Search for a multi-Higgs-boson cascade in W(+)W(-)b(b)over-bar events with the ATLAS detector in pp collisions at root s=8 TeV

A search is presented for new particles in an extension to the Standard Model that includes a heavy Higgs boson (H-0), an intermediate charged Higgs-boson pair (H-+/-), and a light Higgs boson (h(0)). The analysis searches for events involving the production of a single heavy neutral Higgs boson which decays to the charged Higgs boson and a W boson, where the charged Higgs boson subsequently decays into a W boson and the lightest neutral Higgs boson decaying to a bottom-antibottom-quark pair. Such a cascade results in a W-boson pair and a bottom-antibottom-quark pair in the final state. Events with exactly one lepton, missing transverse momentum, and at least four jets are selected from a data sample corresponding to an integrated luminosity of 20.3 fb(-1), collected by the ATLAS detector in proton-proton collisions at root s = 8 TeV at the LHC. The data are found to be consistent with Standard Model predictions, and 95% confidence-level upper limits are set on the product of cross section and branching ratio. These limits range from 0.065 to 43 pb as a function of H-0 and H-+/- masses, with m(h)o fixed at 125 GeV.

High-throughput mutation profiling of CTCL samples reveals KRAS and NRAS mutations sensitizing tumors toward inhibition of the RAS/RAF/MEK signaling cascade

Cutaneous T-cell lymphomas (CTCLs) are malignancies of skin-homing lymphoid cells, which have so far not been investigated thoroughly for common oncogenic mutations. We screened 90 biopsy specimens from CTCL patients (41 mycosis fungoides, 36 Sézary syndrome, and 13 non-mycosis fungoides/Sézary syndrome CTCL) for somatic mutations using OncoMap technology. We detected oncogenic mutations for the RAS pathway in 4 of 90 samples. One mycosis fungoides and one pleomorphic CTCL harbored a KRAS(G13D) mutation; one Sézary syndrome and one CD30(+) CTCL harbored a NRAS(Q61K) amino acid change. All mutations were found in stage IV patients (4 of 42) who showed significantly decreased overall survival compared with stage IV patients without mutations (P = .04). In addition, we detected a NRAS(Q61K) mutation in the CTCL cell line Hut78. Knockdown of NRAS by siRNA induced apoptosis in mutant Hut78 cells but not in CTCL cell lines lacking RAS mutations. The NRAS(Q61K) mutation sensitized Hut78 cells toward growth inhibition by the MEK inhibitors U0126, AZD6244, and PD0325901. Furthermore, we found that MEK inhibitors exclusively induce apoptosis in Hut78 cells. Taken together, we conclude that RAS mutations are rare events at a late stage of CTCL, and our preclinical results suggest that such late-stage patients profit from MEK inhibitors.

Rare decays and MSSM phenomenology

In this article I review some aspects of flavour phenomenology in the MSSM. After an overview of various flavour observables I discuss the constraints on the off-diagonal elements of the squark mass matrices. In this context I present the Fortran code SUSY_FLAVOR which calculates these processes in the generic MSSM including the complete resummation of all chirally enhanced effects as a new feature of version 2. Than I discuss where large new physics effects in the MSSM are still possible. As an example of a model which can give large effects in flavour physics I review a model with "radiative flavour violation" (RFV) and update the results in the light of the recent LHCb measurement of Bs -> \mu \mu. Finally, I recall that the MSSM can generate a sizable right-handed W-coupling which affects B -> \tau\nu and can solve the Vub problem.