Treating cancer by inhibiting angiogenesis: New hopes and potential pitfalls

被引：57

作者：

Rak, J ^{[1
]}

Kerbel, RS ^{[1
]}

机构：

[1] SUNNYBROOK HLTH SCI CTR,DIV CANC BIOL RES,TORONTO,ON M4N 3M5,CANADA

来源：

CANCER AND METASTASIS REVIEWS | 1996年 / 15卷 / 02期

关键词：

angiogenesis dependence; oncogenes; VEGF;

D O I：

10.1007/BF00437476

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

Angiogenesis is essential for progressive solid tumor growth and thus constitutes a very promising therapeutic target. Recent developments in understanding of the molecular mechanisms involved in tumor blood vessel formation provides a rational basis for anti-angiogenic drug development, especially of more selective and effective agents. However, for the very same reason, it is time to think more critically about some of the potential pitfalls and difficulties associated with this treatment strategy and of research needed to define realistic expectations in this area.

引用

页码：231 / 236

页数：6

共 39 条

[21] INHIBITION OF TUMOR ANGIOGENESIS AS A STRATEGY TO CIRCUMVENT ACQUIRED-RESISTANCE TO ANTICANCER THERAPEUTIC AGENTS [J].

KERBEL, RS .

BIOESSAYS, 1991, 13 (01) :31-36

[22]

KIESER A, 1994, ONCOGENE, V9, P963

[23] INHIBITION OF VASCULAR ENDOTHELIAL GROWTH FACTOR-INDUCED ANGIOGENESIS SUPPRESSES TUMOR-GROWTH INVIVO [J].

KIM, KJ ;

LI, B ;

WINER, J ;

ARMANINI, M ;

GILLETT, N ;

PHILLIPS, HS ;

FERRARA, N .

NATURE, 1993, 362 (6423) :841-844

[24] INHIBITION OF FARNESYLTRANSFERASE INDUCES REGRESSION OF MAMMARY AND SALIVARY CARCINOMAS IN RAS TRANSGENIC MICE [J].

KOHL, NE ;

OMER, CA ;

CONNER, MW ;

ANTHONY, NJ ;

DAVIDE, JP ;

DESOLMS, SJ ;

GIULIANI, EA ;

GOMEZ, RP ;

GRAHAM, SL ;

HAMILTON, K ;

HANDT, LK ;

HARTMAN, GD ;

KOBLAN, KS ;

KRAL, AM ;

MILLER, PJ ;

MOSSER, SD ;

ONEILL, TJ ;

RANDS, E ;

SCHABER, MD ;

GIBBS, JB ;

OLIFF, A .

NATURE MEDICINE, 1995, 1 (08) :792-797

[25] GLIOBLASTOMA GROWTH INHIBITED IN-VIVO BY A DOMINANT-NEGATIVE FLK-1 MUTANT [J].

MILLAUER, B ;

SHAWVER, LK ;

PLATE, KH ;

RISAU, W ;

ULLRICH, A .

NATURE, 1994, 367 (6463) :576-579

[26] HYPOXIC INDUCTION OF HUMAN VASCULAR ENDOTHELIAL GROWTH-FACTOR EXPRESSION THROUGH C-SRC ACTIVATION [J].

MUKHOPADHYAY, D ;

TSIOKAS, L ;

ZHOU, XM ;

FOSTER, D ;

BRUGGE, JS ;

SUKHATME, VP .

NATURE, 1995, 375 (6532) :577-581

[27] ENDOTHELIAL RECEPTOR TYROSINE KINASES INVOLVED IN ANGIOGENESIS [J].

MUSTONEN, T ;

ALITALO, K .

JOURNAL OF CELL BIOLOGY, 1995, 129 (04) :895-898

[28] VASCULAR ENDOTHELIAL GROWTH-FACTOR IS A POTENTIAL TUMOR ANGIOGENESIS FACTOR IN HUMAN GLIOMAS INVIVO [J].

PLATE, KH ;

BREIER, G ;

WEICH, HA ;

RISAU, W .

NATURE, 1992, 359 (6398) :845-848

[29]

RAK J, 1995, CANCER RES, V55, P4575

[30] MASSIVE PROGRAMMED CELL-DEATH IN INTESTINAL EPITHELIAL-CELLS INDUCED BY 3-DIMENSIONAL GROWTH-CONDITIONS - SUPPRESSION BY MUTANT C-H-RAS ONCOGENE EXPRESSION [J].

RAK, J ;

MITSUHASHI, Y ;

ERDOS, V ;

HUANG, SN ;

FILMUS, J ;

KERBEL, RS .

JOURNAL OF CELL BIOLOGY, 1995, 131 (06) :1587-1598

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