Basal/myoepithelial cells in chronic sinusitis, respiratory epithelial adenomatoid hamartoma, inverted papilloma, and intestinal-type and nonintestinal-type sinonasal adenocarcinoma: an immunohistochemical study.
BACKGROUND
The pathogenesis of respiratory epithelial adenomatoid hamartoma (REAH) and inverted papilloma (IP) is poorly understood, especially compared with sinonasal adenocarcinoma (SNAC). One feature of malignant glandular lesions is loss of the basal/myoepithelial layer. The immunophenotype of the basal/myoepithelial layer has not been fully examined in benign glandular lesions of the sinonasal tract.


OBJECTIVE
To examine benign and malignant glandular lesions in the sinonasal tract for the immunophenotype of basal/myoepithelial cells, proliferation index, and cytokeratin and intestinal differentiation profiles.


METHODS
Sinonasal adenocarcinoma (intestinal-type adenocarcinoma [ITAC] and nonintestinal type adenocarcinoma [non-ITAC]), REAH, IP, and chronic sinusitis (CS) were stained for cytokeratin (CK) 7, CK20, 34betaE12, CDX-2, p63, Ki-67, smooth muscle actin (SMA), S100 protein, and calponin.


RESULTS
Basal/myoepithelial cells in CS and REAH were positive for p63 and 34betaE12 but negative for SMA, S100 protein, and calponin. Proliferative activity was localized to the compartment containing p63-positive cells. Inverted papilloma demonstrated broad areas staining for p63 and 34betaE12, with intermediate proliferative activity in these areas. Sinonasal adenocarcinoma had the highest Ki-67 labeling index, and p63-positive SNACs had higher proliferation indices than p63-negative SNACs. REAH, IP, CS, and most SNACs expressed CK7. Only SNAC expressed CK20. Sixty percent of morphologic ITACs expressed CDX-2.


CONCLUSIONS
Basal/myoepithelial cells in CS and REAH should be considered basal and not myoepithelial cells. In benign lesions, proliferative activity is limited to the compartments with p63 staining. In SNAC and IP, p63 expression correlates with proliferation index. REAH, IP, and CS share similar immunoprofiles (CK7+, CK20-, and CDX-2-), contrasting with SNAC (CK7+, CK20+/-, CDX-2-/+).
Ozolek
John A
JA
Department of Pathology, Children's Hospital of Pittsburgh, 3705 Fifth Ave, Pittsburgh, PA 15213, USA. ozolekja@upmc.edu
Barnes
E Leon
EL
Hunt
Jennifer L
JL
D000199:Actins / Q000378:metabolism; D000230:Adenocarcinoma / Q000378:metabolism / Q000473:pathology*; D014408:Biomarkers, Tumor / Q000032:analysis; D000071616:CDX2 Transcription Factor; D002135:Calcium-Binding Proteins / Q000378:metabolism; D049109:Cell Proliferation; D002908:Chronic Disease; D003937:Diagnosis, Differential; D004847:Epithelial Cells / Q000473:pathology; D005260:Female; D006222:Hamartoma / Q000378:metabolism / Q000473:pathology*; D018398:Homeodomain Proteins / Q000378:metabolism; D006801:Humans; D007150:Immunohistochemistry; D016130:Immunophenotyping; D007633:Keratins / Q000378:metabolism*; D019394:Ki-67 Antigen / Q000378:metabolism; D008297:Male; D008565:Membrane Proteins / Q000378:metabolism; D008840:Microfilament Proteins / Q000378:metabolism; D008875:Middle Aged; D010212:Papilloma / Q000378:metabolism / Q000473:pathology*; D010255:Paranasal Sinus Neoplasms / Q000378:metabolism / Q000473:pathology*; D009418:S100 Proteins / Q000378:metabolism; D012852:Sinusitis / Q000378:metabolism / Q000473:pathology*; D015534:Trans-Activators / Q000378:metabolism; D000096985:Calponins
D000199:Actins; D014408:Biomarkers, Tumor; D000071616:CDX2 Transcription Factor; D002135:Calcium-Binding Proteins; D018398:Homeodomain Proteins; D007633:Keratins; D019394:Ki-67 Antigen; D008565:Membrane Proteins; D008840:Microfilament Proteins; D009418:S100 Proteins; D015534:Trans-Activators; D000096985:Calponins; C081876:CKAP4 protein, human