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Sökning: WFRF:(Casey G) > Forskningsöversikt

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1.
  • Abazov, V. M., et al. (författare)
  • Evidence for production of single top quarks
  • 2008
  • Ingår i: Physical Review D. - 1550-7998 .- 1550-2368. ; D:78, s. 012005-
  • Forskningsöversikt (refereegranskat)abstract
    • We present first evidence for the production of single top quarks in the D0 detector at the Fermilab Tevatron p (p) over bar collider. The standard model predicts that the electroweak interaction can produce a top quark together with an antibottom quark or light quark, without the antiparticle top-quark partner that is always produced from strong-coupling processes. Top quarks were first observed in pair production in 1995, and since then, single top-quark production has been searched for in ever larger data sets. In this analysis, we select events from a 0.9 fb(-1) data set that have an electron or muon and missing transverse energy from the decay of a W boson from the top-quark decay, and two, three, or four jets, with one or two of the jets identified as originating from a b hadron decay. The selected events are mostly backgrounds such as W + jets and t (t) over bar events, which we separate from the expected signals using three multivariate analysis techniques: boosted decision trees, Bayesian neural networks, and matrix-element calculations. A binned likelihood fit of the signal cross section plus background to the data from the combination of the results from the three analysis methods gives a cross section for single top-quark production of sigma(p (p) over bar -> tb + X, tqb + X) = 4.7 +/- 1.3 pb. The probability to measure a cross section at this value or higher in the absence of signal is 0.014%, corresponding to a 3.6 standard deviation significance. The measured cross section value is compatible at the 10% level with the standard model prediction for electroweak top-quark production. We use the cross section measurement to directly determine the Cabibbo-Kobayashi-Maskawa quark mixing matrix element that describes the Wtb coupling and find vertical bar V(tb)f(1)(L)vertical bar = 1.31(-0.21)(+0.25), where f(1)(L) is a generic vector coupling. This model-independent measurement translates into 0.68 <= 1 at the 95% C.L. in the standard model.
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2.
  • Block, Keith I., et al. (författare)
  • Designing a broad-spectrum integrative approach for cancer prevention and treatment
  • 2015
  • Ingår i: Seminars in Cancer Biology. - : Academic Press. - 1044-579X .- 1096-3650. ; 35, s. S276-S304
  • Forskningsöversikt (refereegranskat)abstract
    • Targeted therapies and the consequent adoption of "personalized" oncology have achieved notable successes in some cancers; however, significant problems remain with this approach. Many targeted therapies are highly toxic, costs are extremely high, and most patients experience relapse after a few disease-free months. Relapses arise from genetic heterogeneity in tumors, which harbor therapy-resistant immortalized cells that have adopted alternate and compensatory pathways (i.e., pathways that are not reliant upon the same mechanisms as those which have been targeted). To address these limitations, an international task force of 180 scientists was assembled to explore the concept of a low-toxicity "broadspectrum" therapeutic approach that could simultaneously target many key pathways and mechanisms. Using cancer hallmark phenotypes and the tumor microenvironment to account for the various aspects of relevant cancer biology, interdisciplinary teams reviewed each hallmark area and nominated a wide range of high-priority targets (74 in total) that could be modified to improve patient outcomes. For these targets, corresponding low-toxicity therapeutic approaches were then suggested, many of which were phytochemicals. Proposed actions on each target and all of the approaches were further reviewed for known effects on other hallmark areas and the tumor microenvironment Potential contrary or procarcinogenic effects were found for 3.9% of the relationships between targets and hallmarks, and mixed evidence of complementary and contrary relationships was found for 7.1%. Approximately 67% of the relationships revealed potentially complementary effects, and the remainder had no known relationship. Among the approaches, 1.1% had contrary, 2.8% had mixed and 62.1% had complementary relationships. These results suggest that a broad-spectrum approach should be feasible from a safety standpoint. This novel approach has potential to be relatively inexpensive, it should help us address stages and types of cancer that lack conventional treatment, and it may reduce relapse risks. A proposed agenda for future research is offered. (C) 2015 The Authors. Published by Elsevier Ltd.
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3.
  • Svensson, Annika, 1975, et al. (författare)
  • Genetic and pharmacologic analyses of the role of Icmt in Ras membrane association and function
  • 2006
  • Ingår i: Methods Enzymol. ; 407, s. 142-159
  • Forskningsöversikt (refereegranskat)abstract
    • After isoprenylation, the Ras proteins and other proteins terminating with a so-called CAAX motif, undergo two additional modifications: (i) endoproteolytic cleavage of the –AAX by Ras converting enzyme 1 (Rce1) and (ii) carboxyl methylation of the isoprenylated cysteine residue by isoprenylcysteine carboxyl methyltransferase (Icmt). Although CAAX protein isoprenylation has been studied in great detail, until recently, very little was known about the biological role and functional importance of Icmt in mammalian cells. Studies over the past few years, however, have begun to fill in the blanks. Genetic experiments showed that Icmt-deficient embryos die at mid-gestation whereas conditional inactivation of Icmt in the liver, spleen, and bone marrow is not associated with obvious pathology. One potential explanation for the embryonic lethality is that Icmt is the only enzyme in mouse cells capable of methylating isoprenylated CAAX proteins—including the Ras proteins. Furthermore, in addition to the CAAX proteins, Icmt methylates the CXC class of isoprenylated Rab proteins. In the absence of carboxyl methylation, the Ras proteins are mislocalized away from the plasma membrane and exhibit a shift in electrophoretic mobility. Given the important role of oncogenic Ras proteins in human tumorigenesis and the mislocalization of Ras proteins in Icmt-deficient cells, it has been hypothesized that inhibition of Icmt could be a strategy to block Ras-induced oncogenic transformation. Recent data provide strong support to that hypothesis: conditional inactivation of Icmt in mouse embryonic fibroblasts and treatment of cells with a novel selective inhibitor of Icmt, termed cysmethynil, results in a striking inhibition of Ras-induced oncogenic transformation.
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