038/nrc1434

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

The cytoplasmic serine/threonine kinase BRAF and receptor tyrosine kinases of the platelet-derived growth factor receptor (PDGFR) family are frequently activated in cancer by mutations of an equivalent amino acid. Structural studies have provided important insights into why these very different kinases share similar oncogenic hot spots and why the PDGFR juxtamembrane region is also a frequent oncogenic target. This research has implications for other kinases that are mutated in human tumours and for the treatment of cancer using kinase inhibitors.

引用

收藏

页码：718 / 727

页数：10

相关论文

共 86 条

[1]

Antonescu CR, 2003, CLIN CANCER RES, V9, P3329

[2] Response to imatinib mesylate in patients with chronic myeloproliferative diseases with rearrangements of the platelet-derived growth factor receptor beta [J].

Apperley, JF ;

Gardembas, M ;

Melo, JV ;

Russell-Jones, R ;

Bain, BJ ;

Baxter, J ;

Chase, A ;

Chessells, JM ;

Colombat, M ;

Dearden, CE ;

Dimitrijevic, S ;

Mahon, FX ;

Marin, D ;

Nikolova, Z ;

Olavarria, E ;

Silberman, S ;

Schultheis, B ;

Cross, NCP ;

Goldman, JM .

NEW ENGLAND JOURNAL OF MEDICINE, 2002, 347 (07) :481-487

[3] Mechanisms of autoinhibition and STI-571/imatinib resistance revealed by mutagenesis of BCR-ABL [J].

Azam, M ;

Latek, RR ;

Daley, GQ .

CELL, 2003, 112 (06) :831-843

[4] Mutational analysis of the tyrosine kinome in colorectal cancers [J].

Bardelli, A ;

Parsons, DW ;

Silliman, N ;

Ptak, J ;

Szabo, S ;

Saha, S ;

Markowitz, S ;

Willson, JKV ;

Parmigiani, G ;

Kinzler, KW ;

Vogelstein, B ;

Velculescu, VE .

SCIENCE, 2003, 300 (5621) :949-949

[5] The structure of phosphorylated P38γ is monomeric and reveals a conserved activation-loop conformation [J].

Bellon, S ;

Fitzgibbon, MJ ;

Fox, T ;

Hsiao, HM ;

Wilson, KP .

STRUCTURE, 1999, 7 (09) :1057-1065

[6] A single amino acid exchange inverts susceptibility of related receptor tyrosine kinases for the ATP site inhibitor STI-571 [J].

Böhmer, FD ;

Karagyozov, L ;

Uecker, A ;

Serve, H ;

Botzki, A ;

Mahboobi, S ;

Dove, S .

JOURNAL OF BIOLOGICAL CHEMISTRY, 2003, 278 (07) :5148-5155

[7]

Buchdunger E, 1996, CANCER RES, V56, P100

[8]

Buchdunger E, 2000, J PHARMACOL EXP THER, V295, P139

[9] Activation mechanism of the MAP kinase ERK2 by dual phosphorylation [J].

Canagarajah, BJ ;

Khokhlatchev, A ;

Cobb, MH ;

Goldsmith, EJ .

CELL, 1997, 90 (05) :859-869

[10] Autoinhibition of the Kit receptor tyrosine kinase by the cytosolic juxtamembrane region [J].

Chang, PM ;

Ilangumaran, S ;

La Rose, J ;

Chakrabartty, A ;

Rottapel, R .

MOLECULAR AND CELLULAR BIOLOGY, 2003, 23 (09) :3067-3078

← 1 2 3 4 5 6 7 8 9 →