Carter-Payne homomorphisms and Jantzen filtrations

We prove a q-analogue of the Carter-Payne theorem in the case where the differences between the parts of the partitions are sufficiently large. We identify a layer of the Jantzen filtration which contains the image of these Carter-Payne homomorphisms and we show how these homomorphisms compose.Comment: 30 page

Schur elements for the Ariki-Koike algebra and applications

We study the Schur elements associated to the simple modules of the Ariki-Koike algebra. We first give a cancellation-free formula for them so that their factors can be easily read and programmed. We then study direct applications of this result. We also complete the determination of the canonical basic sets for cyclotomic Hecke algebras of type $G(l,p,n)$ in characteristic 0.Comment: The paper contains the results of arXiv:1101.146

Global long terminal repeat activation participates in establishing the unique gene expression programme of classical Hodgkin lymphoma

Long terminal repeat (LTR) elements are wide-spread in the human genome and have the potential to act as promoters and enhancers. Their expression is therefore under tight epigenetic control. We previously reported in classical Hodgkin Lymphoma (cHL) that a member of the THE1B class of LTR elements acted as a promoter for the proto-oncogene and growth factor receptor gene CSF1R and that expression of this gene is required for cHL tumour survival. However, to which extent and how such elements participate in globally shaping the unique cHL gene expression programme is unknown. To address this question we mapped the genome-wide activation of THE1-LTRs in cHL cells using a targeted next generation sequencing approach (RACE-Seq). Integration of these data with global gene expression data from cHL and control B cell lines showed a unique pattern of LTR activation impacting on gene expression, including genes associated with the cHL phenotype. We also show that global LTR activation is induced by strong inflammatory stimuli. Together these results demonstrate that LTR activation provides an additional layer of gene deregulation in classical Hodgkin lymphoma and highlight the potential impact of genome-wide LTR activation in other inflammatory diseases

Blocks of cyclotomic Hecke algebras and Khovanov-Lauda algebras

We construct an explicit isomorphism between blocks of cyclotomic Hecke algebras and (sign-modified) Khovanov-Lauda algebras in type A. These isomorphisms connect the categorification conjecture of Khovanov and Lauda to Ariki's categorification theorem. The Khovanov-Lauda algebras are naturally graded, which allows us to exhibit a non-trivial Z-grading on blocks of cyclotomic Hecke algebras, including symmetric groups in positive characteristic.Comment: 32 pages; minor changes to section

Pharmacological restoration and therapeutic targeting of the B-cell phenotype in classical Hodgkin's lymphoma

Classical Hodgkin's lymphoma (cHL), although originating from B-cells, is characterized by the virtual lack of gene products whose expression constitutes the B-cell phenotype. Epigenetic repression of B-cell-specific genes via promoter hypermethylation and histone deacetylation as well as compromised expression of B-cell-committed transcription factors were previously reported to contribute to the lost B-cell phenotype in cHL. Restoring the B-cell phenotype may not only correct a central malignant property, but render cHL susceptible to clinically established antibody therapies targeting B-cell surface receptors or small compounds interfering with B-cell receptor signaling. We conducted now a high-throughput pharmacological screening based on more than 28,000 compounds in cHL cell lines carrying a CD19 reporter to identify drugs that promote re-expression of the B-cell phenotype. Three chemicals were retrieved that robustly enhanced CD19 transcription. Subsequent chromatin immunoprecipitation-based analyses indicated that action of two of these compounds was associated with lowered levels of the transcriptionally repressive lysine 9-trimethylated histone H3 mark at the CD19 promoter. Moreover, the anti-leukemia agents all-trans retinoic acid and arsenic trioxide (ATO) were found to reconstitute the silenced B-cell transcriptional program and reduce viability of cHL cell lines. When applied in combination with a screening-identified chemical, ATO evoked re-expression of the CD20 antigen, which could be further therapeutically exploited by enabling CD20 antibody-mediated apoptosis of cHL cells. Furthermore, restoration of the B-cell phenotype also rendered cHL cells susceptible to the B-cell Non-Hodgkin's lymphoma-tailored small compound inhibitors Ibrutinib and Idelalisib. In essence, we report here a conceptually novel, re-differentiation-based treatment strategy for cHL

The Symbolic and cancellation-free formulae for Schur elements

In this paper we give a symbolical formula and a cancellation-free formula for the Schur elements associated to the simple modules of the degenerate cyclotomic Hecke algebras. As some direct applications, we show that the Schur elements are symmetric with respect to the natural symmetric group action and are integral coefficients polynomials and we give a different proof of Ariki-Mathas-Rui's criterion on the semi-simplicity of degenerate cyclotomic Hecke algebras.Comment: To appear in Monatshefte fur Mathemati

High-dose glucocorticoid treatment of near-fatal Bocavirus lung infection results in rapid recovery

Human Bocavirus(HBoV) has to be considered as life-threatening pathogen inadults with atypical pneumonia. Pulsed high-dose glucocorticoid-treatmentmay be beneficial in patients suffering from severe pulmonary disease caused by HBoV or other viruses

The role of c-FLIP splice variants in urothelial tumours

Deregulation of apoptosis is common in cancer and is often caused by overexpression of anti-apoptotic proteins in tumour cells. One important regulator of apoptosis is the cellular FLICE-inhibitory protein (c-FLIP), which is overexpressed, for example, in melanoma and Hodgkin's lymphoma cells. Here, we addressed the question whether deregulated c-FLIP expression in urothelial carcinoma impinges on the ability of death ligands to induce apoptosis. In particular, we investigated the role of the c-FLIP splice variants c-FLIPlong (c-FLIPL) and c-FLIPshort (c-FLIPS), which can have opposing functions. We observed diminished expression of the c-FLIPL isoform in urothelial carcinoma tissues as well as in established carcinoma cell lines compared with normal urothelial tissues and cells, whereas c-FLIPS was unchanged. Overexpression and RNA interference studies in urothelial cell lines nevertheless demonstrated that c-FLIP remained a crucial factor conferring resistance towards induction of apoptosis by death ligands CD95L and TRAIL. Isoform-specific RNA interference showed c-FLIPL to be of particular importance. Thus, urothelial carcinoma cells appear to fine-tune c-FLIP expression to a level sufficient for protection against activation of apoptosis by the extrinsic pathway. Therefore, targeting c-FLIP, and especially the c-FLIPL isoform, may facilitate apoptosis-based therapies of bladder cancer in otherwise resistant tumours