On q-tensor products of Cuntz algebras

We consider the C∗-algebra Eqn, m, which is a q-twist of two Cuntz-Toeplitz algebras. For the case |q| < 1, we give an explicit formula which untwists the q-deformation showing that the isomorphism class of Eqn, mdoes not depend on q. For the case |q| = 1, we give an explicit description of all ideals in Eqn, m. In particular, we show that Eqn, mcontains a unique largest ideal Mq. We identify Eqn, m/Mq with the Rieffel deformation of On ⊗Om and use a K-theoretical argument to show that the isomorphism class does not depend on q. The latter result holds true in a more general setting of multiparameter deformations

CD157 signaling promotes survival of acute myeloid leukemia cells and modulates sensitivity to cytarabine through regulation of anti-apoptotic Mcl-1.

CD157/BST-1 (a member of the ADP-ribosyl cyclase family) is expressed at variable levels in 97% of patients with acute myeloid leukemia (AML), and is currently under investigation as a target for antibody-based immunotherapy. We used peripheral blood and bone marrow samples from patients with AML to analyse the impact of CD157-directed antibodies in AML survival and in response to cytarabine (AraC) ex vivo. The study was extended to the U937, THP1 and OCI-AML3 AML cell lines of which we engineered CD157-low versions by shRNA knockdown. CD157-targeting antibodies enhanced survival, decreased apoptosis and reduced AraC toxicity in AML blasts and cell lines. CD157 signaling activated the PI3K/AKT/mTOR and MAPK/ERK pathways and increased expression of Mcl-1 and Bcl-XL anti-apoptotic proteins, while decreasing expression of Bax pro-apoptotic protein, thus preventing Caspase-3 activation. The primary CD157-mediated anti-apoptotic mechanism was Bak sequestration by Mcl-1. Indeed, the Mcl-1-specific inhibitor S63845 restored apoptosis by disrupting the interaction of Mcl-1 with Bim and Bak and significantly increased AraC toxicity in CD157-high but not in CD157-low AML cells. This study provides a new role for CD157 in AML cell survival, and indicates a potential role of CD157 as a predictive marker of response to therapies exploiting Mcl-1 pharmacological inhibition

On well-behaved representations of λ-deformed CCR

We study well-behaved *-representations of a ?-deformation of Wick analog of CCR algebra. Homogeneous Wick ideals of degrees two and three are described. Well-behaved irreducible *-representations of quotients by these ideals are classified up to unitary equivalence