bortezomib

In addition, we also found that the NF-κB pathway-related anti-AML effect of bortezomib partially relied on LSP1. This study revealed that LSP1 plays a crucial role in the progression of AML, indicating its potential as a prognostic biomarker and therapeutic target.

At present, there is no established consensus on the treatment of Ph + MPAL, and reports on cases with the atypical e13a3 BCR::ABL1 fusion are particularly scarce. This finding will bring new insights and references for the diagnosis and treatment of Ph + MPAL.

These findings uncover a previously unrecognized role of TRIP13 in regulating mitochondrial integrity under proteotoxic stress, thereby contributing to BTZ resistance. Targeting TRIP13 may represent a novel therapeutic approach to improve outcomes in MM patients.

P2, N=210, Active, not recruiting, Janssen Research & Development, LLC | Recruiting --> Active, not recruiting

P2, N=53, Active, not recruiting, Christian Buske | Trial completion date: Sep 2029 --> Feb 2027

Recent advancements in treatment involve using novel agents like bortezomib, daratumumab, and B-cell maturation antigen-targeted therapy, which are improving outcomes; however, the prognosis for relapsed disease remains poor. The best remission chances come from rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) therapy combined with central nervous system-directed treatment. New research is ongoing for relapsed cases.

Rituximab is now the preferred second-line option for relapsed/refractory patients, comparing favorably with the traditional splenectomy. The latter is increasingly reserved for later lines together with classic immunosuppressants. Several novel treatments are in development for refractory wAIHA, encompassing drugs targeting B-cells (parsaclisib, ibrutinib, rilzabrutinib, zanubrutinib, obexelimab, ianalumab, povetacicept), plasma cells (bortezomib, daratumumab), spleen tyrosine kinase (fostamatinib, sovleplenib), and the neonatal Fc receptor (nipocalimab).

P4, N=450, Active, not recruiting, University of Turin, Italy | Recruiting --> Active, not recruiting

This model underscores the pivotal role of TME components in shaping therapeutic outcomes and offers a scalable, clinically translatable tool for personalized risk stratification. Our findings highlight the necessity of integrating microenvironmental insights into MM prognostication and pave the way for microenvironment-informed therapeutic decision-making.

P2, N=22, Recruiting, University of Utah | Trial primary completion date: Dec 2025 --> Dec 2026

HSP47 inhibition promotes immune evasion by upregulating CD155 via the TRAF2-NF-κB pathway, which impairs CD8+ T cell-mediated antitumor immunity. The combination of HSP47 inhibition with CD155/TIGIT blockade enhances therapeutic efficacy, suggesting a promising strategy for combination cancer therapies.

We constructed a RiskScore model for predicting the survival outcomes based on fibroblasts-related genes. These findings highlighted the role of fibroblasts in GBM development and offered six potential therapeutic targets (VWA1, DUSP6, LOXL1, IGFBP4, CYGB, and ZIC3) for GBM treatment. Additionally, immune infiltration analysis and drug sensitivity prediction further supported the model's utility in guiding personalized treatment of GBM.