[<sup>68</sup>Ga]Pentixafor-PET/CT for imaging of chemokine receptor CXCR4 expression in multiple myeloma - Comparison to [<sup>18</sup>F]FDG and laboratory values.
XIAP and its endogenous inhibitor XAF-1 protein levels and their regulation were assessed by immunoblot analysis in myeloma cell lines or primary myeloma cells.
Xenografts of MM tumors treated with this combination had marked increases in phospho-c-Jun-NH(2)-kinase (JNK)-positive cells and apoptosis, and corresponding reductions in tumor burden, tumor vasculature, and the expression of proliferating cell nuclear antigen and the proangiogenic cytokine vascular endothelial growth factor.
Xenografts of MM tumors treated with this combination had marked increases in phospho-c-Jun-NH(2)-kinase (JNK)-positive cells and apoptosis, and corresponding reductions in tumor burden, tumor vasculature, and the expression of proliferating cell nuclear antigen and the proangiogenic cytokine vascular endothelial growth factor.
Xenografted RPMI 8226 cells also expressed CD10 (CALLA; 44% reactive cells), CD38 (OKTIO; 69%), CD5 (49%), and reacted with the MM monoclonal antibody MM4 (39%).
Xenografted RPMI 8226 cells also expressed CD10 (CALLA; 44% reactive cells), CD38 (OKTIO; 69%), CD5 (49%), and reacted with the MM monoclonal antibody MM4 (39%).
Xenograft studies using human MM cell lines treated with miR-19a and b, and miR-181a and b antagonists resulted in significant suppression of tumor growth in nude mice.
Within the MM sample, 37 IGHV genes were expressed, with 98.9% of all immunoglobulin sequences using the same IGHV gene as the MM clone and 83.0% exhibiting exact nucleotide sequence identity in the IGHV and heavy chain complementarity determining region 3 (HCDR3).
Within the MM sample, 37 IGHV genes were expressed, with 98.9% of all immunoglobulin sequences using the same IGHV gene as the MM clone and 83.0% exhibiting exact nucleotide sequence identity in the IGHV and heavy chain complementarity determining region 3 (HCDR3).
Within the MM sample, 37 IGHV genes were expressed, with 98.9% of all immunoglobulin sequences using the same IGHV gene as the MM clone and 83.0% exhibiting exact nucleotide sequence identity in the IGHV and heavy chain complementarity determining region 3 (HCDR3).
Within the MM sample, 37 IGHV genes were expressed, with 98.9% of all immunoglobulin sequences using the same IGHV gene as the MM clone and 83.0% exhibiting exact nucleotide sequence identity in the IGHV and heavy chain complementarity determining region 3 (HCDR3).
Within MM bone-marrow, the source of BMPs was mainly CD138(+) plasma-cell population, and BMP6 and ACVR1 expression correlated with plasma-cell percentage.
With the use of the Vk*MYC genetically engineered mouse model of myeloma we modeled this competition between subclones for predominance occurring spontaneously and with therapeutic selection.
With the use of the CD40 monoclonal antibody (MoAb) G28-5, we examined CD40 expression and the effect of CD40 binding on MM clonogenic colony (MCC) formation to characterize the IL-6/CD40 loop activity in MM.
With the aim of further exploring the mechanisms underlying the development of MM-related bone disease, here we focused on a possible role of LIGHT in MM patients with active bone disease despite the treatment received.
With similar results, fusions between MUM1 and IgH loci were observed by means of interphase DCFISH in eight (21.1%) out of the 38 MM cases, although no definite relationships between MUM1 status and specific clinical findings could be established.
With similar results, fusions between MUM1 and IgH loci were observed by means of interphase DCFISH in eight (21.1%) out of the 38 MM cases, although no definite relationships between MUM1 status and specific clinical findings could be established.
With several novel agents in the preclinical and early clinical pipeline, among those novel CD38 and BCMA mAbs, immune checkpoint inhibitors, as well as ricolinostat, selinexor, venetoclax, CAR-T cells, and vaccines, further advances in MM patient outcome are expected in the near future.
With several novel agents in the preclinical and early clinical pipeline, among those novel CD38 and BCMA mAbs, immune checkpoint inhibitors, as well as ricolinostat, selinexor, venetoclax, CAR-T cells, and vaccines, further advances in MM patient outcome are expected in the near future.
With several novel agents in the preclinical and early clinical pipeline, among those novel CD38 and BCMA mAbs, immune checkpoint inhibitors, as well as ricolinostat, selinexor, venetoclax, CAR-T cells, and vaccines, further advances in MM patient outcome are expected in the near future.
With several novel agents in the preclinical and early clinical pipeline, among those novel CD38 and BCMA mAbs, immune checkpoint inhibitors, as well as ricolinostat, selinexor, venetoclax, CAR-T cells, and vaccines, further advances in MM patient outcome are expected in the near future.