TICdb: a collection of gene-mapped translocation breakpoints in cancer

BACKGROUND: Despite the importance of chromosomal translocations in the initiation and/or progression of cancer, a comprehensive catalog of translocation breakpoints in which these are precisely located on the reference sequence of the human genome is not available at present. DESCRIPTION: We have created a database that describes the genomic location of 1,225 translocation breakpoints in human tumors, corresponding to 247 different genes, using information from publicly available sources. Junction sequences from reciprocal translocations were obtained from 655 different references (either from the literature or from nucleotide databases), and were mapped onto the reference sequence of the human genome using BLAST. All translocation breakpoints were thus referred to precise nucleotide positions (949 breakpoints) or gene fragments (introns or exons, 276 breakpoints) within specific Ensembl transcripts. CONCLUSION: TICdb is a comprehensive collection of finely mapped translocation breakpoints, freely available at . It should facilitate the analysis of sequences encompassing translocation breakpoints and the identification of factors driving translocation events in human tumors

A simple and a reliable method to quantify antioxidant activity in vitro

The characterization of compounds with antioxidant activity is of great interest due to their ability to reduce reactive oxygen species production and, therefore, prevent some age-related diseases. Its antioxidant capacity can be analyzed by different methods both in vitro and in vivo. Caenorhabditis elegans is an in vivo model widely used in ageing research. Until now, available tests analyze functional effects in the worms, so the antioxidant activity of the compound is indirectly monitored. We have developed a simple and a reliable method to quantify internal antioxidant activity in vivo. To validate this method, we analyzed an aqueous green tea extract and two other compounds with a well-known antioxidant activity and without this activity. The results obtained (EC50 green tea = 21.76 ± 1.28 µg/mL; EC50 positive control = 8.50 ± 0.33 µg/mL; negative control EC50 > 500 µg/mL) can help in the design of further in vivo experiments. Thus, our method can be used as a previous screening capable of reducing the gap between in vitro and in vivo assays

Disruption and aberrant expression of HMGA2 as a consequence of diverse chromosomal translocations in myeloid malignancies

Chromosomal translocations that target HMGA2 at chromosome band 12q14 are seen in a variety of malignancies, notably lipoma, pleomorphic salivary adenoma and uterine leiomyoma. Although some HMGA2 fusion genes have been reported, several lines of evidence suggest that the critical pathogenic event is the expression of truncated HMGA2 isoforms. We report here the involvement of HMGA2 in six patients with myeloid neoplasia, dysplastic features and translocations or an inversion involving chromosome bands 12q13-15 and either 7p12, 8q22, 11q23, 12p11, 14q31 or 20q11. Breaks within or very close to HMGA2 were found in all six cases by molecular cytogenetic analysis, leading to overexpression of this gene as assessed by RT-PCR. Truncated transcripts consisting of HMGA2 exons 1-2 or exons 1-3 spliced to intron-derived sequences were identified in two patients, but were not seen in controls. These findings suggest that abnormalities of HMGA2 play an important and previously unsuspected role in myelodysplasia