DETECTION OF POLYOMAVIRAL DNA-SEQUENCES IN NORMAL AND ADENOMATOUS HUMAN PITUITARY TISSUES USING THE POLYMERASE CHAIN-REACTION

被引:0
作者
WOLOSCHAK, M [1 ]
POST, KD [1 ]
机构
[1] CUNY MT SINAI SCH MED,DEPT NEUROSURG,NEW YORK,NY 10029
关键词
PITUITARY; TUMOR; ADENOMA; VIRUS; POLYMERASE CHAIN REACTION; DNA;
D O I
10.1002/1097-0142(19950801)76:3<490::AID-CNCR2820760320>3.0.CO;2-#
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Background. Tumor viruses are known to have a role in the pathogenesis of many types of benign and malignant human tumors. The possible roles of these viruses in the development of human pituitary tumors have not been investigated. Methods. The polymerase chain reaction was used to screen human pituitary tumors for human papillomaviral (HPV) and Polyomaviral DNA sequences. Sets of consensus primers, which are capable of amplifying HPV Types 16, 18, and 33 and polyomavirus BK, JC, and SV40, were used in these experiments. Results. Amplification products were not detected using HPV consensus primers in 30 tumors. Twenty-six of 30 tumors demonstrated an amplification product with polyomaviral primers that hybridized to SV40 and BK internal probes and was confirmed to be SV40 in one tumor by direct sequencing. Ten normal postmortem pituitary samples then were examined similarly with Polyomaviral consensus primers; 8 of 10 normal samples demonstrated a similar amplification product that also hybridized with SV40 and BK internal probes by Southern blotting. Polyomaviral DNA sequences in normal and tumor samples were not present at levels detectable by genomic Southern blotting. Expressed viral protein (large T antigen) was not demonstrated in positive samples by Western blot analysis. Conclusions. These findings, that polyomaviral DNA sequences are detectable at low levels in certain normal tissues, are in agreement with those of other groups and, to the authors' knowledge, serve as the first report of polyomaviral latency in human pituitary tissue. A role for polyomaviruses in pituitary tumorigenesis could not be established in this analysis.
引用
收藏
页码:490 / 496
页数:7
相关论文
共 63 条
  • [1] CLINICALLY NONFUNCTIONING PITUITARY-TUMORS ARE MONOCLONAL IN ORIGIN
    ALEXANDER, JM
    BILLER, BMK
    BIKKAL, H
    ZERVAS, NT
    ARNOLD, A
    KLIBANSKI, A
    [J]. JOURNAL OF CLINICAL INVESTIGATION, 1990, 86 (01) : 336 - 340
  • [2] ARBEIT JM, 1993, AM J PATHOL, V142, P1187
  • [3] DETECTION OF BK-VIRUS AND JC-VIRUS IN URINE AND BRAIN-TISSUE BY THE POLYMERASE CHAIN-REACTION
    ARTHUR, RR
    DAGOSTIN, S
    SHAH, KV
    [J]. JOURNAL OF CLINICAL MICROBIOLOGY, 1989, 27 (06) : 1174 - 1179
  • [4] DNA-SEQUENCES SIMILAR TO THOSE OF SIMIAN VIRUS-40 IN EPENDYMOMAS AND CHOROID-PLEXUS TUMORS OF CHILDHOOD
    BERGSAGEL, DJ
    FINEGOLD, MJ
    BUTEL, JS
    KUPSKY, WJ
    GARCEA, RL
    [J]. NEW ENGLAND JOURNAL OF MEDICINE, 1992, 326 (15) : 988 - 993
  • [5] A NEW TYPE OF PAPILLOMAVIRUS DNA, ITS PRESENCE IN GENITAL CANCER BIOPSIES AND IN CELL-LINES DERIVED FROM CERVICAL-CANCER
    BOSHART, M
    GISSMANN, L
    IKENBERG, H
    KLEINHEINZ, A
    SCHEURLEN, W
    HAUSEN, HZ
    [J]. EMBO JOURNAL, 1984, 3 (05) : 1151 - 1157
  • [6] TRANSGENIC MICE HARBORING SV40 T-ANTIGEN GENES DEVELOP CHARACTERISTIC BRAIN-TUMORS
    BRINSTER, RL
    CHEN, HY
    MESSING, A
    VANDYKE, T
    LEVINE, AJ
    PALMITER, RD
    [J]. CELL, 1984, 37 (02) : 367 - 379
  • [7] LACK OF JC VIRAL GENOMIC SEQUENCES IN MULTIPLE-SCLEROSIS BRAIN-TISSUE BY POLYMERASE CHAIN-REACTION
    BUCKLE, GJ
    GODEC, MS
    RUBI, JU
    TORNATORE, C
    MAJOR, EO
    GIBBS, CJ
    GAJDUSEK, DC
    ASHER, DM
    [J]. ANNALS OF NEUROLOGY, 1992, 32 (06) : 829 - 831
  • [8] CARBONE M, 1994, ONCOGENE, V9, P1781
  • [9] DEMONSTRATION OF HUMAN PAPILLOMAVIRUS (HPV) TYPE-30 IN ESOPHAGEAL SQUAMOUS-CELL CARCINOMAS BY IN-SITU HYBRIDIZATION
    CHANG, FJ
    SYRJANEN, S
    SYRJANEN, K
    [J]. INTERNATIONAL JOURNAL OF CANCER, 1993, 55 (01) : 171 - 173
  • [10] PERSISTENCE OF DNA-SEQUENCES OF BK VIRUS AND JC VIRUS IN NORMAL HUMAN-TISSUES AND IN DISEASED TISSUES
    CHESTERS, PM
    HERITAGE, J
    MCCANCE, DJ
    [J]. JOURNAL OF INFECTIOUS DISEASES, 1983, 147 (04) : 676 - 684