Maximizing mouse cancer models

被引：498

作者：

Frese, Kristopher K. ^{[1
]}

Tuveson, David A. ^{[1
]}

机构：

[1] Canc Res UK, Cambridge Res Inst, Cambridge CB2 0RE, England

来源：

NATURE REVIEWS CANCER | 2007年 / 7卷 / 09期

关键词：

D O I：

10.1038/nrc2192

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

Animal models of cancer provide an alternative means to determine the causes of and treatments for malignancy, thus representing a resource of immense potential for cancer medicine. The sophistication of modelling cancer in mice has increased to the extent that investigators can both observe and manipulate a complex disease process in a manner impossible to perform in patients. However, owing to limitations in model design and technology development, and the surprising underuse of existing models, only now are we realising the full potential of mouse models of cancer and what new approaches are needed to derive the maximum value for cancer patients from this investment.

引用

页码：645 / 658

页数：14

共 202 条

[21] p53 deficiency rescues the adverse effects of telomere loss and cooperates with telomere dysfunction to accelerate carcinogenesis [J].

Chin, L ;

Artandi, SE ;

Shen, Q ;

Tam, A ;

Lee, SL ;

Gottlieb, GJ ;

Greider, CW ;

DePinho, RA .

CELL, 1999, 97 (04) :527-538

[22] Essential role for oncogenic Ras in tumour maintenance [J].

Chin, L ;

Tam, A ;

Pomerantz, J ;

Wong, M ;

Holash, J ;

Bardeesy, N ;

Shen, Q ;

O'Hagan, R ;

Pantginis, J ;

Zhou, H ;

Horner, JW ;

Cordon-Cardo, C ;

Yancopoulos, GD ;

DePinho, RA .

NATURE, 1999, 400 (6743) :468-472

[23] Mouse models of tumor development in neurofibromatosis type 1 [J].

Cichowski, K ;

Shih, TS ;

Schmitt, E ;

Santiago, S ;

Reilly, K ;

McLaughlin, ME ;

Bronson, RT ;

Jacks, T .

SCIENCE, 1999, 286 (5447) :2172-2176

[24] REQUIREMENT FOR A FUNCTIONAL RB-1 GENE IN MURINE DEVELOPMENT [J].

CLARKE, AR ;

MAANDAG, ER ;

VANROON, M ;

VANDERLUGT, NMT ;

VANDERVALK, M ;

HOOPER, ML ;

BERNS, A ;

RIELE, HT .

NATURE, 1992, 359 (6393) :328-330

[25] Phase II and pharmacodynamic study of the farnesyltransferase inhibitor R115777 as initial therapy in patients with metastatic pancreatic adenocarcinoma [J].

Cohen, SJ ;

Ho, L ;

Ranganathan, S ;

Abbruzzese, JL ;

Alpaugh, RK ;

Beard, M ;

Lewis, NL ;

McLaughlin, S ;

Rogatko, A ;

Perez-Ruixo, JJ ;

Thistle, AM ;

Verhaeghe, T ;

Wang, H ;

Weiner, LM ;

Wright, JJ ;

Hudes, GR ;

Meropol, NJ .

JOURNAL OF CLINICAL ONCOLOGY, 2003, 21 (07) :1301-1306

[26] Cancer gene discovery in solid tumours using transposon-based somatic mutagenesis in the mouse [J].

Collier, LS ;

Carlson, CM ;

Ravimohan, S ;

Dupuy, AJ ;

Largaespada, DA .

NATURE, 2005, 436 (7048) :272-276

[27] Liver-targeted disruption of Apc in mice activates β-catenin signaling and leads to hepatocellular carcinomas [J].

Colnot, S ;

Decaens, T ;

Niwa-Kawakita, M ;

Godard, C ;

Hamard, G ;

Kahn, A ;

Giovannini, M ;

Perret, C .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2004, 101 (49) :17216-17221

[28] Dual functions of E2F-1 in a transgenic mouse model of liver carcinogenesis [J].

Conner, EA ;

Lemmer, ER ;

Omori, M ;

Wirth, PJ ;

Factor, VM ;

Thorgeirsson, SS .

ONCOGENE, 2000, 19 (44) :5054-5062

[29] The CYP2D6 humanized mouse:: Effect of the human CYP2D6 transgene and HNF4α on the disposition of debrisoquine in the mouse [J].

Corchero, J ;

Granvil, CP ;

Akiyama, TE ;

Hayhurst, GP ;

Pimprale, S ;

Feigenbaum, L ;

Idle, JR ;

Gonzalez, FJ .

MOLECULAR PHARMACOLOGY, 2001, 60 (06) :1260-1267

[30] Precancerous lesions upon sporadic activation of β-catenin in mice [J].

Coste, Isabelle ;

Freund, Jean-Noel ;

Spaderna, Simone ;

Brabletz, Thomas ;

Renno, Toufic .

GASTROENTEROLOGY, 2007, 132 (04) :1299-1308

← 1 2 3 4 5 6 7 8 9 10 →