in which this frequency in an R-DEB population was >51% 6 and 10. The discrepancy can be explained by a different constitution of patient populations. The current study involved patients from 32 unrelated families, whereas the 21 families studied by Salas-Alanis et al. included 12 families in

which the mutation had been propagated from a common ancestral allele 6 and 10. Alternatively, there could be a founder effect in the Salas-Alanis study 6 and 10. Founder populations are characterized by low genetic variation, which facilitates the detection of mutations that are rare in the general population (14). When screening the 1000 Genomes Project database for SNPs reported at the location of the c.2470insG mutation (also known as c.2471dupG), chr3:48626191-48626191 (based Selleckchem HDAC inhibitor on Homo sapiens annotation release 105), no data were found (15). This suggests that either the frequency of c2470insG is extremely low in the general population or its occurrence is endemic. Either way, larger cohorts from a larger

geographical area should be studied to elucidate c.2470insG frequency. The presence of healthy individuals with a heterozygous phenotype CDK inhibitor in our population ( Table 1) corroborates that c.2470insG is a recessive allele. R-DEB patients heterozygous for c.2470insG or homozygous for the wild-type probably have another or an additional mutant locus that is responsible for disease. Consequently, a heterozygous

phenotype for c.2470insG is not sufficient for R-DEB screening. Rapamycin chemical structure In conclusion, the allelic discrimination assay by RT-PCR genotyping is a sensitive, specific and effective methodology for detecting the c.2470insG mutation. Larger cohorts should be screened to determine the frequency of the c.2470insG mutation in R-DEB patients. The authors thank the Vicerrectoría Académica of the Universidad de Monterrey for funding of this project. We thank Denisse Martínez Treviño for her help in translating this manuscript. “
“The authorship for the article in Archives of Medical Research 2013;44:514-520 should read as follows: Jun-hui Shen, Qi Ma, Sheng-rong Shen, Guo-Tong Xu, and Undurti N. Das. We apologize for any confusion or inconvenience this may have caused. “
“Adult T-cell leukemia (ATLL) is an aggressive mature T-cell lymphoproliferative disorder linked to the human T-cell lymphotropic virus type 1 (HTLV-I). Usually it is characterized by a monoclonal expansion of the transformed CD4 T lymphocytes 1 and 2. The HTLV-I belongs to the retroviridae family and is endemic in Japan, Caribbean and South America (3). Recently it was demonstrated that leukemic cells of the ATLL have a high potential to invade several tissues from the organism by interacting with the endothelium. The E-selectin adhesion molecule is the main adherence mediator between ATLL cells and endothelial cells.