Genetic progression model for head and neck cancer: implications for field cancerization.

TLDR

The genetic basis of field cancerization in head and neck squamous cell carcinoma remains unclear. The study analyzed 87 head and neck lesions, including preinvasive and benign carcinogen‑exposed lesions, for allelic loss at 10 key chromosomal loci via microsatellite analysis. Chromosomal loss increases progressively from benign hyperplasia to invasive cancer, with adjacent tissues sharing common alterations and more advanced lesions acquiring additional changes, indicating that field cancerization results from expansion and migration of clonally related preneoplastic cells.

Abstract

A genetic progression model of head and neck squamous cell carcinoma has not yet been elucidated, and the genetic basis for "field cancerization" of the aerodigestive tract has also remained obscure. Eighty-seven lesions of the head and neck, including preinvasive lesions and benign lesions associated with carcinogen exposure, were tested using microsatellite analysis for allelic loss at 10 major chromosomal loci which have been defined previously. The spectrum of chromosomal loss progressively increased at each histopathological step from benign hyperplasia to dysplasia to carcinoma in situ to invasive cancer. Adjacent areas of tissue with different histopathological appearance shared common genetic changes, but the more histopathologically advanced areas exhibited additional genetic alterations. Abnormal mucosal cells surrounding preinvasive and microinvasive lesions shared common genetic alterations with those lesions and thus appear to arise from a single progenitor clone. Based on these findings, the local clinical phenomenon of field cancerization seems to involve the expansion and migration of clonally related preneoplastic cells.