Human Papilloma Virus Integration in Oral and Cervical Carcinoma Human papilloma virus (HPV) has been strongly associated with human cervical carcinoma and oral squamous cell carcinoma. Integration of the viral genome into the human genome is a common step in the malignant transformation of the cell. This integration is characterized by breakage and disruption of both viral and human genomes. Investigation of the junctions of human and viral DNA at the integration site will demonstrate any pattern, or lack thereof, in the disruption of protein-coding regions or transcriptional activation regions. Such information can give greater insight into the causes and control of malignancy of oral cancers. The research design involves the screening of clinical samples of cervical and oral malignancy for the presence of HPV by Southern transfer hybridization. Those specimens which are positive for HPV will be subjected to panhandle polymerase chain reaction (PCR), a type of PCR that allows one to amplify a sequence with an unknown end. The junctional regions will be amplified by PCR and then cloned or directly sequenced. The obtained sequence can then be compared with published sequences on computer database and evaluated for homology with open reading frames, transcriptional activator binding sites, and for repetitive sequences. KEY WORDS: Human Papilloma Virus, Keratinocytes, Cervical Carcinoma, Oral Squamous Carcinoma, Polymerase Chain Reaction

Agency
National Institute of Health (NIH)
Institute
National Institute of Dental & Craniofacial Research (NIDCR)
Type
Unknown (K16)
Project #
5K16DE000175-09
Application #
3775609
Study Section
Project Start
Project End
Budget Start
Budget End
Support Year
9
Fiscal Year
1993
Total Cost
Indirect Cost
Name
University of Iowa
Department
Type
DUNS #
041294109
City
Iowa City
State
IA
Country
United States
Zip Code
52242
Perinpanayagam, H; Schneider, G; Holtman, K et al. (2004) Altered Cbfa1 expression and biomineralization in an osteosarcoma cell line. J Orthop Res 22:404-10
Armstrong, Steven R; Vargas, M A; Chung, I et al. (2004) Resin-dentin interfacial ultrastructure and microtensile dentin bond strength after five-year water storage. Oper Dent 29:705-12
Timmons, Sherry R; Nwankwo, Joseph O; Domann, Frederick E (2002) Acetaldehyde activates Jun/AP-1 expression and DNA binding activity in human oral keratinocytes. Oral Oncol 38:281-90
Armstrong, S R; Keller, J C; Boyer, D B (2001) The influence of water storage and C-factor on the dentin-resin composite microtensile bond strength and debond pathway utilizing a filled and unfilled adhesive resin. Dent Mater 17:268-76
Armstrong, S R; Keller, J C; Boyer, D B (2001) Mode of failure in the dentin-adhesive resin-resin composite bonded joint as determined by strength-based (muTBS) and fracture-based (CNSB) mechanical testing. Dent Mater 17:201-10
Armstrong, S R; Boyer, D B; Keller, J C et al. (1998) Effect of hybrid layer on fracture toughness of adhesively bonded dentin-resin composite joint. Dent Mater 14:91-8
Armstrong, S R; Boyer, D B; Keller, J C (1998) Microtensile bond strength testing and failure analysis of two dentin adhesives. Dent Mater 14:44-50
Kurago, Z B; Lutz, C T; Smith, K D et al. (1998) NK cell natural cytotoxicity and IFN-gamma production are not always coordinately regulated: engagement of DX9 KIR+ NK cells by HLA-B7 variants and target cells. J Immunol 160:1573-80
Baumgardner, K R; Walton, R E; Osborne, J W et al. (1996) Induced hypoxia in rat pulp and periapex demonstrated by 3H-misonidazole retention. J Dent Res 75:1753-60
Kurago, Z B; Smith, K D; Lutz, C T (1995) NK cell recognition of MHC class I. NK cells are sensitive to peptide-binding groove and surface alpha-helical mutations that affect T cells. J Immunol 154:2631-41

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