Human papillomavirus infection and TP53 gene mutation in primary cervical carcinoma

被引:18
作者
Kim, JW
Cho, YH
Lee, CG
Kim, JH
Kim, HK
Kim, EJ
Han, KT
Namkoong, SE
机构
[1] CATHOLIC UNIV, COLL MED, CATHOLIC CANC CTR, DEPT OBSTET & GYNECOL, SEOUL, SOUTH KOREA
[2] HANYANG UNIV, SCH MED, DEPT MED GENET, SEOUL 133791, SOUTH KOREA
关键词
D O I
10.3109/02841869709001266
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Tumor specimens obtained from 136 patients with primary carcinoma of the uterine cervix were analyzed for the presence of human papillomavirus (HPV) sequences and for mutation of the TP53 gene. Polymerase chain reaction (PCR) showed that 130 of 136 (96%) tumors contained an oncogenic HPV 16 or Is sequence. HPV 16 was the predominant type in cervical squamous cell carcinomas and HPV IS was significantly associated with cervical adenocarcinomas (p < 0.05). The more dedifferentiated the primary tumor, the more frequent the HPV 16 infection and the more differentiated, the more frequent the HPV 18 infection (p < 0.05). Two out of 136 (1.5%) rumors demonstrated single-strand conformation polymorphism (SSCP) band shifts. One (positive for HPV 18) had a nonsense mutation of codon 101 in exon 4 from AAA to TAA transversion. Another (positive for L1 consensus primer set) showed a point mutation involving codon 179 in exon 5 changing CAT to CGT transition. The three specimens negative for HPV did not contain TP53 gene mutations. Our data show that mutation of TP53 is infrequent in primary cervical carcinoma and there is no inverse correlation between HPV infection and TP53 gene mutation. Other mechanisms independent of TP53 inactivation may also be implicated in tumorigenesis of the uterine cervix.
引用
收藏
页码:295 / 300
页数:6
相关论文
共 35 条
[1]   CHROMOSOME-17P LOSS IN CARCINOMA OF THE CERVIX UTERI [J].
ATKIN, NB ;
BAKER, MC .
CANCER GENETICS AND CYTOGENETICS, 1989, 37 (02) :229-233
[2]   POSSIBLE PROGNOSTIC-SIGNIFICANCE OF HUMAN PAPILLOMAVIRUS TYPE IN CERVICAL-CANCER [J].
BARNES, W ;
DELGADO, G ;
KURMAN, RJ ;
PETRILLI, ES ;
SMITH, DM ;
AHMED, S ;
LORINCZ, AT ;
TEMPLE, GF ;
JENSON, AB ;
LANCASTER, WD .
GYNECOLOGIC ONCOLOGY, 1988, 29 (03) :267-273
[3]   MOLECULAR THEMES IN ONCOGENESIS [J].
BISHOP, JM .
CELL, 1991, 64 (02) :235-248
[4]  
BORRESEN AL, 1992, LANCET, V339, P1350
[5]   A VARIATION IN THE STRUCTURE OF THE PROTEIN-CODING REGION OF THE HUMAN-P53 GENE [J].
BUCHMAN, VL ;
CHUMAKOV, PM ;
NINKINA, NN ;
SAMARINA, OP ;
GEORGIEV, GP .
GENE, 1988, 70 (02) :245-252
[6]   P53 MUTATIONS IN CERVICAL CARCINOGENESIS LOW-FREQUENCY AND LACK OF CORRELATION WITH HUMAN PAPILLOMAVIRUS STATUS [J].
BUSBYEARLE, RMC ;
STEEL, CM ;
WILLIAMS, ARW ;
COHEN, B ;
BIRD, CC .
BRITISH JOURNAL OF CANCER, 1994, 69 (04) :732-737
[7]  
CHIBA I, 1990, ONCOGENE, V5, P1603
[8]   CLONAL P53 MUTATION IN PRIMARY CERVICAL-CANCER - ASSOCIATION WITH HUMAN-PAPILLOMAVIRUS-NEGATIVE TUMORS [J].
CROOK, T ;
WREDE, D ;
TIDY, JA ;
MASON, WP ;
EVANS, DJ ;
VOUSDEN, KH .
LANCET, 1992, 339 (8801) :1070-1073
[9]   OLIGONUCLEOTIDE PRIMERS FOR DNA AMPLIFICATION OF THE EARLY REGION-1, REGION-6, AND REGION-7 FROM HUMAN PAPILLOMAVIRUS TYPE-6, TYPE-11, TYPE-16, TYPE-18, TYPE-31, AND TYPE-33 [J].
EVANDER, M ;
BODEN, E ;
BJERSING, L ;
RYLANDER, E ;
WADELL, G .
ARCHIVES OF VIROLOGY, 1991, 116 (1-4) :221-233
[10]  
FERRE F, 1989, CANCER CEL, V7, P215