On Picard groups of blocks of finite groups

We show that the subgroup of the Picard group of ap-block ofa finite group given by bimodules with endopermutation sources modulo theautomorphism group of a source algebra is determined locally in terms of thefusion system on a defect group. We show that the Picard group of a block overa complete discrete valuation ringOof characteristic zero with an algebraicclosurekofFpas residue field is a colimit of finite Picard groups of blocks overp-adic subrings ofO. We apply the results to blocks with an abelian defectgroup and Frobenius inertial quotient, and specialise this further to blockswith cyclic or Klein four defect groups

Descent of Equivalences and Character Bijections

Categorical equivalences between block algebras of finite groups—such as Morita and derived equivalences—are well known to induce character bijections which commute with the Galois groups of field extensions. This is the motivation for attempting to realise known Morita and derived equivalences over non-splitting fields. This article presents various results on the theme of descent to appropriate subfields and subrings. We start with the observation that perfect isometries induced by a virtual Morita equivalence induce isomorphisms of centres in non-split situations and explain connections with Navarro’s generalisation of the Alperin–McKay conjecture. We show that Rouquier’s splendid Rickard complex for blocks with cyclic defect groups descends to the non-split case. We also prove a descent theorem for Morita equivalences with endopermutation source

The structure of blocks with a Klein four defect group

We prove Erdmann’s conjecture [16] stating that every block with a Klein four defect group has a simple module with trivial source, and deduce from this that Puig’s finiteness conjecture holds for source algebras of blocks with a Klein four defect group. The proof uses the classification of finite simple groups

Stabilization of glucosyl dioxolenium Ions by "dual participation" of the 2,2-dimethyl-2-(ortho-nitrophenyl)acetyl (DMNPA) protection group for 1,2-cis-glucosylation

The stereoselective introduction of glycosidic bonds is of paramount importance to oligosaccharide synthesis. Among the various chemical strategies to steer stereoselectivity, participation by either neighboring or distal acyl groups is used particularly often. Recently, the use of the 2,2-dimethyl-2-(ortho-nitrophenyl)acetyl (DMNPA) protection group was shown to offer enhanced stereoselective steering compared to other acyl groups. Here, we investigate the origin of the stereoselectivity induced by the DMNPA group through systematic glycosylation reactions and infrared ion spectroscopy (IRIS) combined with techniques such as isotopic labeling of the anomeric center and isomer population analysis. Our study indicates that the origin of the DMNPA stereoselectivity does not lie in the direct participation of the nitro moiety but in the formation of a dioxolenium ion that is strongly stabilized by the nitro group.NWONWO-VICI grant VI.C.182.020Bio-organic Synthesi

Sialic acid blockade inhibits the metastatic spread of prostate cancer to bone

Background Bone metastasis is a common consequence of advanced prostate cancer. Bisphosphonates can be used to manage symptoms, but there are currently no curative treatments available. Altered tumour cell glycosylation is a hallmark of cancer and is an important driver of a malignant phenotype. In prostate cancer, the sialyltransferase ST6GAL1 is upregulated, and studies show ST6GAL1-mediated aberrant sialylation of N-glycans promotes prostate tumour growth and disease progression. Methods Here, we monitor ST6GAL1 in tumour and serum samples from men with aggressive prostate cancer and using in vitro and in vivo models we investigate the role of ST6GAL1 in prostate cancer bone metastasis. Findings ST6GAL1 is upregulated in patients with prostate cancer with tumours that have spread to the bone and can promote prostate cancer bone metastasis in vivo. The mechanisms involved are multi-faceted and involve modification of the pre-metastatic niche towards bone resorption to promote the vicious cycle, promoting the development of M2 like macrophages, and the regulation of immunosuppressive sialoglycans. Furthermore, using syngeneic mouse models, we show that inhibiting sialylation can block the spread of prostate tumours to bone. Interpretation Our study identifies an important role for ST6GAL1 and α2-6 sialylated N-glycans in prostate cancer bone metastasis, provides proof-of-concept data to show that inhibiting sialylation can suppress the spread of prostate tumours to bone, and highlights sialic acid blockade as an exciting new strategy to develop new therapies for patients with advanced prostate cancer. Funding Prostate Cancer Research and the Mark Foundation For Cancer Research, the Medical Research Council and Prostate Cancer UK