Citations

AbstractThere is increasing evidence that vitamin D may protect against breast cancer. Some studies have suggested that dietary and supplemental vitamin D is associated with reduced mammographic density, which is highly associated with breast cancer risk, although this evidence is not entirely consistent. We investigated a possible association between circulating 25-hydroxyvitamin D (25OHD), the best indicator of vitamin D status, and quantitative mammographic density in the Minnesota Breast Cancer Family Study. Mean values of mammographic density (both percent and area densities) and circulating levels of 25OHD were compared across categories of covariates using ANOVA. Models were adjusted for age and body mass index, as well as other covariates, and also stratified by dietary calcium intake, menopause, and season. Serum, mammographic density, and questionnaire data were available from 487 women [133 premenopausal and 354 postmenopausal; mean age, 56.4 years (range, 27-85 years)] without breast cancer, and for 73%, the blood was drawn within 1 year of their mammogram. No evidence was found for an association between 25OHD and either percent density or total dense area. There was also no evidence for any association when the data were stratified by season of sample (winter and summer) or menopause. However, both percent density and dense area were lowest among those in the highest vitamin D quartile with calcium intake above the median. Unlike some previous reports, vitamin D does not seem to be related to mammographic density in this cohort. (Cancer Epidemiol Biomarkers Prev 2006;15(10):1988–92)

Transforming growth factor α (TGF-α) is produced by and required for the growth of epithelial cells and is angiogenic in vivo. Since epidermal hyperplasia and angiogenesis are hallmarks of psoriasis, TGF-α gene expression was analyzed in epidermal biopsies of normal and psoriatic skin. TGF-α messenger RNA and protein are much more abundant in lesional psoriatic epidermis than in normal-appearing skin of psoriatic patients or in normal epidermis. In contrast, messenger RNA levels of transforming growth factor β1 (TGF-β1), which inhibits epithelial cell growth, are not significantly different in normal, uninvolved, and lesional psoriatic epidermis. Thus, psoriatic epidermal hyperplasia may involve increased expression of a keratinocyte mitogen (TGF-α) rather than deficient expression of a growth inhibitor (TGF-β1).

The gene for von Recklinghausen neurofibromatosis (NF1), one of the most common autosomal-dominant disorders of humans, was recently mapped to chromosome 17 by linkage analysis. The identification of two NF1 patients with balanced translocations that involved chromosome 17q11.2 suggests that the disease can arise by gross rearrangement of the NF1 locus, and that the NF1 gene might be identified by cloning the region around these translocation breakpoints. To further define the region of these translocations, a series of chromosome 17 Not I-linking clones has been mapped to proximal 17q and studied by pulsed-field gel electrophoresis. One clone, 17L1 (D17S133), clearly identifies the breakpoint in an NF1 patient with a t(1;17) translocation. A 2.3-megabase pulsed-field map of this region was constructed and indicates that the NF1 breakpoint is only 10 to 240 kilobases away from 17L1. This finding prepares the way for the cloning of NF1 .

Dopamine-β-hydroxylase activity accumulated above a ligature on biopsy samples of normal human sural nerves incubated in vitro. The rate of accumulation indicated that this enzyme was transported distally at a velocity of 2 millimeters per hour. Axoplasmic transport of dopamine-β-hydroxylase was greatly reduced in sural nerves from a few patients with peripheral neuropathies.