Genetic alterations in cancer as a result of breakage at fragile sites

被引：91

作者：

Popescu, NC ^{[1
]}

机构：

[1] NCI, Mol Cytogenet Sect, Expt Carcinogenesis Lab, Ctr Canc Res, Bethesda, MD 20814 USA

来源：

CANCER LETTERS | 2003年 / 192卷 / 01期

关键词：

fragile site; DNA replication; genomic DNA; oncogenic virus; gene alteration; oncogenes; tumor suppressor gene; chromosome translocations;

D O I：

10.1016/S0304-3835(02)00596-7

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

The organization and replication of DNA render fragile sites (FSs) prone to breakage, recombination as well as becoming preferential targets for mutagens-carcinogens and integration. of oncogenic viruses. For many years, attempts to link FSs and cancer generated mostly circumstantial evidence. The discoveries that chromosome translocations, amplification of protooncogenes, deletion of tumor suppressor. genes, and integration of oncogenic viruses all result from the specific breakage of genomic DNA at FSs, however, have provided compelling support for such a link, further suggesting a causative role for FSs in cancer. (C) 2002 Elsevier Science Ireland Ltd. All rights reserved.

引用

页码：1 / 17

页数：17

共 137 条

[21] INFLUENCE OF CHROMOSOMAL INTEGRATION ON GLUCOCORTICOID-REGULATED TRANSCRIPTION OF GROWTH-STIMULATING PAPILLOMAVIRUS GENES E6 AND E7 IN CERVICAL-CARCINOMA CELLS [J].

DOEBERITZ, MV ;

BAUKNECHT, T ;

BARTSCH, D ;

HAUSEN, HZ .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1991, 88 (04) :1411-1415

[22] The DIRC1 gene at chromosome 2q33 spans a familial RCC-associated t(2;3)(q33;q21) chromosome translocation [J].

Druck, T ;

Podolski, J ;

Byrski, T ;

Wyrwicz, L ;

Zajaczek, S ;

Kata, G ;

Borowka, A ;

Lubinski, J ;

Huebner, K .

JOURNAL OF HUMAN GENETICS, 2001, 46 (10) :583-589

[23] PAPILLOMAVIRUS SEQUENCES INTEGRATE NEAR CELLULAR ONCOGENES IN SOME CERVICAL CARCINOMAS [J].

DURST, M ;

CROCE, CM ;

GISSMANN, L ;

SCHWARZ, E ;

HUEBNER, K .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1987, 84 (04) :1070-1074

[24]

Einstein MH, 2002, CLIN CANCER RES, V8, P549

[25] RODENT COMMON FRAGILE SITES - ARE THEY CONSERVED - EVIDENCE FROM MOUSE AND RAT [J].

ELDER, FFB ;

ROBINSON, TJ .

CHROMOSOMA, 1989, 97 (06) :459-464

[26]

Fang JM, 2001, GENE CHROMOSOME CANC, V30, P292, DOI 10.1002/1098-2264(2000)9999:9999<::AID-GCC1095>3.0.CO

[27]

2-F

[28] Muir-Torre-like syndrome in Fhit-deficient mice [J].

Fong, LYY ;

Fidanza, V ;

Zanesi, N ;

Lock, LF ;

Siracusa, LD ;

Mancini, R ;

Siprashvili, Z ;

Ottey, M ;

Martin, SE ;

Druck, T ;

McCue, PA ;

Croce, CM ;

Huebner, K .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2000, 97 (09) :4742-4747

[29] INTEGRATION SITE OF HUMAN PAPILLOMAVIRUS TYPE-18 DNA IN CHROMOSOME BAND-8Q22.1 OF C4-1 CERVICAL-CARCINOMA - DNASE-I HYPERSENSITIVITY AND METHYLATION OF CELLULAR FLANKING SEQUENCES [J].

GALLEGO, MI ;

ZIMONJIC, DB ;

POPESCU, NC ;

DIPAOLO, JA ;

LAZO, PA .

GENES CHROMOSOMES & CANCER, 1994, 9 (01) :28-32

[30] The hereditary renal cell carcinoma 3;8 translocation fuses FHIT to a patched-related gene, TRC8 [J].

Gemmill, RM ;

West, JD ;

Boldog, F ;

Tanaka, N ;

Robinson, LJ ;

Smith, DI ;

Li, F ;

Drabkin, HA .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1998, 95 (16) :9572-9577

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