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Objectives: We aim to contribute to the assessment of the screening performance in Flanders (Belgium) and to identify valuable mammograms for subsequent studies and training., Materials and Methods: Initially negative prior screening mammograms (sMx) of 210 women with confirmed breast cancer detected by the Flemish screening programme between 2011-2013 were reviewed by a highly experienced radiologist. The review of the prior sMx was performed in three steps: 1) only prior mammograms available; 2) with index sMx (=subsequent positive sMx) present; 3) with index sMx and clinical information present., Results: The radiological review yielded 94 (45%) mammograms 'without suspicious lesions', 77 (37%) 'with minimal signs in at least one breast', and 39 (19%) 'with clearly visible tumours'. In univariate analyses, the reclassification of prior sMx was significantly associated with the date of the prior sMx, the need for a third reader for arbitration, image quality and the detector system used (computed radiography versus direct readout digital radiography), and it was not associated with the interval between screening rounds, age at prior sMx, breast density, or tumour characteristics (

The 22q11.2 deletion syndrome is a common dominant genetic disorder characterized by a heterozygous deletion of a cluster of genes on chromosome 22q11.2. TBX1, a transcription factor belonging to the T-box gene family, is a key player in the syndrome. However, heterozygosity of Tbx1 in mouse models does not fully recapitulate the phenotypes characteristic of the disease, which may point to the involvement of other genes in the deleted chromosomal region. Hence, we investigated the contribution of the catenin ARVCF, another gene that is deleted in 22q11.2DS. During Xenopus development, ARVCF mRNA is expressed in the pharyngeal arches and depleting either ARVCF or Tbx1 results in delayed migration of the cranial neural crest cells and in defects in the craniofacial skeleton and aortic arches. Moreover, double depletion of ARVCF and Tbx1 revealed that they act cooperatively, indicating that decreased ARVCF levels may also contribute to 22q11.2DS-associated phenotypes., (Copyright © 2011 Wiley Periodicals, Inc.)

The hepatitis B virus, as is the case of the hepatitis C virus, can be categorized in several genotypes. The genotyping of HBV is based on the nucleotide sequence divergence encoding the amino acids constituting the HBV surface proteins. Since the genotype of the hepatitis C virus is shown to be related to epidemiology and response to interferon therapy, one wonders whether this also holds for the hepatitis B virus. HBV genotypes clearly are found to be different in various geographical areas of infection. In Europe, genotypes A and D are predominant, whereas in Asian patients genotypes B and C are more frequent, and in the Middle-East the genotype D. Data concerning the clinical relevance are less clear but it seems that in Europe, the genotype A has a higher HBeAg clearance rate and a better outcome. In Asia, genotype B (and especially the genotype Bj) is associated with a higher HBeAg clearance and with less development of cirrhosis and HCC. The impact on spontaneous or therapy induced viral resolution is not yet clearly identified. Further evaluation in different countries is needed to delineate the impact of the genotype relative to other factors such as age at infection, level of serum transaminases and viral load, on the course of infection, complication, outcome of treatment and prognosis.

During Xenopus development, p120 transcripts are enriched in highly morphogenetic tissues. We addressed the developmental function of p120 by knockdown experiments and by expressing E-cadherin mutants unable to bind p120. This resulted in defective eye formation and provoked malformations in the craniofacial cartilage structures, derivatives of the cranial neural crest cells. Closer inspection showed that p120 depletion impaired evagination of the optic vesicles and migration of cranial neural crest cells from the neural tube into the branchial arches. These morphogenetic processes were also affected by p120-uncoupled cadherins or E-cadherin containing a deletion of the juxtamembrane domain. Irrespective of the manipulation that caused the malformations, coexpression of dominant-negative forms of either Rac1 or LIM kinase rescued the phenotypes. Wild-type RhoA and constitutively active Rho kinase caused partial rescue. Our results indicate that, in contrast to invertebrates, p120 is an essential factor for vertebrate development and an adequate balance between cadherin activity and cytoskeletal condition is critical for correct morphogenetic movements.