Disruption of the E1 and E2 reading frames of HPV 16 in cervical carcinoma is associated with poor prognosis

被引:118
作者
Kalantari, M
Karlsen, F
Kristensen, G
Holm, R
Hagmar, B
Johansson, B
机构
[1] Huddinge Univ Hosp, Dept Clin Virol, S-14186 Huddinge, Sweden
[2] Norwegian Radium Hosp, Dept Pathol, Oslo, Norway
[3] Norwegian Radium Hosp, Dept Gynecol Oncol, Oslo, Norway
[4] Norwegian Rikshosp, Dept Pathol, Oslo, Norway
关键词
cervical cancer; HPV; 16; E1; E2; integration; deletion; disruption; PCR;
D O I
10.1097/00004347-199804000-00009
中图分类号
R71 [妇产科学];
学科分类号
100211 ;
摘要
The E1 and E2 reading frames of 158 cervical carcinoma samples containing human papillomavirus (HPV) 16 were mapped using polymerase chain reaction (PCR). The reading frames were amplified using primers spanning the entire genes. Of the analyzed samples, 23% showed no amplification with the E1 primers and 29% showed no amplification with the E2 primers. There was an overlap, but not complete identity, between the E1- and E2-disrupted groups. All E1- and E2-negative samples were further analyzed with primers spanning subsections of the E1 and E2 reading frames, which together covered the entire genes. Of the 35 samples negative for E1, 11 were positive in specific amplification of the 3' end of the E1 gene. Several different subsections of E2 could be amplified from most samples negative for the entire gene (37/46). Five classes of patterns were found, in which either all subsections of the E2 gene or subsections in the 5', middle, or 3' end were disrupted. Although a variable pattern of disruption/deletion In the E1-E2 area of the HPV 16 genome was found in cervical carcinoma, the 5' end disruption was the most common one in both E1 and E2. Patients with carcinomas showing disruptions in E1/E2 had a poorer survival than those without such changes, and E1 disruptions were the most important prognostically.
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页码:146 / 153
页数:8
相关论文
共 55 条
[41]   DISRUPTION OF EITHER THE E1-REGULATORY OR THE E2-REGULATORY GENE OF HUMAN PAPILLOMAVIRUS TYPE-16 INCREASES VIRAL IMMORTALIZATION CAPACITY [J].
ROMANCZUK, H ;
HOWLEY, PM .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1992, 89 (07) :3159-3163
[42]   STRUCTURE AND TRANSCRIPTION OF HUMAN PAPILLOMAVIRUS SEQUENCES IN CERVICAL-CARCINOMA CELLS [J].
SCHWARZ, E ;
FREESE, UK ;
GISSMANN, L ;
MAYER, W ;
ROGGENBUCK, B ;
STREMLAU, A ;
HAUSEN, HZ .
NATURE, 1985, 314 (6006) :111-114
[43]   DETECTION OF HUMAN PAPILLOMAVIRUS TYPE-16 DNA AND EVIDENCE FOR INTEGRATION INTO THE CELL-DNA IN CERVICAL DYSPLASIA [J].
SHIRASAWA, H ;
TOMITA, Y ;
KUBOTA, K ;
KASAI, T ;
SEKIYA, S ;
TAKAMIZAWA, H ;
SIMIZU, B .
JOURNAL OF GENERAL VIROLOGY, 1986, 67 :2011-2015
[44]  
STANLEY M, 1994, PAPILLOMAVIRUS REP, V5, P141
[45]   HUMAN PAPILLOMAVIRUS TYPE-16 AND TYPE-18 GENE-EXPRESSION IN CERVICAL NEOPLASIAS [J].
STOLER, MH ;
RHODES, CR ;
WHITBECK, A ;
WOLINSKY, SM ;
CHOW, LT ;
BROKER, TR .
HUMAN PATHOLOGY, 1992, 23 (02) :117-128
[46]   CELLULAR PROTEINS INVOLVED IN PAPILLOMAVIRUS-INDUCED TRANSFORMATION [J].
SWAN, DC ;
VERNON, SD ;
ICENOGLE, JP .
ARCHIVES OF VIROLOGY, 1994, 138 (1-2) :105-115
[47]   DURING NEGATIVE REGULATION OF THE HUMAN PAPILLOMAVIRUS-16 E6 PROMOTER, THE VIRAL E2 PROTEIN CAN DISPLACE SP1 FROM A PROXIMAL PROMOTER ELEMENT [J].
TAN, SH ;
GLOSS, B ;
BERNARD, HU .
NUCLEIC ACIDS RESEARCH, 1992, 20 (02) :251-256
[48]   ANALYSIS OF INTEGRATED HUMAN PAPILLOMAVIRUS TYPE-16 DNA IN CERVICAL CANCERS - AMPLIFICATION OF VIRAL SEQUENCES TOGETHER WITH CELLULAR FLANKING SEQUENCES [J].
WAGATSUMA, M ;
HASHIMOTO, K ;
MATSUKURA, T .
JOURNAL OF VIROLOGY, 1990, 64 (02) :813-821
[49]  
*WHO, 1995, IARC MON, V94
[50]   IDENTIFICATION OF HPV-16 EARLY GENES RETAINED IN CERVICAL CARCINOMAS [J].
WILCZYNSKI, SP ;
PEARLMAN, L ;
WALKER, J .
VIROLOGY, 1988, 166 (02) :624-627