No abstract

The different nature of the Te and N binding sites of bis(2pyridyl)ditellane -o Py 2 Te 2 -(1) in reactions with halogen, hydrohalic acids and a metal salt were explored in this work in order to obtain seven compounds: H o PyTeCl 2 (2), H o PyTeBr 2 (3), o PyTeI (4), H o PyTeI 2 (5), H o PyTeI 4 (6), Me o PyTeI 2 (7), and [ o PyTeCuCl] 2 (8). The compounds were structurally characterized by X-ray diffraction, which revealed, in almost all of the compounds, the presence of hypervalent chalcogen adducts containing a formal negative charge located on the Te II or Te IV atom stabilized by the protonated (2, 3, and 5) and methylated (7) pyridyl group. Compound 4 has a dimeric structure built up by association of highly unstable monomeric ArTeX units (X = Cl, Br, I) through Te-N interactions while compound 8 is a binuclear coordination complex, in which 1 behaves as a tridentate ligand, with k 2 N 2 , Te 8 coordination for one Cu I ion and kN 10 coordination for the other Cu I ion.

The genome sequence of the hemibiotrophic fungus Moniliophthora perniciosa revealed genes possibly participating in the RNAi machinery. Therefore, studies were performed in order to investigate the efficiency of gene silencing by dsRNA. We showed that the reporter gfp gene stably introduced into the fungus genome can be silenced by transfection of in vitro synthesized gfpdsRNA. In addition, successful dsRNA-induced silencing of endogenous genes coding for hydrophobins and a peroxiredoxin were also achieved. All genes showed a silencing efficiency ranging from 18% to 98% when compared to controls even 28d after dsRNA treatment, suggesting systemic silencing. Reduction of GFP fluorescence, peroxidase activity levels and survival responses to H(2)O(2) were consistent with the reduction of GFP and peroxidase mRNA levels, respectively. dsRNA transformation of M. perniciosa is shown here to efficiently promote genetic knockdown and can thus be used to assess gene function in this pathogen.

The sentinel lymph node (SLN) is considered to be the first axillary node that contains malignant cells in metastatic breast tumors, and its positivity is currently used in clinical practice as an indication for axillary lymph node dissection. Therefore, accurate evaluation of the SLN for the presence of breast metastatic cells is essential. The main aim of our study is to characterize the genomic changes present in the SLN metastatic samples with the ultimate goal of improving the predictive value of SLN evaluation. Twenty paired samples of SLN metastases and their corresponding primary breast tumors (PBT) were investigated for DNA copy number changes using comparative genomic hybridization (CGH). Non-random DNA copy number changes were observed in all the lesions analyzed, with gains being more common than losses. In 75% of the cases there was at least one change common to both PBT and SLN. The most frequent changes detected in both lesions were gains of 1pter→p32, 16, 17, 19, and 20 and losses of 6q13→q23 and 13q13→q32. In the PBT group, alterations on chromosomes 1, 16, and 20 were the most frequent, whereas chromosomes 1, 6, and 19 were the ones with the highest number of changes in the SLN metastatic group. A positive correlation was found between the DNA copy number changes per chromosome in each of the groups. Our findings indicate the presence of significant DNA copy number changes in the SLN metastatic lesions that could be used in the future as additional markers to improve the predictive value of SLN biopsy procedure.

Aim: The evaluation of allelic losses at the FHIT and the BRCA1 genes and at three other loci at the 17q region in a series of 34 sporadic breast cancer cases from Southern Brazil. Methods: The samples were evaluated for loss of heterozygosity (LOH) at the FHIT and the BRCA1 genes and at three other microsatellite markers at 17q, and the findings were correlated with clinicopathological parameters. Results: The BRCA1 intragenic marker, D17S855, had the highest frequency of LOH, detected in 10 of 24 informative cases, followed by the D17S579 (six of 23 informative cases), D17S806 (five of 21 informative cases), and D17S785 markers (five of 21 informative cases). LOH at the FHIT intragenic marker, D3S1300, was found in six of 25 informative cases. In four of the six cases with LOH of the FHIT gene, there was concomitant loss of the BRCA1 intragenic marker. Conclusions: The frequency of allelic losses in the FHIT and BRCA1 loci in the Southern Brazilian population is similar to that described in the general population. No correlations were found when the total LOH frequency was compared with tumour size, grade, or presence of axillary lymph node metastasis. Further studies using larger sporadic breast cancer samples and additional markers would be useful to confirm these findings, in addition to establishing more specific associations with clinicopathological parameters in this specific population. B reast cancer is the most common malignancy in women and one in eight Brazilian women will probably develop breast cancer in their lifetime.1 Among the genetic alterations involved in the development and progression of breast cancer, allelic losses at particular chromosomal regions are common, and may indicate deletion of tumor suppressor genes. 2Loss of heterozygosity (LOH) at 17q has been reported in about 30-60% of sporadic breast cancer cases and in many studies involves the BRCA1 gene located at 17q21. [3][4][5] However, in sporadic breast cancer, somatic mutations inactivating the BRCA1 gene are rare, 6 and it has been suggested that epigenetic mechanisms of inactivation, in addition to LOH at this locus, may take place. The region 3p14, where the FHIT gene is located, is a common site for chromosomal rearrangements in breast cancer, 8 and contains the most active common fragile site in the human genome, the FRA3B locus.9 Genetic alterations with reduced expression of this gene are found in about 30% of breast cancers.10-12 LOH studies have shown allelic losses at 3p14 in about 25% of primary breast carcinomas, suggesting that FHIT may have suppressor-like properties.10 13 In familial breast cancer kindreds, early studies 14 demonstrated a higher frequency of allelic imbalance at 3p14 compared with that seen in the sporadic breast cancers. More recent studies in BRCA2 positive tumours have shown a high frequency of FHIT LOH and reduced expression of the FHIT protein. 12In our study, we evaluated LOH at the BRCA1 and FHIT loci, in addition to three other loci on 17q, in a series of 34 sporadic breast cancer cases f...