Changing Epidemiology of Head and Neck Cancer

摘要: ead and neck (HN muco -epidermoid in the parotid gland andadenocarcinoma paranasal sinuses.Papillary is main histologic type inthyroid cancer, all other histologiesrepresenting less than 3% of cases [1].We have focused our attention particularon sites for which an increased incidence hasbeen recorded. Oropharynx oral cavity squamouscell cancerA slight increase tonsiland tongue cancer has emerged from SEERdata, against a reduction mortality. Over last few years human papillomavirus (HPV) infection been recognized tohave pathogenetic role approximately25% oropharynx carcinomas. Lingual andpalatine tonsils are most involved sitescompared to H&N sites, reasonfor this behaviour being still unknown. Morethan 120 different HPV types so farsingled out among high riskoncogenic such as 16, 18, 31, 33,35, 16 (90-95% ofcases) squamous cell cancer. The method transmission seems berelated sex, particular there strongassociation between positive tumoursand specific sexual behaviors, oralsex oral-anal intercourse. If relationshipbetween genital HPVinfection exists, it be defined. Thistopic analyzed study including172 women with immunodeficiencyvirus (HIV) 86 HIV negativewomen. Oral infections seem lesscommon cervical bothgroups, were morecommon concomitant cervicalHPV presence ofsimultaneous bythe same rare, although thelatter condition was present more womenthan expected, making HPVinfections two related entities [2].Younger age, nonsmokers, nondrinkers,with risk developmentamong both genders demographiccharacteristics tumors.Morphologically, basaloid histology apoorly differentiated grade morefrequently associated positivecancer. Molecularly, cancers containingintegrated transcriptionally activeHPV16, generally carry wild TP53.Indeed TP53 functionally inactivated byviral E6 oncoprotein happensfor pRb, by viraloncoprotein E7. These molecular features arecompletely those recorded inHPV negative tumors, where oftenmutated due carcinogens tobacco smokeand amplification cyclin D1. Besides, tumours, inactivation ofp16 alters pRb pathway [3]. Probably dueto origin, HPVpositive better prognosis, whichalong secondtumour development [4], contributes toimprove patient survival. In evidence ofpathogenic evident.