No abstract

In vitro models are required for the study of these cancers, and several cell lines have already been established and characterised (Lafargues & Ozzello, 1958;Soule et al., 1973;Cailleau et al., 1974;Engel et al., 1978;Whitehead et al., 1983;Yamane et al., 1984;Chu et al., 1985;Vandewalle et al., 1987). Nevertheless, owing to the heterogenity and the diversity of mammary cancers, a great number of cell models is necessary to understand the reasons for this diversity and the effect of anticancer drugs on tumour cells.Cytogenetic studies of mammary adenocarcinoma cell lines are essential for comprehension of the pathogenesis of these cancers (Trent, 1985;Gebhart et al., 1986). The implication of chromosomal alterations in these pathologies has opened a new and promising route towards better knowledge of these cancers (Cervenka & Koulischer, 1973). Chromosomal alterations are generally numerous, and markers often demonstrate hyperploidy in these cancers (Sandberg, 1980). Demonstration of the minimum genetic alterations indispensable for cell transformation is difficult, and might be easier on cells with a karyotype closer to normal. Sandberg and Wolman mentioned the existence of such cells, but most of their results concerned karyotype studies without chromosome banding (Sandberg, 1980;Wolman, 1983 [-', hyaluronidase 25 IU for 20 ml, Hepes buffer 4.8 g 1' in distilled water). Cells were then fixed in acetic acid:methanol (1:3) and dropped onto grease-free, cooled slides for chromosome counting and examination. R bands were obtained by heat denaturation of the chromosomes according to the method of Dutrillaux and Lejeune (1971). Xenografted CAL51 cells were plated and studied in vitro in the same manner.

Permanent human osteosarcoma cell lines are important tools for the study of bone cancer. As representative of an osteoblastic phenotype, they partly reflect their normal osteoblastic counterparts and, thus, may represent appropriate models to investigate the mechanisms involved in bone remodelling and in haematopoietic differentiation. In the present work, we describe a new human cell line, CAL 72, obtained from an osteosarcoma of the knee of a 10‐year‐old boy. These cells grow in continuous culture, and karyotypic analysis has revealed clonal abnormalities in number and structure, especially loss of chromosome Y. These cells exhibit morphological, immuno‐histochemical and molecular characteristics of the osteoblastic lineage. Using RT‐PCR, we have shown that the CAL 72 cell line expresses high levels of mRNA coding for several cytokines, such as G‐CSF, GM‐CSF, IL‐1β and IL‐6. In view of this expression profile, the CAL 72 phenotype appears to be closer to normal primary osteoblasts than other reported osteosarcomas. Moreover, these cells express mRNA for both HGF and its receptor c‐MET, suggesting that this autocrine loop might contribute to the invasiveness of the tumour from which CAL 72 originated. Int. J. Cancer82:282–285, 1999. © 1999 Wiley‐Liss, Inc.

We describe here two new human urothelial carcinoma cell lines, CAL 29 and CAL 185, established from two patients with high-grade tumours and which display very different properties in vitro. We have shown that CAL 29 cells were tumorigenic in mice and expressed characteristic features of both cell scattering and transition from epithelial to mesenchymal phenotype (EMT) after triggering by the EGF receptor ligands, TGFα and EGF. At the opposite, the CAL 185 cells were not tumorigenic in mice and neither scattered nor expressed vimentin intermediary filaments in the presence of growth factors. We further demonstrated that CAL 29 cell scattering was reversible after growth factor removal and that both scattering and EMT were markedly impaired after treatment with MEK, Src and PI3-kinase inhibitors suggesting that these kinases might be important components of the cellular responses to EGF and TGF-α leading to scattering and EMT. These agents could help to understand the intracellular pathways involved in invasiveness and to find new targets for limiting metastasis. In conclusion, these two new cell lines could be good models to dissect the molecular mechanisms involved in invasion and metastasis development in human bladder cancer. © 2001 Cancer Research Campaign http://www.bjcancer.com

No abstract