Quark-gluon vertex in general kinematics

The original publication can be found at www.springerlink.com Submitted to Cornell University’s online archive www.arXiv.org in 2007 by Jon-Ivar Skullerud. Post-print sourced from www.arxiv.org.We compute the quark–gluon vertex in quenched lattice QCD in the Landau gauge, using an off-shell mean-field O(a)-improved fermion action. The Dirac-vector part of the vertex is computed for arbitrary kinematics. We find a substantial infrared enhancement of the interaction strength regardless of the kinematics.Ayse Kizilersu, Derek B. Leinweber, Jon-Ivar Skullerud and Anthony G. William

Genomically Complex Human Angiosarcoma and Canine Hemangiosarcoma Establish Convergent Angiogenic Transcriptional Programs Driven by Novel Gene Fusions

Sporadic angiosarcomas are aggressive vascular sarcomas whose rarity and genomic complexity present significant obstacles in deciphering the pathogenic significance of individual genetic alterations. Numerous fusion genes have been identified across multiple types of cancers, but their existence and significance remain unclear in sporadic angiosarcomas. In this study, we leveraged RNA-sequencing data from 13 human angiosarcomas and 76 spontaneous canine hemangiosarcomas to identify fusion genes associated with spontaneous vascular malignancies. Ten novel protein-coding fusion genes, including TEX2-PECAM1 and ATP8A2-FLT1, were identified in seven of the 13 human tumors, with two tumors showing mutations of TP53. HRAS and NRAS mutations were found in angiosarcomas without fusions or TP53 mutations. We found 15 novel protein-coding fusion genes including MYO16-PTK2, GABRA3-FLT1, and AKT3-XPNPEP1 in 11 of the 76 canine hemangiosarcomas; these fusion genes were seen exclusively in tumors of the angiogenic molecular subtype that contained recurrent mutations in TP53, PIK3CA, PIK3R1, and NRAS. In particular, fusion genes and mutations of TP53 cooccurred in tumors with higher frequency than expected by random chance, and they enriched gene signatures predicting activation of angiogenic pathways. Comparative transcriptomic analysis of human angiosarcomas and canine hemangiosarcomas identified shared molecular signatures associated with activation of PI3K/AKT/mTOR pathways. Our data suggest that genome instability induced by TP53 mutations might create a predisposition for fusion events that may contribute to tumor progression by promoting selection and/or enhancing fitness through activation of convergent angiogenic pathways in this vascular malignancy. IMPLICATIONS: This study shows that, while drive events of malignant vasoformative tumors of humans and dogs include diverse mutations and stochastic rearrangements that create novel fusion genes, convergent transcriptional programs govern the highly conserved morphologic organization and biological behavior of these tumors in both species

List of significantly associated haplotypes.

<p>List of significantly associated haplotypes.</p

Two neighboring loci on chromosome 5 are independently associated with disease risk.

<p>A. The top SNP of the first peak (29 Mb) is in high LD with nearby variants and shows no evidence of linkage to the top SNPs in the second peak (33 Mb). B. The 29 Mb peak is comprised of two haplotype blocks, and C. the risk haplotypes for the 29 Mb peak are rather common in the population. Similarly, D. the second peak also shows no linkage with the first peak in the combined analysis, whereas E. analysis of only B-cell lymphoma shows SNPs in strong LD within the second peak and in moderate LD with SNPs in the first peak. The top SNPs in the combined analysis and B-cell-lymphoma-only analysis are independent, and F. make up separate haplotypes at the second locus. G. Both risk haplotypes at the second locus are rare. Color-coding of SNPs in A, D, E, reflects their r² value relative the top SNP of that region, ranging from grey (not in LD) to red (strong LD).</p

Top 10 differentially expressed genes by the risk haplotype at each locus.

<p>Top 10 differentially expressed genes by the risk haplotype at each locus.</p

Differentially expressed genes by the risk alleles at 29 Mb and 33 Mb play important role in T-cell immunity.

<p>A. The risk allele at the 29 Mb at homozygous state has a clear cis-regulation effect on the expression levels of <i>TRPC6</i>, <i>KIAA1377</i>, and <i>ANGPTL5</i>, three of the most proximal genes. <i>BIRC3</i>, which is also proximal to the 29 Mb risk locus, had a significant p-value, however the FDR value was slightly above the threshold of 0.05. The risk allele at 29 Mb was also associated with a regulatory effect on genes near the 33 Mb locus and a change in the expression of <i>PIK3R6</i> significantly. B. A large network of molecules that play a major role in activation of T-lymphocyte and other immune cells (IPA category: cell-to-cell signaling and interaction, hematological system development and function). This network includes 15 molecules of which expressions are significantly altered in individuals carrying at least one copy of the shared risk allele at the 33 Mb locus. The outcomes of such expression changes are significantly linked to decrease in T-cell activation.</p