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B Conclusion: b With a 51% OS-rate at 12 months CART seem to be a very effective therapeutic option in heavily pre-treated r/r PCNSL or SCNSL, particularly for pts being refractory to prior therapy. Pts with involvement of the CNS were excluded from most CART trials; however, anecdotal reports suggest that CART might be an effective treatment option for such pts. B Introduction: b The prognosis of patients (pts) with diffuse large B-cell lymphoma (DLBCL) and involvement of the central nervous system (CNS) remains dismal. [Extracted from the article]

PROGNOSTIC SCORING SYSTEMS FOR SEVERE CRS AND ICANS AFTER AUTOLOGOUS ANTI-CD19 CAR T CELLS IN LARGE B-CELL LYMPHOMA: A DESCAR-T REGISTRY STUDY FORM THE LYSA B Background: b Cytokine release syndrome (CRS) and immune effector cell-associated neurotoxicity syndrome (ICANS) are common immune-related toxicities associated with chimeric antigen receptor (CAR)-T-cell therapy. B S. Legouill b Honoraria: Janssen-Cilag, Kite/Gilead and Novartis B G. Cartron b Honoraria: Roche, Bristol Myers Squibb, Onwards Therapeutics, MedxCell, EmerCell, MabQ, Sanofi, Abbvie, Takeda, Roche, Janssen, Roche, Novartis and Myltenyi B D. Beauvais b Honoraria: Kite/Gilead B F. Gros b Honoraria: Bristol Myers Squibb, Novartis and Kite/Gilead B P. Bories b Honoraria: Bristol Myers Squibb, Kite/Gilead, Novartis and Abbvie B M. Rubio b Honoraria: Novartis and Kite/Gilead. [Extracted from the article]

B82L mouse fibroblasts respond to fibronectin or vitronectin via a syndecan-1-mediated activation of the αvβ5 integrin. Cells attached to syndecan-1-specific antibody display only filopodial extension. However, the syndecan-anchored cells extend lamellipodia when the antibody-substratum is supplemented with serum, or low concentrations of adsorbed vitronectin or fibronectin, that are not sufficient to activate the integrin when plated alone. Integrin activation is blocked by treatment with (Arg-Gly-Asp)-containing peptides and function-blocking antibodies that target αv integrins, as well as by siRNA-mediated silencing of β5 integrin expression. In addition, αvβ5-mediated cell attachment and spreading on high concentrations of vitronectin is blocked by competition with recombinant syndecan-1 ectodomain core protein and by downregulation of mouse syndecan-1 expression by mouse-specific siRNA. Taking advantage of the species-specificity of the siRNA, rescue experiments in which human syndecan-1 constructs are expressed trace the activation site to the syndecan-1 ectodomain. Moreover, both full-length mouse and human syndecan-1 co-immunoprecipitate with the β5 integrin subunit, but fail to do so if the syndecan is displaced by competition with soluble, recombinant syndecan-1 ectodomain. These results suggest that the ectodomain of the syndecan-1 core protein contains an active site that assembles into a complex with the αvβ5 integrin and regulates αvβ5 integrin activity. [ABSTRACT FROM AUTHOR]