Mathematical models of targeted cancer therapy

被引：38

作者：

Abbott, L. H.

Michor, F. ^{[1
]}

机构：

[1] Harvard Univ, Soc Fellows, Cambridge, MA 02138 USA

[2] Harvard Univ, Program Evolutionary Dynam, Cambridge, MA 02138 USA

来源：

BRITISH JOURNAL OF CANCER | 2006年 / 95卷 / 09期

关键词：

targeted cancer therapy; mathematical biology; chronic myeloid leukaemia;

D O I：

10.1038/sj.bjc.6603310

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

Improved understanding of the molecular underpinnings of cancer initiation and progression has led to the development of targeted cancer therapies. The importance of these new methods of cancer treatment necessitates further research into the dynamic interactions between cancer cells and therapeutic agents, as well as a means of analysing their relationship quantitatively. The present review outlines the application of mathematical modelling to the dynamics of targeted cancer therapy, focusing particular attention on chronic myeloid leukaemia and its treatment with imatinib (Glivec).

引用

收藏

页码：1136 / 1141

页数：6

相关论文

共 38 条

[1] A mathematical model of combination therapy using the EGFR signaling network [J].

Araujo, RP ;

Petricoin, EF ;

Liotta, LA .

BIOSYSTEMS, 2005, 80 (01) :57-69

[2] Persistence of malignant hematopoietic progenitors in chronic myelogenous leukemia patients in complete cytogenetic remission following imatinib mesylate treatment [J].

Bhatia, R ;

Holtz, M ;

Niu, N ;

Gray, R ;

Snyder, DS ;

Sawyers, CL ;

Arber, DA ;

Slovak, ML ;

Forman, SJ .

BLOOD, 2003, 101 (12) :4701-4707

[3] Detection of BCR-ABL mutations in patients with CML treated with imatinib is virtually always accompanied by clinical resistance, and mutations in the ATP phosphate-binding loop (P-loop) are associated with a poor prognosis [J].

Branford, S ;

Rudzki, Z ;

Walsh, S ;

Parkinson, I ;

Grigg, A ;

Szer, J ;

Taylor, K ;

Herrmann, R ;

Seymour, JF ;

Arthur, C ;

Joske, D ;

Lynch, K ;

Hughes, T .

BLOOD, 2003, 102 (01) :276-283

[4]

Branford S, 2003, BLOOD, V102, p414A

[5]

Charusanti P, 2004, DISCRETE CONT DYN-B, V4, P99

[6] Detection of BCR-ABL kinase mutations in CD34+ cells from chronic myelogenous leukemia patients in complete cytogenetic remission on imatinib mesylate treatment [J].

Chu, S ;

Xu, H ;

Shah, NP ;

Snyder, DS ;

Forman, SJ ;

Sawyers, CL ;

Bhatia, R .

BLOOD, 2005, 105 (05) :2093-2098

[7] Cancer drugs - Smart weapons prove tough to design [J].

Couzin, J .

SCIENCE, 2002, 298 (5593) :522-+

[8] The development of imatinib as a therapeutic agent for chronic myeloid leukemia [J].

Deininger, M ;

Buchdunger, E ;

Druker, BJ .

BLOOD, 2005, 105 (07) :2640-2653

[9] Activity of a specific inhibitor of the BCR-ABL tyrosine kinase in the blast crisis of chronic myeloid leukemia and acute lymphoblastic leukemia with the philadelphia chromosome. [J].

Druker, BJ ;

Sawyers, CL ;

Kantarjian, H ;

Resta, DJ ;

Reese, SF ;

Ford, JM ;

Capdeville, R ;

Talpaz, M .

NEW ENGLAND JOURNAL OF MEDICINE, 2001, 344 (14) :1038-1042

[10] INITIATION OF DEREGULATED GROWTH OF MULTIPOTENT PROGENITOR CELLS BY BCR-ABL INVITRO [J].

GISHIZKY, ML ;

WITTE, ON .

SCIENCE, 1992, 256 (5058) :836-839

← 1 2 3 4 →