bortezomib

High plasma cell-like phenotype signatures were linked to poorer progression-free survival (PFS) but greater benefit from R-CHOP plus bortezomib, while low-signature patients achieved better PFS with R-CHOP alone. These findings characterize the transcriptomic features of distinct plasma cell-like phenotypes in DLBCL, providing new insights into its prognostic relevance and potential for individualized treatment strategies.

Co-treatment of BoHV-1 with either bortezomib or lenalidomide increased anti-MM cytotoxicity. Finally, BoHV-1 upregulated CD38 on both MM cells and immune effectors, thereby increasing sensitivity to the anti-CD38 daratumumab. These findings establish BoHV-1 as a promising immunovirotherapy agent, effective as a single agent and in combination strategies, by coupling direct oncolysis with broad immune remodeling of the BM microenvironment.

Venetoclax-based regimens, combined venetoclax with either hypomethylating agents or low-dose cytarabine, have markedly improved treatment outcomes in elderly patients with acute myeloid leukemia (AML). Importantly, the combination of bortezomib and venetoclax significantly prolongs the survival of mice inoculated with venetoclax-resistant AML cell line harboring BAX mutations, which are commonly observed in relapsed AML following venetoclax-based regimens and confer resistance to venetoclax by inhibiting BAX-dependent apoptotic pathway. Collectively, this study provides a rationale for venetoclax-bortezomib combination as a potential strategy to overcome venetoclax resistance in certain AML subsets.

In contrast, the methylation status of histone H3 lysine 4 (H3K4me1/3) on the PERK promoter remains unaltered, regardless of the complex state. Taken together, the findings of this study underscore the key role of KDM5C as a driving force behind MM progression and BTZ resistance, indicating that KDM5C represents a novel and promising therapeutic target for the treatment of BTZ-resistant MM.

P1, N=15, Active, not recruiting, National Cancer Institute (NCI) | Trial completion date: Mar 2026 --> Mar 2027

P1/2, N=466, Active, not recruiting, Celgene | Trial completion date: Feb 2028 --> Jul 2028

IDE emerges as a novel biomarker and therapeutic vulnerability in MM. This study demonstrates the relevance of IDE inhibitors as boosters of PIs to better treat patients with resistant MM.

Manufacturing CAR-T cells in the presence of bortezomib, an FDA-approved proteasome inhibitor, prevents T cell exhaustion and improves therapeutic efficacy. Our findings identify a proteasome-guided haem signalling axis, governed by mitochondrial integrity, as a regulator of CD8+ T cell exhaustion and propose innovative therapeutic strategies that exploit this pathway to optimize adoptive cellular immunotherapy.

P3, N=200, Recruiting, Children's Cancer Group, China | Trial primary completion date: Dec 2025 --> Dec 2026

The patient demonstrated only a transient response to initial therapy with R-CHOP plus bortezomib, following which she had rapid disease progression, resulting in an overall survival of 10 months. It also provides important insights into the biology of DLBCL-to-PBL evolution. These findings highlight the need for more precise molecular diagnostic tools and novel approaches to improve outcomes for patients with such highly aggressive lymphoma.

In MM patients, compared with poor response, patients with a favorable response to bortezomib exhibited a significant reduction in cfTFEB and miR-1246 levels from the baseline levels after treatment. The plasma cfTFEB and miR-1246 may serve as potential biomarkers for evaluating the efficacy of bortezomib in the treatment of multiple myeloma.

P2, N=60, Not yet recruiting, GlaxoSmithKline | Trial completion date: Feb 2032 --> Dec 2032 | Trial primary completion date: Aug 2027 --> Dec 2032