Andrea Arenz1, Johannes Patze1, Evelyn Kornmann2, Jochen Wilhelm3, Frank Ziemann1, Steffen Wagner4, Andrea Wittig1,5, Ulrike Schoetz1, Rita Engenhart-Cabillic1, Ekkehard Dikomey1,6, Barbara Fritz2. 1. Department of Radiotherapy and Radiooncology, Philipps-University, University Hospital Giessen and Marburg, Marburg, Germany. 2. Center of Human Genetics, Philipps-University, Marburg, Germany. 3. Department of Pathology, Justus-Liebig-University, Giessen, Germany. 4. Department of Otorhinolaryngology, Head and Neck Surgery, Justus-Liebig University, Giessen, Germany. 5. Department of Radiation Oncology, Friedrich-Schiller-University, Jena, Germany. 6. Laboratory of Radiobiology & Experimental Radiooncology, University Medical Center Hamburg Eppendorf, Hamburg, Germany.
Abstract
BACKGROUND: It was tested whether the difference in carcinogenesis between noxa and human papillomavirus (HPV)-driven head and neck squamous cell carcinoma (HNSCC) is associated with a variation in genomic instability. METHODS: Conventional and molecular cytogenetics in HPV-positive and HPV-negative HNSCC cell lines. RESULTS: Numerical aneuploidy determined by multicolor fluorescence in situ hybridization and DNA ploidy was very similar for both entities with most chromosomes being present either in quadruplicate or triplicate, and only few are still diploid with, however, a striking similarity in the overall pattern. A clear difference was seen concerning the translocations formed, with no difference in the total amount but with a significantly higher genomic instability of HPV-positive cell lines at chromosome 3 as compared to HPV-negative cells. CONCLUSION: The different processes of carcinogenesis of HPV-positive and HPV-negative HNSCC appear to result in a similar pattern of numerical but a clear difference in structural chromosomal aberrations.
BACKGROUND: It was tested whether the difference in carcinogenesis between noxa and human papillomavirus (HPV)-driven head and neck squamous cell carcinoma (HNSCC) is associated with a variation in genomic instability. METHODS: Conventional and molecular cytogenetics in HPV-positive and HPV-negative HNSCC cell lines. RESULTS: Numerical aneuploidy determined by multicolor fluorescence in situ hybridization and DNA ploidy was very similar for both entities with most chromosomes being present either in quadruplicate or triplicate, and only few are still diploid with, however, a striking similarity in the overall pattern. A clear difference was seen concerning the translocations formed, with no difference in the total amount but with a significantly higher genomic instability of HPV-positive cell lines at chromosome 3 as compared to HPV-negative cells. CONCLUSION: The different processes of carcinogenesis of HPV-positive and HPV-negative HNSCC appear to result in a similar pattern of numerical but a clear difference in structural chromosomal aberrations.