A b s t r a c tThe aim of this study was to analyze the prevalence of BK virus, Human Papillomavirus and Epstein-Barr virus in oropharyngeal cancer, and to test our hypothesis that BKV/HPV/EBV co-infection plays a role in oropharyngeal squamous cell carcinoma. The correlation between viral infection, OSCC, anatomic location, pre-treatment staging, evidence of metastases to lymph nodes, and grading was also investigated. The examination samples were collected from 62 patients from paraffin tissue blocks. Males (90.3%) with, smoking (83.9%) and alcohol abuse (67.7%) problems prevailed in the studied group. G2 histological type was recognized in 80.6% cases. T4 (77.4%) and N2 (56.5%) traits occurred in the majority of patients. No cases of metastasis were observed (M0 100%). HPV -24.2%, EBV -27.4% and BKV 17.7% were detected in the studied samples. We observed co-infection EBV/BKV in 8% of cases, HPV/BKV in 4.8%, and HPV/EBV in 9% cases. Only in two cases co-infection of all three viruses was found.

Introduction and objective. Colorectal cancer is one of the most common cancers worldwide. In Poland, it is the second most common cancer, regardless of gender. The aim of study was to analyze the incidence of HPV and BKV in the tissue of colorectal cancer and to determine the relationship between the presence of these viruses and the development of this cancer. Materials and method. The experiments were conducted using 50 colorectal cancer tissues collected from histological sections. The clinical material was embedded in paraffin blocks. Next, DNA extraction was performed. Isolates of colorectal cancer tissue were tested for the presence of HPV DNA. BKV DNA was detected by PCR using specific primers and then differentiated from JCV by digestion with BamHI enzyme. Results. In clinical specimens taken from patients with colorectal cancer, HPV DNA was detected in 20% of cases. In 10% of cases the presence of HPV type 18 was confirmed, in the other 90% of the samples HPV type 16 was detected, while the presence of BKV was confirmed in 30% of cases. Coinfection with HPV and BKV was shown in 12% of patients. In one case, BK virus coexisted with HPV type 18, in the remaining 5 cases with HPV type 16. Conclusions. Developing colorectal cancer can show no symptoms, even for many years. This is why it is so important to become familiar with as many etiological factors as possible. The development of many human neoplasms is often initiated by exposure to infectious agents -such as bacterial or viral infections. Similar to the human papillomavirus, the BK virus was detected in clinical specimens. It seems that HPV and BKV infections can contribute to the neoplastic process, which requires detailed studies on a larger group of patients.

The Epstein-Barr virus (EBV) was discovered in 1964 by Michael Anthony Epstein and Yvonne Barr, who discovered a herpesvirus-like infectious agent in a biopsy specimen from a patient with Burkitt's lymphoma. This virus belongs to the Herpesviridae family (subfamily Gammaherpesvirinae, genus Lymphocryptovirus). EBV is a ubiquitous herpesvirus that is causally associated with various malignant tumours. According to the current nomenclature, it was named human herpesvirus type 4 (human herpesvirus 4 -HHV-4). Primary infection usually occurs in childhood. In developing countries, the infection rate among young children is higher than in developed countries. It was the first human tumour virus and it is currently categorized as a group-1 carcinogen due to its association with various cancers. It is estimated that over 90% of the adult population has been infected with this pathogen, but only a minority will develop the disease. EBV establishes latent infection characterized by the expression of a limited number of viral genes called latent genes. Moreover, during its life cycle, EBV periodically reactivates and can be transmitted to other susceptible hosts. The oral cavity is the main site of EBV occurrence and the most common source of infection. This study discusses EBV frequency and its association with the occurrence of malignant tumours and the pathways of tumour progression.

According to current World Health Organization data, worldwide, cancer is second to cardiovascular diseases as the leading cause of death. The p53 protein is a translation product of the TP53 gene, and it has many functions in cells. Indeed, for this, it is commonly called the “guardian of the genome”. The aim of this study was to evaluate the prevalence of mutation and methylation in the promoter of the TP53 gene in cells affected with squamous cell carcinoma of the head and neck. The research material consisted of 34 DNA samples isolated from surgically removed tissue fragments of head and neck tumors. In this work, analysis of all samples for the presence of mutations proved negative. This result simultaneously revealed an absence of mutation in the TP53 gene promoter in the analyzed material. However, the detection of changes in the methylation profile status of the promoter of the TP53 gene in the DNA samples revealed the presence of both methylated alleles in 76.5% of the sample population, while in the remaining 23.5%, methylation was present in only one allele of the studied gene. In our work, we assumed that samples displaying methylation involving two alleles will show greater predisposition to the development of a malignant tumor. The obtained results reveal that despite the lack of mutation in the TP53 gene promoter, its functioning may be impaired by other mechanisms – either epigenetic or environmental.

TP 53 promoter methylation was examined in frozen tumor tissue taken from patients with oropharyngeal carcinoma with EBV, HPV and co-infection EBV/HPV. This pilot study was performed on 48 patients. Initial studies indicate a high frequency of methylation in HPV-associated (57.1%) and EBV - associated OSCC (60%) cases, whilst the highest exists in co-infection HPV/EBV (75%). Future studies on a larger group of patients, of the mechanisms of co-infection and their role in oral squamous cell carcinoma, are necessary.