Dysplasia, in situ carcinoma, and progression to invasive squamous cell carcinoma of the upper aerodigestive tract

Abstract

Invasive squamous cell carcinoma (SCC) in the upper aerodigestive tract (UADT) is usually preceded by severe keratinizing dysplasia, a manifestation of intraepithelial neoplasia. Despite the presence of surface maturation (keratosis), severe keratinizing dysplasia has a higher frequency of progression to SCC than full-thickness classic carcinoma in situ (CIS) as defined in the gynecologic tract. For this reason, we recommend that severe UADT dysplasia be combined with CIS under the rubric of 'squamous intraepithelial neoplasia (SIN) grade III' to convey to the clinician the prognostic importance of these two diagnoses. Microinvasive carcinoma in the UADT includes a microfocus of submucosal invasion within 1-2 mm of the overlying epithelial basal lamina that is completely surrounded by nonneoplastic tissue. This conservative definition of microinvasion has a low risk, or no risk, for regional metastatic spread. Immunohistologic demonstration of basal lamina components is often absent in severe intraepithelial neoplasia (SIN III). Paradoxically, basal lamina is often observed in invasive SCC, especially neoplasms forming large cohesive aggregates and cords of invasive tumor. This finding negates the usefulness of basal lamina to identify microinvasive carcinoma, but its presence does appear to correlate with a low rate of progression of SCC invading with large cohesive tumor cords.