Cancellation of UV Divergences in the N=4 SUSY Nonlinear Sigma Model in Three Dimensions

We study the UV properties of the three-dimensional ${\cal N}=4$ SUSY nonlinear sigma model whose target space is $T^*(CP^{N-1})$ (the cotangent bundle of $CP^{N-1}$) to higher orders in the 1/N expansion. We calculate the $\beta$-function to next-to-leading order and verify that it has no quantum corrections at leading and next-to-leading orders.Comment: 10 pages, 2 figures. references adde

The Noncommutative Supersymmetric Nonlinear Sigma Model

We show that the noncommutativity of space-time destroys the renormalizability of the 1/N expansion of the O(N) Gross-Neveu model. A similar statement holds for the noncommutative nonlinear sigma model. However, we show that, up to the subleading order in 1/N expansion, the noncommutative supersymmetric O(N) nonlinear sigma model becomes renormalizable in D=3. We also show that dynamical mass generation is restored and there is no catastrophic UV/IR mixing. Unlike the commutative case, we find that the Lagrange multiplier fields, which enforce the supersymmetric constraints, are also renormalized. For D=2 the divergence of the four point function of the basic scalar field, which in D=3 is absent, cannot be eliminated by means of a counterterm having the structure of a Moyal product.Comment: 15 pages, 7 figures, revtex, minor modifications in the text, references adde

Vector Positronium States in QED3

The homogeneous Bethe-Salpeter equation is solved in the quenched ladder approximation for the vector positronium states of 4-component quantum electrodynamics in 2 space and 1 time dimensions. Fermion propagator input is from a Rainbow approximation Dyson-Schwinger solution, with a broad range of fermion masses considered. This work is an extension of earlier work on the scalar spectrum of the same model. The non-relativistic limit is also considered via the large fermion mass limit. Classification of states via their transformation properties under discrete parity transformations allows analogies to be drawn with the meson spectrum of QCD.Comment: 24 pages, 2 encapsulated postscript figure

Holography of the N=1 Higher-Spin Theory on AdS4

We argue that the N=1 higher-spin theory on AdS4 is holographically dual to the N=1 supersymmetric critical O(N) vector model in three dimensions. This appears to be a special form of the AdS/CFT correspondence in which both regular and irregular bulk modes have similar roles and their interplay leads simultaneously to both the free and the interacting phases of the boundary theory. We study various boundary conditions that correspond to boundary deformations connecting, for large-N, the free and interacting boundary theories. We point out the importance of parity in this holography and elucidate the Higgs mechanism responsible for the breaking of higher-spin symmetry for subleading N.Comment: 19 page

Series Expansions for three-dimensional QED

Strong-coupling series expansions are calculated for the Hamiltonian version of compact lattice electrodynamics in (2+1) dimensions, with 4-component fermions. Series are calculated for the ground-state energy per site, the chiral condensate, and the masses of `glueball' and positronium states. Comparisons are made with results obtained by other techniques.Comment: 13 figure

Pan-cancer analysis of whole genomes

Cancer is driven by genetic change, and the advent of massively parallel sequencing has enabled systematic documentation of this variation at the whole-genome scale(1-3). Here we report the integrative analysis of 2,658 whole-cancer genomes and their matching normal tissues across 38 tumour types from the Pan-Cancer Analysis of Whole Genomes (PCAWG) Consortium of the International Cancer Genome Consortium (ICGC) and The Cancer Genome Atlas (TCGA). We describe the generation of the PCAWG resource, facilitated by international data sharing using compute clouds. On average, cancer genomes contained 4-5 driver mutations when combining coding and non-coding genomic elements; however, in around 5% of cases no drivers were identified, suggesting that cancer driver discovery is not yet complete. Chromothripsis, in which many clustered structural variants arise in a single catastrophic event, is frequently an early event in tumour evolution; in acral melanoma, for example, these events precede most somatic point mutations and affect several cancer-associated genes simultaneously. Cancers with abnormal telomere maintenance often originate from tissues with low replicative activity and show several mechanisms of preventing telomere attrition to critical levels. Common and rare germline variants affect patterns of somatic mutation, including point mutations, structural variants and somatic retrotransposition. A collection of papers from the PCAWG Consortium describes non-coding mutations that drive cancer beyond those in the TERT promoter(4); identifies new signatures of mutational processes that cause base substitutions, small insertions and deletions and structural variation(5,6); analyses timings and patterns of tumour evolution(7); describes the diverse transcriptional consequences of somatic mutation on splicing, expression levels, fusion genes and promoter activity(8,9); and evaluates a range of more-specialized features of cancer genomes(8,10-18).Peer reviewe

