C1S (Complement C1s)

Subsequent chemotherapy with polatuzumab vedotin, rituximab, cyclophosphamide, doxorubicin, and prednisolone resulted in further improvement in anemia. This case highlights the importance of reassessing underlying conditions through BMB in cases where sutimlimab treatment is ineffective.

Only dK58β2m in combination with IFN-γ caused apoptosis and cell death. Our findings highlight the modular nature of a β2m-induced macrophage response, potentiated by dK58β2m and IFN-γ, and provide information on the underlying mechanisms responsible for the immune activation properties of β2m.

Our findings highlight the dynamic alterations in the post-NCRT ESCC microenvironment and provide a foundation for the development of personalized treatment and immunotherapeutic approaches. Future studies are warranted to further validate these findings and explore their clinical implications.

Our findings were further validated via glioma tissue microarray immunohistochemical analysis and an M2 macrophage infiltration assay. Together, these findings revealed the underlying critical role of C1S in glioma tumorigenesis, progression, and the tumor immune microenvironment, contributing to further understanding of glioma pathogenesis and guiding immunotherapy.

Additionally, gene-drug association analysis identified ciclosporin, ouabain and 6- mercaptopurine, which all exhibit immunosuppressive properties, as potential therapeutic options for tumor patients exhibiting high F3, PLAT or C1S expression, respectively. In summary, our findings provide a bioinformatics perspective on VRGs in pan-cancer, highlighting the pivotal roles of F3, PLAT and C1S, which could potentially be therapeutically exploited and targeted in several cancers, especially in GBMLGG.

Notably, C1s knockdown significantly inhibited ESCC cell proliferation and enhanced their apoptosis. C1s suppressed ESCC cell proliferation via Wnt1/β-catenin pathway and promoted their apoptosis through modulating the expression of Bcl2, Bax, and cleaved-caspase3.

Long-term SUT maintained mean Hb levels >11 g/dL, normalized bilirubin, and improved FACIT-Fatigue scores with a favorable safety profile.

Long-term SUT treatment was well-tolerated, and was associated with sustained efficacy, with improvements in anemia, hemolysis and QoL. Figure: Autoimmune hemolytic anemia (AIHA)

This abstract was previously presented at EHA 2022. Keyword : Cold aglutinin disease, Sutimlimab, CARDINAL study, Hemolytic markers, FACIT-Fatigue score

Improvements in anemia, inhibition of hemolysis and favourable effects on QoL were rapidly achieved and sustained to a similar extent in those patients administered SUT throughout the study and those who switched to SUT treatment in Part B. This abstract was previously presented at ASH 2022. Keyword : Cold aglutinin disease, Sutimlimab, Hemolysis, Hemoglobin, Quality of life

Long-term treatment with SUT, an anti-C1s CP inhibitor, maintained mean Hb levels >11 g/dL, achieved sustained normalization of bilirubin and led to clinically meaningful improvements of FACIT-Fatigue scores, while maintaining a favourable safety profile. Improvements in anemia, inhibition of hemolysis and favourable effects on QoL were rapidly achieved and sustained to a similar extent in those patients administered SUT throughout the study and those who switched to SUT treatment in Part B.

Sutimlimab continued to improve FACIT-Fatigue scores, with no newly identified safety concerns at 2 years of treatment. This study has demonstrated that sutimlimab is an effective and well-tolerated long-term therapy for the management of chronic CAD through continued upstream inhibition of the classical CP.