Conservation of the organization of the pre-B cell specific VpreB1/VpreB2/lambda 5 loci in the genus Mus.
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Animals↗
Biomedical subjects
S R Bauer
Publications and source records attributed to S R Bauer.
The human Vpre B gene is located on chromosome 22 near a cluster of V lambda gene segments.
The chromosomal location of the human VpreB gene was determined by Southern blotting analysis of restriction enzyme-digested DNAs from a panel of 17 mouse-human somatic cell hybrids. The pattern of hybridization of a Vpre B-specific probe in conjunction with earlier analysis of several marker genes allowed the following conclusions: 1) Vpre B is on human chromosome 22 within band 22q11.2 distal to the bcr-like gene, bcr-2 and proximal to the bcr-like gene, bcr-4. 2) Vpre B has been localized relative to several constitutional and tumor-specific breakpoints within 22q11.2, segregates in hybrids retaining 22q- chromosomes with some but not with all members of the V lambda 1 subgroup of the V lambda genes, and is amplified with these genes in K562 cells. 3) The order of the loci on chromosome 22 is centromere----bcr-2, Vpre B, V lambda 1----bcr-4----C lambda----bcr-1----bcr-3----sis.
B-Lymphocytes↗
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↗
Mutations which stabilize myc transcripts and enhance myc transcription in two mouse plasmacytomas.
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Animals↗
Chromosome translocations clustered 5' of the murine c-myc gene qualitatively affect promoter usage: implications for the site of normal c-myc regulation.
Five novel murine plasma cell (PC) tumors with chromosome translocations 350-500 bp 5' of the first c-myc exon are described. The t(12;15)s of TEPC 1194, ABPC 33 and TEPC 1165 position the intact c-myc locus 5' of the Cu, C gamma 2a and C alpha IgCH genes respectively. In ABPC 17, the IgH enhancer element and adjacent switch (Su) sequences were found 5' of the first c-myc exon while this enhancer is associated with the reciprocal products of the TEPC 1194, ABPC 33 and TEPC 1033 translocations. Quantitative S1 nuclease analyses demonstrate that the ratios of transcription from the two c-myc promoters (P1 and P2) are increased 4-to 7-fold in these five tumors. With the exception of TEPC 1165, (which contains a small deletion in exon 1), such increases in P1:P2 ratios appear to be manifested by a reduction in P2 usage in comparison to other tumors without such promoter shifts. A survey of 27 additional PC and non-PC B lymphoid tumors and cell lines revealed that myc promoter shifts of this magnitude are unique to PC tumors with 5'-proximal translocations. We propose that (i) these clustered breakpoints identify a normal c-myc regulatory element located at least 350 bp 5' of c-myc exon 1; (ii) the loss or disruption of this cis-acting upstream element and the linkage of c-myc to the IgCH locus would result in abnormal expression of this oncogene in these as well as most other PC tumors.
Animals↗
DNA rearrangement and altered RNA expression of the c-myb oncogene in mouse plasmacytoid lymphosarcomas.
Three types of tumors termed plasmacytomas (ABPC's), lymphosarcomas (ABLS's), and plasmacytoid lymphosarcomas (ABPL's) arise in BALB/c mice treated with pristane and Abelson murine leukemia virus (A-MuLV). While most ABPC's and BLS's contain integrated A-MuLV proviral genome and synthesize the v-abl RNA, most ABPL's do not. The ABPL tumors were examined for the expression of other oncogenes that may be associated with their transformed state, in the absence of transforming virus. These tumors expressed abundant c-myb RNA of unusually large size and showed DNA rearrangements of the c-myb locus.
Abelson murine leukemia virus↗
Increased expression of myc-related oncogene mRNA characterizes most BALB/c plasmacytomas induced by pristane or Abelson murine leukemia virus.
RNA blots of poly(A)-containing RNA from normal livers and spleens and from a number of transplantable hematopoietic and lymphoid BALB/c tumors, including early and late generation plasmacytomas, were hybridized with probes for four onc genes. abl RNA was abundant only in those tumors producing Abelson virus, bas RNA was found in approximately equal amounts in normal tissues and plasmacytomas, and myb RNA was absent in normal liver and plasmacytomas. Normal liver and spleen RNA showed faint traces of myc hybridization, but myc RNA was increased in most plasmacytomas. In one plasmacytoma, TEPC 1165, a particularly abundant amount of myc RNA was found, principally as a 3.5-kilobase band. In the other plasmacytomas, bands of 2.4- or 1.8-kilobase myc RNA were found. Southern blots of DNA from tumors that contained 2.4-kilobase or larger myc RNA showed myc hybridization to an EcoRI fragment of about 21 kilobase pairs, similar to the myc band in normal DNA. EcoRI digests of DNA from two tumors that expressed myc RNA of 1.8 kilobases showed an additional smaller myc band, suggesting that the myc gene is rearranged in these plasmacytomas. The basis for increased myc gene transcription in plasmacytomas is not understood, but the evidence suggests that different mechanisms may be operating in different plasmacytomas. Apparently, neither myc gene amplification nor myc gene rearrangement is required for increased myc transcription.
Abelson murine leukemia virus↗
A comparative study of iodine uptake by thyroid and thymus glands of male and female Sprague-Dawley rats of different ages.
The iodine concentrating ability of thyroid glands, thymus gland and skin in Sprague-Dawley rats was assessed by determining the tissue/blood radioiodide concentration ratios. Tissue/blood ratios are significantly affected by the age of the rats, however, thymus/blood radioiodide ratios never exceeded unity. The comparative uptake of 131I by thymus and thyroid tissue expressed as thymus/thyroid (%) for neonate animals was 10-16 times greater than those obtained for older rats. Moreover, the fraction of injected dose of radioiodide in thymus tissue never exceeded that of the thyroid or skin and paralleled the concentration of radio-activity in the blood. These results indicate that although neonate thymus tissue contains a significantly greater amount of radioactivity than the thymus of older rats, an active iodide concentration mechanism is not involved.
Age Factors↗
Self-image disparity, repression-sensitization, and extraversion-introversion: a unitary dimension?
To determination (1) whether self-image disparity, repression-sensitization, and extraversion-introversion intercorrelated to a degree indicative of a unitary personality dimension and, (2) whether the interrelationships among these variables was accounted for by cognitive developmental variance, Byrne's Revised Repression-Sensitization Scale, Giedt and Downing's Extraversion-Introversion Scale, and two measures of self-image disparity were administered to 20 male college freshmen and 20 male seniors. All the correlations among the four measures were significant, but none correlated significantly with cognitive development, as measured by SATs. Factor analysis yielded a clearcut personality factor and a clearcut cognitive factor, indicating that the personality measures reflect a unitary dimension, even after cognitive developmental variance is extracted.
Adolescent↗