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Search for human papillomavirus, herpes simplex virus and c‐ myc oncogene in human genital tumors
Author(s) -
Di Luca D.,
Costa S.,
Monini P.,
Rotola A.,
Terzano P.,
Savioli A.,
Grigioni W.,
Cassai E.
Publication year - 1989
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/ijc.2910430407
Subject(s) - carcinogenesis , sex organ , biology , herpes simplex virus , capsid , virology , oncogene , dna , homology (biology) , bamhi , virus , microbiology and biotechnology , cancer research , pathology , gene , medicine , genetics , plasmid , cell cycle
We tested grade III cervical intra‐epithelial neoplasms (CIN III), genital invasive carcinomas and healthy genital tissues for the presence of a number of viral and cellular parameters, considered to be risk factors in genital oncogenesis. The results show that: (1) about 30% of genital tumors had homology to HSV‐2 BgIII N and/or BamHI E DNA fragments; (2) positivity to HSV‐2‐specific protein ICP10, encoded by sequences within the HSV‐2 BamHI E DNA fragment, was detected in 29/55 neoplastic genital tissues but not in healthy genital tissues or tumors at other sites; (3) HPV‐16 DNA was found in about 50% of tumor samples, but none of the positive tissues reacted to HPV capsid protein or to the protein encoded by the HPV‐16 E6 ORF; (4) 6/8 tumor samples showing homology to HSV‐2 DNA fragments also hybridized to HPV‐16 DNA; (5) c‐ myc amplification was not detected in any of the analyzed samples, but tissues from 4 patients were positive for c‐ myc expression. None of the considered factors was present in all the analyzed samples; nevertheless, some tissues showed the simultaneous involvement of several parameters, suggesting that a number of risk factors may be involved in different steps of human genital oncogenesis.