CD38 overexpression

The expression of CD38+ monocytes in bone marrow of MM patients is closely related to the prognosis and clinical characteristics. CD38+ monocytes maybe used to predict prognosis and guide treatment decisions.

In vitro we have shown that the addition of TGF-β1 antibody or CD38 antibody can effectively inhibit the proportion of CD38high Tregs. This study describes the characteristics of DHMM based on bicentric data, which is helpful to better provide theoretical support for the treatment of DHMM.

Our study shows that the accumulation of peripheral CD8+CD57+T cells, CD8+CD38high T cells, and CD8+HLA-DR+CD38high T cells is reflective of an ongoing antitumor T cell response and a progressive immune dysfunction in MM. During chemotherapy, the recovery of immune function can be monitored by detecting the proportion of activated molecules of T lymphocytes.

This mouse V8-12 similar to human V2-5, and V2-5 showed several cancers with macrophages/neutrophils generated hepcidin+ ironlow or some showed hepcidin- iron+ with tumor, and mouse V8-12 with different Vk19-17 generate MZ B cells strongly increased macrophage++ in old aged and generated intestine/colon tumor. Conclusion, neonate generated TC-ATA B1 cells in old aged tumor generation are CD11b+ in the leukemia CLL together with lymphoma cancer with hepcidin-related Hamp2++ in B-1 cell generation to control iron.

P=N/A, N=330, Recruiting, The Second Affiliated Hospital of Chongqing Medical University

In sum, BN-CD38 induces an effective T cell synapse and IFNγ release, while concomitantly blocking the clonogenicity and inducing CD38 expression on LSCs. These studies suggest a new mechanism to unmask and target LSCs, providing the rationale for using BN-CD38 to effectively treat AML.

Anti-CD38 monoclonal antibodies (mAbs), daratumumab (dara) and isatuximab (isa), are approved to treat multiple myeloma (MM) in the first line and relapsed/refractory settings. Following characterization of a deletion, FISH could be used to monitor the clonal level longitudinally. Our suggestion that the presence of a CD38 deletion in >25% of malignant PC clones predicts for reduced CD38 mAb efficacy requires prospective validation.

However, the anti-CD38 monoclonal antibodies daratumumab and isatuximab have been associated with mobilisation impairment, yet the mechanism remains unclear. Finally, direct in vitro effect of isatuximab in upregulating JCAD and CLEC3B was confirmed by quantitative PCR. These findings suggest that upregulated adhesion-related interactions, rather than killing of CD34 cells by effector mechanisms, could be leading causes of decreased mobilisation efficacy in MM patients treated with anti-CD38 therapy.

Introduction: The implementation of CD38-targeting antibodies daratumumab and isatuximab into combination regimens including a proteasome inhibitor (PI) significantly improved outcome and prolonged survival of patients with multiple myeloma (MM)...In order to improve myeloma therapy, recently a phase II trial for RRMM patients was initiated combining the CD47 blocking antibody magrolimab with daratumumab or PIs (NCT04892446)...In responsive MM cell lines, ADCP mediated by CD38 antibodies in combination with the CD47 blocking antibody was slightly, but not significantly enhanced by pre-treatment with carfilzomib. Our findings demonstrate that blocking the CD47-SIRPa axis with a CD47 blocking antibody can improve ADCP of myeloma cells by therapeutic antibodies targeting CD38 and that PI treatment may enhance phagocytosis. Our findings demonstrate that blocking the CD47-SIRPa axis with a CD47 blocking antibody can improve ADCP of myeloma cells by therapeutic antibodies targeting CD38 and that PI treatment may enhance phagocytosis. Interestingly, there might be also MM cells with particular phenotypes rendering them resistant to phagocytosis. Further investigating these factors may help to identify MM patients that benefit from CD47 blockade.

A high frequency of tertiary lymphoid structures composed of CD31highCD38high plasma cells was associated with reduced recurrence after surgery in HNSCC. This data supports the notion that the structural architecture of the tumor immune microenvironment plays an essential role in tumor progression and indicates that type 1 tertiary lymphoid structures and long-lived CD31highCD38high plasma cells are associated with good prognosis in HNSCC.

O + D demonstrated no new toxicity concerns and yielded a clinically meaningful PFS6 rate and durable OTRs across several cancers with HRR defects, including rare cancers.

The novel striking finding of this study was an independent link between SF3B1 mutational status and poor response to RG7388. Overall, SF3B1 mutations in CLL patient samples were associated with resistance to treatment with RG7388 ex vivo, and patients with the wild type for both SF3B1 and TP53 are more likely to benefit from treatment with MDM2 inhibitors.