Chapter 6 Mouth cancer By Professor Crispian Scully CBE, Professor emeritus, UCL, London and Mr Nicholas Kalavrezos, Maxillofacial & Reconstructive Surgeon of The Head, Face & Neck, University College London Hospital and The Harley Street Clinic.
Introduction Cancer is caused by DNA mutations, which lead to altered cell proteins and function. Mutations can be spontaneous or caused by various mutagens such as tobacco, alcohol or viruses (Figure 1). Several DNA mutations are necessary before the affected cells change appearance and behaviour to a recognisably pre- or potentially malignant cell characterised by an ability to proliferate in a less-controlled fashion than normal (they become autonomous). The effects of these changes may be seen under the microscope as dysplasia – disordered cell size and arrangement, with abnormal cell divisions (mitoses). This can transform to cancer - characterised by malignant epithelial cells (keratinocytes) which proliferate and invade across the epithelial basement membranes as a ‘growth’ into the underlying tissues. The mass is termed a malignant neoplasm. Ultimately, the cancer spreads locally, often causing a swelling (tumour) and, via lymphatics and blood (metastasis –or ‘secondary’ growth) spreads to lymph nodes, bone, brain, liver and elsewhere. Finally, even with treatment, many cancers recur and can be fatal. People with one particular cancer are also predisposed to develop another malignant neoplasm - a second primary cancer (second primary tumour; SPT) - in the case of mouth cancer, SPTs may be in the mouth, or aerodigestive tract (pharynx, larynx, bronchi, oesophagus).
Figure 1 The early progression of cell mutation
46