Abstract
An individual pulmonary tumor induced by a chemical carcinogen often shows complex histologic features associated with different cellular and structural atypias which suggest tumor progression in the tumorigenesis. Analysis of their cellular characteristics is important to elucidate tumor cell origin and the relationship between tumor histology and cell origin. For this purpose, we examined lectin binding affinities in various types of pulmonary tumor induced by 3-methylcholanthrene (3-MC) in mice.
3-MC induced proliferative lesions of the A/J mouse lung were classified into four basic histological types : hyperplasia (HP), alveolar adenoma (AA), papillary adenoma (PA), and papillary adenocarcinoma (PC), and their combined type : PA in AA, PC in AA, PC in PA, etc. Frequency of PA, PC, and combined type tumors increased as a function of time after carcinogen administration. Binding affinities of cells in normal respiratory epithelia and 3-MC induced proliferative lesions to four perox-idase-conjugated lectins, Maclura pomifera agglutinin (MPA), Arachis hypogea agglutinin (PNA), Ricinus communis agglutinin (RCA), and wheat germ agglutinin (WGA) were examined. In normal epithelia, both Clara cells and type II alveolar cells showed strong affinity to MPA and WGA. Cells of HP and AA showed fairly strong affinity to all four lectins. PA and PC cells, however, lost their binding affinity to MPA, PNA, and RCA, but not to WGA. A distinct difference in lectin binding affinity between HP/AA and PA/PC was clearly shown in this experiment and the evidence obtained was supportive of progressive development of mouse pulmonary tumors.
