title: Detection of oncogenic DNA viruses in colorectal cancer.
abstract: BACKGROUND
  As a part of our search for oncogenic viruses as potential etiological agents in human malignancies, our studies on human papillomaviruses (HPV) were extended to analysis of the 3 polyomaviruses (SV40, BKV and JCV) in colorectal carcinomas.
  
  
  METHODS
  Archival tumour samples from 71 patients with colorectal cancer were analyzed for the sequences of SV40, BKV, JCV and HPV using PCR-based techniques. HPV genotypes were determined using sequencing and reverse blot hybridization (InnoLipa).
  
  
  RESULTS
  Amplification of BKV and JCV with the primer pair PEP-1 and PEP-2 and subsequent restriction digestion of the amplified products with BamH I disclosed BKV in 6/66 (9%) of the samples, whereas none contained JCV. SV40 was amplified in 10/66 (15.1%) samples and confirmed by sequencing analysis. In pair-wise analysis for co-infections, the samples were significantly different in their BKV-JCV and JCV-SV40 status, in contrast to their BKV-SV40 co-infection status. HPV DNA was detected in 22/66 (33.3%) of the samples analysed with either the MY09/11 or SPF primer mix. Of these 22 HPV infections, 7 were single-type infections and 15 contained multiple HPV types. HPV detection or type distribution showed no relationship to the gender of the patients or histological grade of the tumour. HPV status was not significantly related to detection of BKV, JCV or SV40. Similarly, in pair-wise analysis for co-infections, the samples were significantly different in their status of HPV-BKV (p=0.0006), HPV-JCV (p=0.0001), and HPV-SV40 (p=0.019), implicating that HPV and the 3 polyomaviruses are rarely detected concomitantly in the same samples.
  
  
  CONCLUSIONS
  Taking the known molecular mechanisms of action of these individual viruses, there is a chance that these viruses could alter the mechanisms of cell cycle control and inhibit apoptosis, thus potentially causing chromosomal instability and promoting colorectal oncogenesis.
authors.affiliation: Laboratory of Molecular Virology, University Hospital Tor Vergata, Rome, Italy.
authors.forename: Laura
authors.initials: L
authors.lastname: Giuliani
authors.forename: Corrado
authors.initials: C
authors.lastname: Ronci
authors.forename: Daniela
authors.initials: D
authors.lastname: Bonifacio
authors.forename: Luigi
authors.initials: L
authors.lastname: Di Bonito
authors.forename: Cartesio
authors.initials: C
authors.lastname: Favalli
authors.forename: Carlo Federico
authors.initials: CF
authors.lastname: Perno
authors.forename: Kari
authors.initials: K
authors.lastname: Syrjänen
authors.forename: Marco
authors.initials: M
authors.lastname: Ciotti
mesh_terms: D000230:Adenocarcinoma / Q000821:virology*; D001739:BK Virus / Q000302:isolation & purification; D015179:Colorectal Neoplasms / Q000821:virology*; D004279:DNA, Viral / Q000302:isolation & purification; D006801:Humans; D007577:JC Virus / Q000302:isolation & purification; D027383:Papillomaviridae / Q000235:genetics / Q000302:isolation & purification; D030361:Papillomavirus Infections / Q000150:complications / Q000821:virology; D016612:Paraffin Embedding; D011120:Polyomavirus / Q000302:isolation & purification*; D027601:Polyomavirus Infections / Q000150:complications* / Q000821:virology; D013539:Simian virus 40 / Q000302:isolation & purification; D014412:Tumor Virus Infections / Q000150:complications* / Q000821:virology
chemical_list: D004279:DNA, Viral