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We consider the class of inclusive hadron collider processes in which one or more energetic jets are produced, possibly accompanied by colourless particles. We provide a general formulation of a slicing scheme for this class of processes, by identifying the various contributions that need to be computed up to next-to-leading order (NLO) in QCD perturbation theory. We focus on two novel observables, the one-jet resolution variable ∆Et and the n-jet resolution variable kTness , and explicitly compute all the ingredients needed to carry out NLO computations using these variables. We contrast the behaviour of these variables when the slicing parameter becomes small. In the case of kTness we also present results for the hadroproduction of multiple jets.

We consider the class of inclusive hadron collider processes in which several energetic jets are produced, possibly accompanied by colorless particles [such as Higgs boson(s), vector boson(s) with their leptonic decays, and so forth]. We propose a new variable that smoothly captures the N+1 to N-jet transition. This variable, that we dub kTness, represents an effective transverse momentum controlling the singularities of the N+1-jet cross section when the additional jet is unresolved. The kTness variable offers novel opportunities to perform higher-order calculations in quantum chromodynamics by using nonlocal subtraction schemes. We study the singular behavior of the N+1-jet cross section as kTness→0 and, as a phenomenological application, we use the ensuing results to evaluate next-to-leading-order corrections to H+jet and Z+2-jet production at the LHC. We show that kTness performs extremely well as a resolution variable and appears to be very stable with respect to hadronization and multiple-parton interactions.

We consider the associated production of a vector or Higgs boson with a jet in hadronic collisions. When the transverse momentum qT of the boson-jet system is much smaller than its invariant mass Q, the QCD perturbative expansion is affected by large logarithmic terms that must be resummed to all orders. We discuss the all-order resummation structure of the logarithmically enhanced contributions up to next-to-leading logarithmic accuracy. Resummation is performed at the differential level with respect to the kinematical variables of the boson-jet system. Soft-parton radiation produces azimuthal correlations that are fully accounted for in our framework. We present explicit analytical results for the resummation coefficients up to next-to-leading order and next-to-leading logarithmic accuracy, that include the exact dependence on the jet radius.

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Contains fulltext : 190745.pdf (publisher's version ) (Closed access), Individuals with acute myeloid leukemia (AML) harboring an internal tandem duplication (ITD) in the gene encoding Fms-related tyrosine kinase 3 (FLT3) who relapse after allogeneic hematopoietic cell transplantation (allo-HCT) have a 1-year survival rate below 20%. We observed that sorafenib, a multitargeted tyrosine kinase inhibitor, increased IL-15 production by FLT3-ITD(+) leukemia cells. This synergized with the allogeneic CD8(+) T cell response, leading to long-term survival in six mouse models of FLT3-ITD(+) AML. Sorafenib-related IL-15 production caused an increase in CD8(+)CD107a(+)IFN-gamma(+) T cells with features of longevity (high levels of Bcl-2 and reduced PD-1 levels), which eradicated leukemia in secondary recipients. Mechanistically, sorafenib reduced expression of the transcription factor ATF4, thereby blocking negative regulation of interferon regulatory factor 7 (IRF7) activation, which enhanced IL-15 transcription. Both IRF7 knockdown and ATF4 overexpression in leukemia cells antagonized sorafenib-induced IL-15 production in vitro. Human FLT3-ITD(+) AML cells obtained from sorafenib responders following sorafenib therapy showed increased levels of IL-15, phosphorylated IRF7, and a transcriptionally active IRF7 chromatin state. The mitochondrial spare respiratory capacity and glycolytic capacity of CD8(+) T cells increased upon sorafenib treatment in sorafenib responders but not in nonresponders. Our findings indicate that the synergism of T cells and sorafenib is mediated via reduced ATF4 expression, causing activation of the IRF7-IL-15 axis in leukemia cells and thereby leading to metabolic reprogramming of leukemia-reactive T cells in humans. Therefore, sorafenib treatment has the potential to contribute to an immune-mediated cure of FLT3-ITD-mutant AML relapse, an otherwise fatal complication after allo-HCT.