Oral cancer; tobacco, virus, alcohol and malignant cell transformation
Lifestyle aspects, tobacco, alcohol, infections, diet and oral hygiene comprise risk factors for developing oral cancer. We are developing methods to help tobacco users, both those who are healthy and those who are sick and are being treated in the hospital for their acquired problems, to quit. Once patients have quit using tobacco an increased risk for developing malignancy remains among those who continue to use nicotine. We know that tobacco use increases the risk of developing oral cancer and even human papilloma virus (HPV) infection. A sharp increase has been noted in the number of tumours containing HPV. In cases where the virus can be demonstrated, the prognosis is usually better and more treatment options are available. We are attempting to clarify the various biological processes associated with tobacco and alcohol-induced tumors as well as those due to viral manifestation by studying molecular changes in the development of cancer, which are still essentially unknown.
Oncogenic HPV codes for the early E6 and E7 proteins that inactivate tumor suppressors pRB (E7) and p53 (E6) and inhibit apoptosis, which is significant in the tumor development process, in contrast to tobacco and alcohol-associated tumors that cause mutation of tumor suppressor genes. Since lifestyle plays an important role, researchers are studying changes in the oral mucosa of smokers and smokeless tobacco users with various diagnoses and differing degrees of cellular changes who come from regions in Asia, Africa and Scandinavia, regions covering the spectrum from low to high socioeconomic standards. The overall aim is to study clinical, immunological and genetic parameters of importance for malignant cell transformation.