Clinical applications of tumor suppressor genes and oncogenes in cancer

被引:9
作者
Diamandis, EP [1 ]
机构
[1] UNIV TORONTO, DEPT CLIN BIOCHEM, TORONTO, ON M5G 1L5, CANADA
关键词
oncogenes; tumor suppressors; cancer diagnosis; tumor markers BRCA-1; BRCA-2;
D O I
10.1016/S0009-8981(96)06442-X
中图分类号
R446 [实验室诊断]; R-33 [实验医学、医学实验];
学科分类号
1001 ;
摘要
In the search for new ways to better diagnose and monitor cancer, scientists have turned to oncogenes and tumor suppressor genes. These genes are involved in cell differentiation, communication and proliferation and their alteration is frequently associated with cancer. Such alterations include mutations, translocations, amplifications and deletions. In this review, I give examples of using the detection of such alterations for patient diagnosis and monitoring. The practical examples an restricted to a few cancer types, but the identification of new tumor suppressor genes, like BRCA-1 and BRCA-2, is creating new possibilities for determining cancer risk of individual family members. There is no doubt that the cloning of new genes which predispose to sporadic cancer will lead to the introduction of widespread testing to assess risk and to the application of preventive measures. Copyright (C) 1997 Elsevier Science B.V.
引用
收藏
页码:157 / 180
页数:24
相关论文
共 127 条
[71]   NEW LINK FOUND BETWEEN P53 AND DNA-REPAIR [J].
MARX, J .
SCIENCE, 1994, 266 (5189) :1321-1322
[72]   Cancer research - A second breast cancer susceptibility gene is found [J].
Marx, J .
SCIENCE, 1996, 271 (5245) :30-31
[73]  
MIDGLEY CA, IN PRESS J CELL SCI
[74]   A STRONG CANDIDATE FOR THE BREAST AND OVARIAN-CANCER SUSCEPTIBILITY GENE BRCA1 [J].
MIKI, Y ;
SWENSEN, J ;
SHATTUCKEIDENS, D ;
FUTREAL, PA ;
HARSHMAN, K ;
TAVTIGIAN, S ;
LIU, QY ;
COCHRAN, C ;
BENNETT, LM ;
DING, W ;
BELL, R ;
ROSENTHAL, J ;
HUSSEY, C ;
TRAN, T ;
MCCLURE, M ;
FRYE, C ;
HATTIER, T ;
PHELPS, R ;
HAUGENSTRANO, A ;
KATCHER, H ;
YAKUMO, K ;
GHOLAMI, Z ;
SHAFFER, D ;
STONE, S ;
BAYER, S ;
WRAY, C ;
BOGDEN, R ;
DAYANANTH, P ;
WARD, J ;
TONIN, P ;
NAROD, S ;
BRISTOW, PK ;
NORRIS, FH ;
HELVERING, L ;
MORRISON, P ;
ROSTECK, P ;
LAI, M ;
BARRETT, JC ;
LEWIS, C ;
NEUHAUSEN, S ;
CANNONALBRIGHT, L ;
GOLDGAR, D ;
WISEMAN, R ;
KAMB, A ;
SKOLNICK, MH .
SCIENCE, 1994, 266 (5182) :66-71
[75]   COTRANSLATION OF ACTIVATED MUTANT P53 WITH WILD-TYPE DRIVES THE WILD-TYPE P53 PROTEIN INTO THE MUTANT CONFORMATION [J].
MILNER, J ;
MEDCALF, EA .
CELL, 1991, 65 (05) :765-774
[76]   THE RELATIONSHIP BETWEEN SERUM P53 AUTOANTIBODIES AND CHARACTERISTICS OF HUMAN BREAST-CANCER [J].
MUDENDA, B ;
GREEN, JA ;
GREEN, B ;
JENKINS, JR ;
ROBERTSON, L ;
TARUNINA, M ;
LEINSTER, SJ .
BRITISH JOURNAL OF CANCER, 1994, 69 (06) :1115-1119
[77]  
MURAKAMI Y, 1991, CANCER RES, V51, P3356
[78]  
MUTHUSWAMY SK, 1995, ONCOGENE, V11, P271
[79]   P53 PROTEIN ACCUMULATION AND GENE MUTATION IN THE PROGRESSION OF HUMAN PROSTATE CARCINOMA [J].
NAVONE, NM ;
TRONCOSO, P ;
PISTERS, LL ;
GOODROW, TL ;
PALMER, JL ;
NICHOLS, WW ;
VONESCHENBACH, AC ;
CONTI, CJ .
JOURNAL OF THE NATIONAL CANCER INSTITUTE, 1993, 85 (20) :1657-1669
[80]  
NOGUCHI M, 1994, ONCOL REP, V1, P1157