Focus on head and neck cancer Li Mao, Waun K Hong, Vassiliki A Papadimitrakopoulou  Cancer Cell  Volume 5, Issue 4, Pages 311-316 (April 2004) DOI: 10.1016/S1535-6108(04)00090-X

Figure 1 Multistep process and field effect in HNSCC tumorigenesis Chronic exposure to tobacco carcinogens in the upper aerodigestive tract causes genetic and epigenetic damage in epithelial cells. Accumulation of this damage leads to the development of premalignant lesions and invasive cancers. Understanding the common genetic and epigenetic alterations that are important in the tumorigenic process is critical in the development of molecularly based management strategies. Cancer Cell 2004 5, 311-316DOI: (10.1016/S1535-6108(04)00090-X)

Figure 2 Field cancerization versus clonal spread The diagram shows the sites of 14 oral lesions that developed in a patient over 10 years. There were nine invasive cancers and five premalignant lesions. Each lesion was treated by complete resection at the time of diagnosis. Each lesion is numbered according to the sequence of diagnosis. Lesions with the same color shared identical genetic alterations, suggesting the same clonal origin based on results of genetic analysis and a mathematic model. Four independent clones might have been responsible for the development of all 14 oral lesions in this patient. Cancer Cell 2004 5, 311-316DOI: (10.1016/S1535-6108(04)00090-X)

Figure 3 Simplified scheme of the molecular abnormalities within signal transduction pathways in HNSCC that are possible targets for intervention with targeted therapies C225, cetuximab; IGF, insulin-like growth factor; Abs, antibodies; RTKIs, receptor tyrosine kinase inhibitors; FTI, farnesyl transferase inhibitors; Cdk, cyclin-dependent kinase. Cancer Cell 2004 5, 311-316DOI: (10.1016/S1535-6108(04)00090-X)