The two pion decay of the Roper resonance

We evaluate the two pion decay of the Roper resonance in a model where explicit re-scattering of the two final pions is accounted for by the use of unitarized chiral perturbation theory. Our model does not include an explicit $\epsilon$ or $\sigma$ scalar-isoscalar meson decay mode, instead it generates it dynamically by means of the pion re-scattering. The two ways, explicit or dynamically generated, of introducing this decay channel have very different amplitudes. Nevertheless, through interference with the other terms of the model we are able to reproduce the same phenomenology as models with explicit consideration of the $\epsilon$ meson.Comment: 17 latex pages, 11 eps figures. A few misprints corrected. A few new references. Version accepted for publication in Phys. Rev.

Molecular and clinical diversity in primary central nervous system lymphoma

International audienceBackground: Primary central nervous system lymphoma (PCNSL) is a rare and distinct entity within diffuse large B cell lymphoma presenting with variable response rates probably to underlying molecular heterogeneity.Patients and methods: To identify and characterize PCNSL heterogeneity and facilitate clinical translation, we performed a comprehensive multi-omic analysis (whole-exome sequencing, RNA-seq, methyl-seq, and clinical features) in a discovery cohort of 147 fresh-frozen immunocompetent PCNSLs and a validation cohort of formalin-fixed, paraffin-embedded (FFPE) 93 PCNSLs with RNA-seq and clinico-radiological data.Results: Consensus clustering of multi-omics data uncovered concordant classification of four robust, non-overlapping, prognostically significant clusters (CS). The CS1 and CS2 groups presented an immune-cold hypermethylated profile but distinct clinical behavior. The "immune-hot" CS4 group, enriched with mutations increasing the JAK-STAT and NF-κB activity, had the most favorable clinical outcome while the heterogeneous-immune CS3 group had the worse prognosis probably due to its association with meningeal infiltration and enriched HIST1H1E mutations. The CS1 was characterized by high Polycomb repressive complex 2 activity and CDKN2A/B loss leading to higher proliferation activity. Integrated analysis on proposed targets suggests potential use of immune checkpoint inhibitors/JAK1 inhibitors for CS4, cyclin D-Cdk4,6 plus PI3K inhibitors for CS1, lenalidomide/demethylating drugs for CS2, and EZH2 inhibitors for CS3. We developed an algorithm to identify the PCNSL subtypes using RNA-seq data from either FFPE or FF tissue.Conclusions: The integration of genome-wide data from multi-omics data revealed four molecular patterns in PCNSL with a distinctive prognostic impact that provides a basis for future clinical stratification and subtype-based targeted interventions