Field Cacerization

The concept of “field cancerization” was first introduced by Slaughter et al. in 1953 when studying the presence of histologically abnormal tissue surrounding oral squamous cell carcinoma.  It was proposed to explain the development of multiple primary tumors and locally recurrent cancer.  Organ systems in which field cancerization has been described since then are: head and neck (oral cavity, oropharynx, and larynx), lung, vulva, esophagus, cervix, breast, skin, colon, and bladder.  Recent molecular findings support the carcinogenesis model in which the development of a field with genetically altered cells plays a central role. (Cancer Res. 2003; 63:1727-1730.)

According to one model of field cancerization, one cell sustains an initiating mutation.  Following extensive proliferation, some of its clonal descendants may subsequently acquire a second mutant allele, and the doubly mutated “initiated” cells may then proliferate and eventually occupy a large patch of epithelium.  While these cells have already undergone several of the early steps of multi-step tumor progression, they continue to form an epithelium that is histologically normal.  Subsequently, two cells located at different sites within this large patch of initiated cells may independently acquire additional mutations; both of these cells will now advance over the boundary to acquire a histologically abnormal appearance, spawning hyperplastic, dysplastic, or even neoplastic growths.  These two tumors will appear to have arisen independently even though they derive from the same clone of initiated cells. (The Biology of Cancer 2007)