University of Groningen

About: University of Groningen is a education organization based out in Groningen, Groningen, Netherlands. It is known for research contribution in the topics: Population & Poison control. The organization has 36346 authors who have published 69116 publications receiving 2940370 citations. The organization is also known as: Rijksuniversiteit Groningen & RUG.

On the equilibrium states in quantum statistical mechanics

Abstract: Representations of theC*-algebra\(\mathfrak{A}\) of observables corresponding to thermal equilibrium of a system at given temperatureT and chemical potential μ are studied. Both for finite and for infinite systems it is shown that the representation is reducible and that there exists a conjugation in the representation space, which maps the von Neumann algebra spanned by the representative of\(\mathfrak{A}\) onto its commutant. This means that there is an equivalent anti-linear representation of\(\mathfrak{A}\) in the commutant. The relation of these properties with the Kubo-Martin-Schwinger boundary condition is discussed.

Burkitt lymphoma pathogenesis and therapeutic targets from structural and functional genomics

Abstract: Burkitt's lymphoma (BL) can often be cured by intensive chemotherapy, but the toxicity of such therapy precludes its use in the elderly and in patients with endemic BL in developing countries, necessitating new strategies. The normal germinal centre B cell is the presumed cell of origin for both BL and diffuse large B-cell lymphoma (DLBCL), yet gene expression analysis suggests that these malignancies may use different oncogenic pathways. BL is subdivided into a sporadic subtype that is diagnosed in developed countries, the Epstein-Barr-virus-associated endemic subtype, and an HIV-associated subtype, but it is unclear whether these subtypes use similar or divergent oncogenic mechanisms. Here we used high-throughput RNA sequencing and RNA interference screening to discover essential regulatory pathways in BL that cooperate with MYC, the defining oncogene of this cancer. In 70% of sporadic BL cases, mutations affecting the transcription factor TCF3 (E2A) or its negative regulator ID3 fostered TCF3 dependency. TCF3 activated the pro-survival phosphatidylinositol-3-OH kinase pathway in BL, in part by augmenting tonic B-cell receptor signalling. In 38% of sporadic BL cases, oncogenic CCND3 mutations produced highly stable cyclin D3 isoforms that drive cell cycle progression. These findings suggest opportunities to improve therapy for patients with BL.