J. Hanley-Hyde

TL;DR: It is shown that cross-linkage of FcεRI on a series of non-transformed murine mast cell lines, or treatment of these cells with calcium ionophores, stimulates increased messenger RNA levels and secretion of a group of lymphokines classically produced by a subset of murine T cell lines (TH2cells).

TL;DR: The notion that DHFR gene amplification as a consequence of c-Myc deregulation may occur in a variety of cell lines irrespective of their cell type and species origins is supported.

TL;DR: The data suggest that Myc-induced genomic instability may contribute to neoplasia by increasing the levels of a cell cycle-regulating protein, cyclin D2, via intrachromosomal amplification of its gene or generation of extrachROMosomal copies.

TL;DR: Through Southern blot analyses of DNA from backcross and cogenic mice, recombinant inbred strains, and somatic cell hybrids, the genetic loci that produce the cyclin B1-related sequences were mapped on mouse chromosomes 5, 1, 17, 4, 14, 13, 7, X, and 8, respectively.

TL;DR: The actions of the proto-oncogene, c-Myc, are considered, which may contribute to both steps of carcinogenesis, including B-cell neoplasia.