Four Permanent Cell Lines Established from Human Malignant Gliomas

Rat model of the human “Triton” tumor: direct genetic evidence for the myogenic differentiation capacity of schwannoma cells using the mutant neu gene as a cell lineage marker

“…Interpretations of this phenomenon usually refer to the pronounced differentiation capacity of neural crest cells during embryonal development, which has been particularly well documented in lower vertebrates [26,271, and it is assumed that at least part of the progeny of these cells retain this capacity during the process of malignant transformation [lo, 211. The observation of skeletal muscle differentiation in dissociated cells of the optic nerves of 10-day-old rats [51], the pineal glands of neonatal rats [14], and in rat and human glioma cell lines 14, 18,281 points to the same direction. Additional evidence comes from the present study where: (1) spontaneous myogenic differentiation was observed in cultures established from primary malignant schwannomas enriched for cells expressing the rat Schwann cell-specific cell surface antigen specified by Mab 217c [12, 431; (2) cells with transitional phenotypes between embryonal rhabdomyoblasts and atypical Schwann cells were found in the tumors after reimplantation of cells from cultures undergoing myogenic differentiation.…”

“…Note the significant decrease in the number of fluorescent cells. Histograms[16][17][18] show the result of a control experiment omitting the first antibody vidual myotubes and in 25-30 cycles in all other cases (temperature profile: 94" C, 30 s; 55" C, 1 min; 72" C, 2 min), with elongation…”

The Role of Stem Cells in Skeletal and Cardiac Muscle Repair

“…They may be derived from fibroblasts or may correspond to pericytes closely associated with blood vessels, and they can be derived from embryonic stem cells in the presence of PDGF and stem cell factor (Powell et al 1999;Walker et al 2001). Myofibroblasts are usually identified by expression of the cytoskeletal protein desmin (which is Table 2 Older literature related to other sources of myoblasts (Grounds 1990) Neuroectodermal origin Thymus Myoblasts (Ketelsen and Werkerle 1976;Kamo et al 1984; Nakamura and Ayer-Le Lievre 1986) Pineal Myoblasts (Freschi et al 1979;Watanabe 1986) Neural cell lines/brain tumors Myoblasts (Lennon and Petersen 1979;Wright 1984;Jacobsen et al 1987 (Blau et al 1985) Chick muscle nuclei activate muscle genes in rat neural cell lines (Wright 1984) present in smooth, skeletal, and cardiac muscle), often in addition to vimentin (which is a marker for fibroblasts) and by smooth muscle ␣ -actin, but they do not express cardiac or skeletal ␣ -actin (Powell et al 1999). Expression of the skeletal muscle-specific genes for MyoD, myogenin, and sarcomeric myosins in myofibroblasts in culture and also in rat liver stellate cells in vivo confirms that they also have some properties of skeletal muscle (Mayer and Leinwand 1997;Walker et al 2001).…”

Immunohistochemical localisation of tissue plasminogen activator in human brain tumours

“…Lymphokines have also been shown to have a similar inductive effect on endothelium (Tiku & Tomasi, 1985). These observations provide support for the view that the phenotypically transformed t-PA and FN producing cells derived in vitro from human malignant gliomas are of vascular origin and are responding to factors produced by neoplastic glial cells (Manoury, 1977;Franks & Burrow, 1986;Jacobsen et al, 1987;McKeever et al, 1987;Rutka et al, 1987). Clearly a broader study of endothelium in other sites (neoplastic, reactive and normal) and the response of cultured cells to glioma-derived factors would be of interest.…”

“…The latter cell type has been considered by some to be a less differentiated neoplastic glial cell whose growth is enhanced by culture, a view apparently strengthened by the observation that its growth pattern is aberrant and not contact-inhibited (Kennedy et al, 1987;Frame et al, 1984). A contrary view holds that these cells are not of parenchymal origin but instead derive from mesenchymal or endothelial elements responding to growth factors produced by the tumours (Manoury, 1977;Franks & Burrow, 1986;Jacobsen et al, 1987;McKeever et al, 1987;Rutka et al, 1987). The finding that similar growth properties and antigen expression can be observed in endothelial cells derived from non-neoplastic tissues (Laug et al, 1980;McAuslan et al, 1980) supports this latter view.…”