2,956 research outputs found

    Hunting the Scalar Glueball: Prospects for BES III

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    The search for the ground state scalar glueball G_0 is reviewed. Spin zero glueballs will have unique dynamical properties if the amplitude is suppressed by chiral symmetry, as it is to all orders in perturbation theory: for instance, mixing of G_0 with \bar qq mesons would be suppressed, radiative J/psi decay would be a filter for new physics in the spin zero channel, and the decay G_0 \to \bar KK could be enhanced relative to G_0 \to \pi \pi. These properties are consistent with the identification of f_0(1710) as the largely unmixed ground state scalar glueball, while recent BES data implies that f_0(1500) does not contain the dominant glueball admixture. Three hypotheses are discussed: that G_0 is 1) predominantly f_0(1500) or 2) predominantly f_0(1710) or 3) is strongly mixed between f_0(1500) and f_0(1710).Comment: 10 pages, talk presented at CHARM 2006, Beijing IHEP, June 5-7, 2006, to be published in the proceeding

    Improved prognostic classification of breast cancer defined by antagonistic activation patterns of immune response pathway modules.

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    BACKGROUND: Elucidating the activation pattern of molecular pathways across a given tumour type is a key challenge necessary for understanding the heterogeneity in clinical response and for developing novel more effective therapies. Gene expression signatures of molecular pathway activation derived from perturbation experiments in model systems as well as structural models of molecular interactions ("model signatures") constitute an important resource for estimating corresponding activation levels in tumours. However, relatively few strategies for estimating pathway activity from such model signatures exist and only few studies have used activation patterns of pathways to refine molecular classifications of cancer. METHODS: Here we propose a novel network-based method for estimating pathway activation in tumours from model signatures. We find that although the pathway networks inferred from cancer expression data are highly consistent with the prior information contained in the model signatures, that they also exhibit a highly modular structure and that estimation of pathway activity is dependent on this modular structure. We apply our methodology to a panel of 438 estrogen receptor negative (ER-) and 785 estrogen receptor positive (ER+) breast cancers to infer activation patterns of important cancer related molecular pathways. RESULTS: We show that in ER negative basal and HER2+ breast cancer, gene expression modules reflecting T-cell helper-1 (Th1) and T-cell helper-2 (Th2) mediated immune responses play antagonistic roles as major risk factors for distant metastasis. Using Boolean interaction Cox-regression models to identify non-linear pathway combinations associated with clinical outcome, we show that simultaneous high activation of Th1 and low activation of a TGF-beta pathway module defines a subtype of particularly good prognosis and that this classification provides a better prognostic model than those based on the individual pathways. In ER+ breast cancer, we find that simultaneous high MYC and RAS activity confers significantly worse prognosis than either high MYC or high RAS activity alone. We further validate these novel prognostic classifications in independent sets of 173 ER- and 567 ER+ breast cancers. CONCLUSION: We have proposed a novel method for pathway activity estimation in tumours and have shown that pathway modules antagonize or synergize to delineate novel prognostic subtypes. Specifically, our results suggest that simultaneous modulation of T-helper differentiation and TGF-beta pathways may improve clinical outcome of hormone insensitive breast cancers over treatments that target only one of these pathways.RIGHTS : This article is licensed under the BioMed Central licence at http://www.biomedcentral.com/about/license which is similar to the 'Creative Commons Attribution Licence'. In brief you may : copy, distribute, and display the work; make derivative works; or make commercial use of the work - under the following conditions: the original author must be given credit; for any reuse or distribution, it must be made clear to others what the license terms of this work are
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