Comprehensive analysis of chromothripsis in 2,658 human cancers using whole-genome sequencing

Chromothripsis is a mutational phenomenon characterized by massive, clustered genomic rearrangements that occurs in cancer and other diseases. Recent studies in selected cancer types have suggested that chromothripsis may be more common than initially inferred from low-resolution copy-number data. Here, as part of the Pan-Cancer Analysis of Whole Genomes (PCAWG) Consortium of the International Cancer Genome Consortium (ICGC) and The Cancer Genome Atlas (TCGA), we analyze patterns of chromothripsis across 2,658 tumors from 38 cancer types using whole-genome sequencing data. We find that chromothripsis events are pervasive across cancers, with a frequency of more than 50% in several cancer types. Whereas canonical chromothripsis profiles display oscillations between two copy-number states, a considerable fraction of events involve multiple chromosomes and additional structural alterations. In addition to non-homologous end joining, we detect signatures of replication-associated processes and templated insertions. Chromothripsis contributes to oncogene amplification and to inactivation of genes such as mismatch-repair-related genes. These findings show that chromothripsis is a major process that drives genome evolution in human cancer

Retrospective evaluation of whole exome and genome mutation calls in 746 cancer samples

Funder: NCI U24CA211006Abstract: The Cancer Genome Atlas (TCGA) and International Cancer Genome Consortium (ICGC) curated consensus somatic mutation calls using whole exome sequencing (WES) and whole genome sequencing (WGS), respectively. Here, as part of the ICGC/TCGA Pan-Cancer Analysis of Whole Genomes (PCAWG) Consortium, which aggregated whole genome sequencing data from 2,658 cancers across 38 tumour types, we compare WES and WGS side-by-side from 746 TCGA samples, finding that ~80% of mutations overlap in covered exonic regions. We estimate that low variant allele fraction (VAF < 15%) and clonal heterogeneity contribute up to 68% of private WGS mutations and 71% of private WES mutations. We observe that ~30% of private WGS mutations trace to mutations identified by a single variant caller in WES consensus efforts. WGS captures both ~50% more variation in exonic regions and un-observed mutations in loci with variable GC-content. Together, our analysis highlights technological divergences between two reproducible somatic variant detection efforts

Sex differences in oncogenic mutational processes

Sex differences have been observed in multiple facets of cancer epidemiology, treatment and biology, and in most cancers outside the sex organs. Efforts to link these clinical differences to specific molecular features have focused on somatic mutations within the coding regions of the genome. Here we report a pan-cancer analysis of sex differences in whole genomes of 1983 tumours of 28 subtypes as part of the ICGC/TCGA Pan-Cancer Analysis of Whole Genomes (PCAWG) Consortium. We both confirm the results of exome studies, and also uncover previously undescribed sex differences. These include sex-biases in coding and non-coding cancer drivers, mutation prevalence and strikingly, in mutational signatures related to underlying mutational processes. These results underline the pervasiveness of molecular sex differences and strengthen the call for increased consideration of sex in molecular cancer research.Sex differences have been observed in multiple facets of cancer epidemiology, treatment and biology, and in most cancers outside the sex organs. Efforts to link these clinical differences to specific molecular features have focused on somatic mutations within the coding regions of the genome. Here we report a pan-cancer analysis of sex differences in whole genomes of 1983 tumours of 28 subtypes as part of the ICGC/TCGA Pan-Cancer Analysis of Whole Genomes (PCAWG) Consortium. We both confirm the results of exome studies, and also uncover previously undescribed sex differences. These include sex-biases in coding and non-coding cancer drivers, mutation prevalence and strikingly, in mutational signatures related to underlying mutational processes. These results underline the pervasiveness of molecular sex differences and strengthen the call for increased consideration of sex in molecular cancer research.Peer reviewe