SummaryThe expression of heat shock proteins (HSP) of the 65kD family (groEL) has been observed by flow cytometry using murine monoclonal antibody (MoAb) anti-HSP 65kD (ML30) on the surface of B (Daudi) or T (H9) lymphoma cells, on a moncyte cell line (U937) and also on a primary culture of a human pancreatic carcinoma (HPC). Moreover Heat Shock Proteins (HSP) represent a family of highly conserved molecules that under stress conditions play an important physiological role in folding and unfolding of proteins (Lindquist & Craig, 1988). HSP expression is strictly related to cell cycle and oncogene activation (Pechan, 1991), and it is important to note that HSP are often tumour associated antigens (Ulrich & Robinson, 1986;Srivistava & Maki, 1990). In fact, myc-overexpressing cells show viral myc-proteins nuclearly colocalised with nuclear HSP70 (Koshinen et al., 1991). The myc-oncogene is functionally similar to the adenovirus Ela and is able to collaborate with activated ras-oncogene to transform primary fibroblasts (Ralston, 1991). It has been reported also that the adenoviral Ela products induce HSP70 synthesis by acting as transcriptional activator. However, it is not yet clear whether increased levels of HSP may facilitate tumoural and viral proliferation. In Hela cells, HSP70 interacts with other cellular proteins in a cell cycle-dependent manner; synthesis of HSP has been shown to increase during mitosis (Pechan, 1991). Other HSP such as HSP90 and HSP70 have been found to reach abnormally high levels in transformed cells (Bensaude & Morange, 1983). Proteins belonging to the HSP70 family were shown to interact with nuclear oncogenes such as p53, and the stability of this interaction might influence transformation (Finlay et al., 1988
SCID miceThe SCID mutation (Bosma et al., 1983) occurred in the C.B-171cr (C.B-17) inbred strain, an immunoglobulin heavy chain (Igh) congenic partner strain of BALB/cAnIcr (BALB/ c). These mice have a severe combined immune deficiency as a result of their inability to rearrange correctly their immunoglobulin and T-cell receptor genes, and for this reason are permissive for the growing of transformed human Correspondence: V. Colizzi,