Role of extended histological examination in the assessment of local recurrence of tongue and floor of the mouth cancer

AimThe aim is to find out why the rate of recurrence of tongue and floor of the mouth cancer is so high despite radical surgical treatment combined with radiochemotherapy.BackgroundOropharyngeal cancer is the second most common head and neck cancer in Poland. Tongue cancers account for 40% of all oral cavity tumours. A frequent reason for a failure in treatment of tongue and floor of the mouth cancers is local recurrence. Based on that examination, cancer treatment can be precisely planned.Materials and methodsThe study comprised a group of 56 tongue and floor of the mouth cancer patients. 9 patients who showed local recurrence were given an extended histopathological examination. The infiltration of the vessels, nerves and muscles was examined. The examination also checked the largest dimension of the tumour, the greatest depth of invasion from the mucous membrane, invasive front of the cancer, vessel embolisms, intra- and perineural infiltrations in the cancer invasive front. Tumour aggressiveness was assessed according to M. Brandwein-Gensler.ResultsIn five patients, primary tumours were found to be histologically aggressive as indicated by the infiltration of the vessels, nerves and muscles. Tumours which penetrate these structures were characterized with peri- and intraneural infiltration and were correlated with the depth of invasion from the mucous membrane, the occurrence of embolisms, and a high risk assessment as proposed by M. Brandwein-Gensler.ConclusionThe progression of cancer depends strongly on histopathological traits. The incidence of penetration of the vessels, nerves and muscles correlates with aggressiveness of the tumour front

Comprehensive genomic characterization of head and neck squamous cell carcinomas

The Cancer Genome Atlas profiled 279 head and neck squamous cell carcinomas (HNSCCs) to provide a comprehensive landscape of somatic genomic alterations. Here we show that human-papillomavirus-associated tumours are dominated by helical domain mutations of the oncogene PIK3CA, novel alterations involving loss of TRAF3, and amplification of the cell cycle gene E2F1. Smoking-related HNSCCs demonstrate near universal loss-of-function TP53 mutations and CDKN2A inactivation with frequent copy number alterations including amplification of 3q26/28 and 11q13/22. A subgroup of oral cavity tumours with favourable clinical outcomes displayed infrequent copy number alterations in conjunction with activating mutations of HRAS or PIK3CA, coupled with inactivating mutations of CASP8, NOTCH1 and TP53. Other distinct subgroups contained loss-of-function alterations of the chromatin modifier NSD1, WNT pathway genes AJUBA and FAT1, and activation of oxidative stress factor NFE2L2, mainly in laryngeal tumours. Therapeutic candidate alterations were identified in most HNSCCsclose9