The toxicologic and carcinogenic potential of naphthalene was studied by exposing groups of male and female B 6 U F , mice to atmospheres containing 0 (7.5 mice per sex), 70 ppm (7.5 mice per sex), or 30 ppm (150 mice per sex) of the chemical for 6 h daily, 5 dayslwk for 703 wk. The final mean body weights of mice exposed to naphthalene were similar to those of the controls. The survival of control male mice was significantly lower than that of the exposed males. The lower survival was attributed to wound trauma and secondary infection related to fighting among the group-housed control animals. There was no significant difference in survival between control and exposed female mice. Under the conditions of this 2-yr study, naphthalene was not carcinogenic to male mice. In female mice it caused an increase in the incidence of pulmonary alveolar/bronchiolar adenomas. Naphthalene also caused an increase in the incidence and severity of chronic inflammation, olfactory epithelium metaplasia of hyperplasia of the nasal respiratory epithelium, and chronic nasal inflammation in the lungs of mice of each sex.A complete account for this study was presented in National Toxicology Program Technical Report 410 entitled "Toxicology and Carcinogenesis Studies of Naphthalene." 393 Inhalation Toxicology, 4993409,1992 Copyright 0 1992 by Hemisphere Publishing Corporation Inhalation Toxicology Downloaded from informahealthcare.com by McMaster University on 02/20/15 For personal use only. 394 K. M. ABDO ET AL.

Here we report a transgenic mouse line that exhibits significant deviations from a classic pattern of parental imprinting. When the transgene is passed through the female germline, it is completely silenced in some offspring while in others expression is reduced. This variable expressivity does not appear to be the result of differences in the presence of unlinked modifiers. Female transmission of the transgene is associated with hypermethylation. The transgene is generally reactivated on passage through the male germline. Extended pedigrees reveal complex patterns of inheritance of the phenotype. The most likely explanation for this result is that the imprint is not completely erased and reset when passed through the germline of either sex. FISH analysis reveals that the transgene has integrated into chromosome 3 band E3, a region not known to carry imprinted genes, and the integration site shows no sign of allele-specific differential methylation. These findings, in conjunction with other recent

Herein, we describe the analysis and mapping of cDNA clones encoding variant forms of the human homolog of the canine 180-kDa ribosome receptor (p180). One form, similar to the chicken ES/130 homolog, possesses a large uninterrupted C-terminal region composed predominantly of heptad repeats predicted to form an alpha-helical double-stranded coiled-coil rod. Other forms contain in addition a 10-amino acid consensus motif, NQGKKAEGAQ, repeated up to 54 times in tandem close to the N-terminus. Such repeats in canine p180 represent a ribosome-binding domain. The cDNA hybridized to a major 6-kb transcript in all tissues examined, where very high expression was observed in tissues that carry out a high level of secretion such as pancreas, liver, and placenta. The ES130/p180 gene was mapped to chromosome 20p12, and a potential pseudogene appears to reside on chromosome 7. In summary, the data suggest that p180 exists in humans in different forms because of complete removal of tandem repeats, or partial intraexonic splicing, creating different repeat lengths with potentially novel ribosome-binding characteristics.

An unusually high level of latent HHV-6 infection has been documented in the peripheral blood and/or bone marrow cells of a small group of patients with predominantly malignant lymphoid disorders, and in at least one healthy individual. We have shown previously in peripheral blood mononuclear cells (PBMCs) of three patients, two with a history of lymphoma and one with multiple sclerosis, a specific target site for latent integration of the full-length HHV-6 viral genome on the distal short arm of chromosome 17, in band p13.3. Fluorescence in situ hybridization (FISH) procedures were used to map more precisely the location of the viral integration site in one of those patients, relative to two known oncogenes mapped previously, namely CRK, and the more telomeric ABR oncogene. It is shown that the HHV-6 integration site is located at least 1,000 kb telomeric of ABR, and is very likely to map close to or within the telomeric sequences of 17p. This finding is significant given that human telomeric-like repeats flank the terminal ends of the HHV-6 genome. Cytogenetic studies showed evidence of karyotype instability in the peripheral blood cells infected latently.

The closely related small GTP-binding proteins Rac1, Rac2, and Rac3 are part of a larger Rho subfamily of Ras proteins. Because disruption of Ras signaling pathways is relevant to the pathogenesis of a wide variety of cancers, it is important to clearly define the structural and functional characteristics of the participating proteins and their encoding genes. Rho subfamily members are involved in a range of signal transduction pathways relevant to cell growth, differentiation, motility, and stress, and Rac proteins are now recognised as a necessary component of Ras-mediated cellular transformation. We previously mapped RAC3 to chromosome band 17q23→ q25, a region that contains a number of candidate tumour suppressor genes. Because of its oncogenic potential, we have now further refined the location of this gene. Here we confirm that RAC3 maps to chromosome band 17q25.3 and further show that it maps some distance telomeric of a well-characterised minimal breast and ovarian candidate tumour suppressor gene region, BROV. The genomic structure of RAC3, including exon and intron boundaries, is also presented.