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Biomedical subjects

M Potter

Publications and source records attributed to M Potter.

At least 181 records · Page 10Linked to original sources
PubMed1988

Mapping of the bcl-2 oncogene on mouse chromosome 1.

Two bcl-2 alleles have been identified in inbred strains of mice by restriction fragment length polymorphism (RFLP). Analysis of a bcl-2 RFLP in a series of bilineal congenic strains (C.D2), developed as a tool for chromosomal mapping studies, revealed linkage of bcl-2 to the Idh-1/Pep-3 region of murine chromosome 1. The co-segregation of bcl-2 alleles with allelic forms of two other chromosome 1 loci, Ren-1,2 and Spna-1, in a set of back-cross progeny, positions bcl-2 7.8 cM centromeric from Ren-1,2.

Animals↗
PubMed1987

Avian v-myc replaces chromosomal translocation in murine plasmacytomagenesis.

Deregulation of c-myc expression in association with chromosomal translocations occurs in over 95% of murine plasmacytomas, rat immunocytomas, and human Burkitt lymphomas. Infection with a murine retrovirus (J-3) containing an avian v-myc rapidly induced plasmacytomas in pristane-primed BALB/cAn mice. Only 17% of the induced plasmacytomas that were karyotyped showed the characteristic chromosomal translocations involving the c-myc locus. Instead, all of the translocation-negative tumors demonstrated characteristic J-3 virus integration sites that were actively transcribed. Thus, the high levels of v-myc expression have replaced the requirement for chromosomal translocation in plasmacytomagenesis and accelerated the process of transformation.

Animals↗
PubMed1986

A macrophage-derived factor required by plasmacytomas for survival and proliferation in vitro.

Plasmacytoma (PCT) cell lines dependent for proliferation and survival on a factor elaborated by the murine macrophage cell line, P388D1, were established in vitro. Adherent peritoneal cells induced by pristane produced 50-fold greater amounts of this activity in vitro than did resident cells. The molecules responsible for plasmacytoma growth were distinct from a number of characterized factors including interleukin-1, -2, and -3, macrophage colony-stimulating factor, B-cell stimulatory factor-1, B-cell growth factor II, epidermal growth factor, transforming growth factor-beta, and gamma- and beta-interferon, none of which were able to support the growth of the factor-dependent PCT cell lines. These results suggest that PCT growth factor may be a novel factor that has not been previously characterized and, further, that its production is associated with the pristane-induced, chronic peritoneal inflammatory response that precedes plasmacytoma formation.

Animals↗
PubMed1986

Clonal relationship of the lymphoblastic cell line P388 to the macrophage cell line P388D1 as evidenced by immunoglobulin gene rearrangements and expression of cell surface antigens.

A lymphocytic tumor of early B cell lineage, P388, and a mature macrophage tumor, P388D1, appear to have been derived from a common precursor based on identical immunoglobulin gene rearrangements and shared cell surface antigens. These cell lines may have resulted from differential maturation of a transformed cell that is an immediate cellular precursor to both the B cell and myeloid lineages. This supports earlier findings that suggest a close relationship between early B cell and myeloid differentiation pathways.

Animals↗