Head and neck cancer are a group that start in the head and neck. Most originate from the mucosa, occurring in upper airway and digestive tract. A subset containing sequences of human papillomavirus (HPV), which differ in biological and clinical features and molecular pathogenesis (gene expression, mutations, amplifications and deletions and alterations epigenome) with respect to non driven by the virus. Depending on the anatomic location of the tumor, HPV prevalence is estimated between 23 and 36%.
Contents
- Tumor process is triggers by the virus by several mechanisms
- Integration of the virus into the host genome
- References
HPV is known to trigger tumor development through the action of its oncoproteins E6 and E7 led to numerous cellular pathways, including inactivating p53 and the retinoblastoma protein, and played an important role in immune evasion together with E5. Subsequently are characterizing other mechanisms by which the virus can interact with the host genome also tumorigenic process further triggering of these proteins.
Tumor process is triggers by the virus by several mechanisms
The human papillomavirus can induce tumor by several mechanisms:
- E6 and E7 oncogenic proteins.
- Disruption of tumor suppressor genes.
- High-level DNA amplifications, for example, oncogenes.
- Generating alternative transcripts nonfunctional.
- interchromosomal rearrangements.
- Distinct host genome methylation and expression patterns, producing too when virus isn't integrated in host genome.
Integration of the virus into the host genome
An important step in the process is the integration of the virus into the host genome, being necessary to differentiate between tumors in which the virus is integrated and which not, as has been seen each other tumors has clinical, biological and different pathological features. Complete sequencing of the genome of HPV-positive tumor cells has allowed the identification of various virus integration points besides the distinction between tumors in which the virus is integrated and which not. Viral integration is nonrandom because in almost all cases this remains intact viral proteins E6 and E7. This integration tends to occur in or near genes producing changes mentioned in the previous point and it is for this reason that the integration of the virus can greatly contribute to the development of tumor characteristics.