The murine B-cell tumor, BCL?1?, originally described by Slavin and Strober, was adapted to in vitro tissue culture by Gronowicz, et al., and was subcloned in our laboratory by Brooks, et al. The in vitro-adapted clones of BCL?1? cells are phenotypically similar to the parent line. We have recently found that when the clones of BCL?1? cells are blocked (by excess thymidine) at the G?1?/S border and then released from the blockade, the medium from these cells contains a growth factor (GF) which is functionally very similar to T-cell-derived BCGF and acts on normal B cells. It might, therefore, be postulated that these neoplastic B cells produce an autostimulatory BCGF. It is conceivable that this GF is a product of an activated cellular oncogene, as is the case for platelet-derived GF. The purpose of this research will be to investigate the structure/function relationships between conventional T-cell-derived BCGF and the BCL?1?-derived BCGF. The approaches to be used are: (1) the biochemical isolation and characterization of the BCL?1?-BCGF; (2) the generation of monoclonal anti-BCL?1?-BCGF antibodies; and (3) an attempt to clone the BCGF gene from the BCL?1? cells. If and when BCGF can be purified by one of the above methods, we will study its mode of action, e.g., its binding to specific receptors on activated cells, its similarity to T-cell-derived BCGF and other GF, and the possibility that it acts (like some other GF) as a tyrosine-specific protein kinase. (HF)
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