GENOMIC INSTABILITY DUE TO GERMLINE P53 MUTATIONS DRIVES PRENEOPLASTIC PROGRESSION TOWARD CANCER IN HUMAN-CELLS

被引：35

作者：

TAINSKY, MA ^{[1
]}

BISCHOFF, FZ ^{[1
]}

STRONG, LC ^{[1
]}

机构：

[1] UNIV TEXAS,MD ANDERSON CANCER CTR,DEPT EXPTL PEDIAT,HOUSTON,TX 77030

来源：

CANCER AND METASTASIS REVIEWS | 1995年 / 14卷 / 01期

关键词：

P53; GERMLINE MUTATIONS; RDS ONCOGENE; GENOMIC INSTABILITY;

D O I：

10.1007/BF00690210

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

[No abstract available]

引用

页码：43 / 48

页数：6

共 16 条

[1]

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[2]

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[3]

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[4]

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[5] SUSCEPTIBILITY FOR N-RAS-MEDIATED TRANSFORMATION REQUIRES LOSS OF TUMOR SUPPRESSOR ACTIVITY [J].

KRIZMAN, DB ;

GIOVANELLA, BC ;

TAINSKY, MA .

SOMATIC CELL AND MOLECULAR GENETICS, 1990, 16 (01) :15-27

[6]

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[7]

LI FP, 1969, J NATL CANCER I, V43, P1365

[8]

LITTLE JB, 1987, CANCER RES, V47, P4229

[9] ALTERED CELL-CYCLE ARREST AND GENE AMPLIFICATION POTENTIAL ACCOMPANY LOSS OF WILD-TYPE P53 [J].

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WHITE, A ;

SPROUSE, J ;

LIVANOS, E ;

JACKS, T ;

TISTY, TD .

CELL, 1992, 70 (06) :923-935

[10]

LUSTBADER ED, 1992, AM J HUM GENET, V51, P344

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