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Classification of human colorectal adenocarcinoma cell lines.
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1976
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Tumor BiologyStem LineElectron MicroscopyGastrointestinal OncologyCytogeneticsMedicineHistopathologyColorectal CancerPathologyCell LinesGastrointestinal PathologyMolecular PathologyOncologyCell BiologyTumor MicroenvironmentCancer Research
Eleven human colorectal adenocarcinoma cell lines were classified into three groups based on morphology, chromosome number, and carcinoembryonic antigen synthesis. The three groups differed in morphology, chromosome number, and CEA production, with Group 1 showing tight epithelial clusters and ~47 chromosomes, Group 2 being more dedifferentiated and hyperdiploid, and Group 3 exhibiting ultrastructural microvesicular bodies, variable chromosome counts, and higher CEA, yet no correlation was found with tumor grade, supporting Nowell’s hypothesis that each solid tumor has a distinct stem line.
Eleven human colorectal adenocarcinoma cell lines established in this laboratory were classified into three groups based on morphological features (light and electron microscopy), modal chromosome number, and ability to synthesize carcinoembryonic antigen (CEA). Group 1 cell lines contained both dedifferentiated and differentiating cells growing in tight clusters or islands of epithelium-like cells; their modal chromosome number was about 47, and they synthesized small to moderate amounts of CEA. Group 2 cell lines were more dedifferentiated, were hyperdiploid, and synthesized small amounts of CEA. Group 3 cell lines were morphologically similar to those of Group 1 by light microscopy. They differed ultrastructurally by containing microvesicular bodies; the modal chromosome number varied from hyperdiploid to hypertriploid or they had bimodal populations of hypodiploid and hypertriploid cells, and they synthesized relatively large amounts of CEA. No correlation could be found between Broder's grade or Duke's classification of the original tumor and modal chromosome number or ability to synthesize CEA. These findings support Nowell's hypothesis that the stem line is different for each solid tumor, which makes it difficult to relate chromosomal changes to the initiation of the neoplastic state.