Genetically altered fields in head and neck cancer and second field tumor

Abstract

The concept of field cancerization has been ever changing since its first description by Slaughter et al in 1953. Field cancerization explains the mechanisms by which second primary tumors (SPTs) develop. SPTs are the tumors, which develop in the oral cavity in succession to the primary malignant tumors, which might vary in duration ranging from few months to years. Conceivably, a population of daughter cells with early genetic changes (without histopathology) remains in the organ, demonstrating the concept of field cancerization. This review explains the concept of field cancerization and various field theories along with molecular basis of field formation.

Open questions and novel concepts in oral cancer surgery

“…This observation has been confirmed in several reports [2,76,77]. About 50 years later, Billroth, Warren and Gate [78] established a few criteria to distinguish SPTs from LRs.…”

“…The term field cancerization was first used by Slaughter et al [1], based on the theory of multistep carcinogenesis, which describes the transformation of a normal cell into a malignant cell as a result of the progressive accumulation of genetic mutations [2,3].…”

Patterns of concurrent cigarette, alcohol, and e‐cigarette use: Off‐setting or additive behaviors?

“…The prognosis and management of patients with head and neck malignancies arising in the setting of high risk cigarette and alcohol use may be different than those without these risk factors because these cancers may be less responsive to therapy . In addition, these risky behaviors tend to create a field cancerization effect whereby patients are more likely to develop second primary malignancies of the head and neck and may need to be more closely followed for longer periods of time . Thus, we here examine the patterns of the concurrent use of conventional tobacco cigarettes (Ccigs), e‐cigarettes (Ecigs), and alcohol in a large adult sample.…”

Queratosis actínicas: un modelo de campo de cancerización

“…Se ha propuesto que desde la piel normal hasta el desarrollo de un CEC invasivo se acumularían alteraciones en 17p, 3p, 8p, 9p, 18q y 11q. Los principales genes alterados son p16 (INK4a, localizado en el cromosoma 9p21), p14 (ARF), p15 (INK4b) y p53 13,[16][17][18] .…”