title: Glycoprotein CD44 expression in benign, premalignant and malignant epithelial lesions of the larynx: an immunohistochemical study including correlation with Rb, p53, Ki-67 and PCNA.
abstract: CD44 is an integral membrane glycoprotein that has diverse functions in cell-cell and cell-substrate interactions. It has been suggested that it may be a determinant of metastatic and invasive behavior in carcinomas. The immunohistochemical expression of CD44 was examined in a series of 34 squamous cell carcinomas, 13 in situ carcinomas, 35 cases with various degrees of epithelial dysplasia, 10 papillomas and 17 cases of keratosis. We used the monoclonal mouse anti-human phagocytic glycoprotein-1 CD44 (clone DF 1485), on formalin-fixed, paraffin-embedded tissue. CD44 expression was correlated with the expression of Rb and p53 proteins, with the proliferative indices Ki-67 and PCNA as well as with conventional clinicopathological data. The mean value of CD44 expression was 78.84 in squamous cell carcinomas, 78.04 in situ carcinomas, 54.93 in dysplasia, 26.8 in papillomas and 24.97 in keratosis. There was no significant difference of CD44 expression between in situ and invasive carcinomas. However, a strong difference of reaction between carcinomas and the other cases was observed. CD44 expression was statistically higher in dysplastic lesions than the cases of keratosis (p < 0.0001) and papillomas (p = 0.01). In the group of invasive carcinomas, CD44 expression was statistically correlated with pRb (p = 0.011), while in preinvasive lesions it was correlated with PCNA (p = 0.016). The relationship with the degree of dysplasia or grade of carcinoma and p53 protein expression was insignificant. These observations suggest that CD44 expression may be involved in the multiple mechanism of the development and progression of laryngeal lesions and may help to predict the risk of transformation of the benign or precancerous lesions to cancer.
authors.affiliation: Department of Pathology, Medical School, University of Ioannina, Greece.
authors.forename: E
authors.initials: E
authors.lastname: Ioachim
authors.forename: D
authors.initials: D
authors.lastname: Assimakopoulos
authors.forename: A C
authors.initials: AC
authors.lastname: Goussia
authors.forename: D
authors.initials: D
authors.lastname: Peschos
authors.forename: A
authors.initials: A
authors.lastname: Skevas
authors.forename: N J
authors.initials: NJ
authors.lastname: Agnantis
mesh_terms: D000818:Animals; D002278:Carcinoma in Situ / Q000378:metabolism / Q000473:pathology; D002294:Carcinoma, Squamous Cell / Q000378:metabolism / Q000473:pathology; D006801:Humans; D018960:Hyaluronan Receptors / Q000096:biosynthesis*; D007642:Keratosis / Q000378:metabolism / Q000473:pathology; D019394:Ki-67 Antigen / Q000096:biosynthesis*; D007820:Laryngeal Mucosa / Q000378:metabolism* / Q000473:pathology; D007822:Laryngeal Neoplasms / Q000378:metabolism / Q000473:pathology; D051379:Mice; D010212:Papilloma / Q000378:metabolism / Q000473:pathology; D011230:Precancerous Conditions / Q000378:metabolism* / Q000473:pathology; D018809:Proliferating Cell Nuclear Antigen / Q000096:biosynthesis*; D016160:Retinoblastoma Protein / Q000096:biosynthesis*; D016159:Tumor Suppressor Protein p53 / Q000096:biosynthesis*
chemical_list: D018960:Hyaluronan Receptors; D019394:Ki-67 Antigen; D018809:Proliferating Cell Nuclear Antigen; D016160:Retinoblastoma Protein; D016159:Tumor Suppressor Protein p53