bortezomib

P1, N=24, Active, not recruiting, National Cancer Institute (NCI) | Trial completion date: Mar 2026 --> Mar 2027

P2, N=67, Active, not recruiting, University of Cologne | Recruiting --> Active, not recruiting | N=160 --> 67 | Trial completion date: Dec 2029 --> Dec 2031 | Trial primary completion date: Dec 2029 --> Mar 2025

P2, N=50, Active, not recruiting, PETHEMA Foundation | Completed --> Active, not recruiting

P2, N=50, Completed, PETHEMA Foundation | Not yet recruiting --> Completed

P2, N=24, Recruiting, Memorial Sloan Kettering Cancer Center | Trial completion date: Feb 2026 --> Feb 2027 | Trial primary completion date: Feb 2026 --> Feb 2027

A novel prediction model was constructed based on seven RB-related signature genes for prognostic prediction in HCC patients. Targeted inhibition of CGREF1 may represent a potential strategy to improve therapeutic outcomes in HCC.

P2, N=20, Recruiting, Institute of Hematology & Blood Diseases Hospital, China | Trial primary completion date: Apr 2025 --> Jun 2026

P2, N=67, Completed, Bristol-Myers Squibb | Active, not recruiting --> Completed

Among patients receiving bortezomib, lenalidomide, and dexamethasone (VRd) induction therapy, those with cytogenetic abnormalities showed significantly lower deep response rates (complete response + very good partial response). Furthermore, RB1 deletion or D13S319 deletion combined with other high-risk indicators further shortened PFS. These findings indicate that integrating expanded cytogenetic markers optimises MM risk stratification and provides a basis for individualised treatment strategies.

P2, N=62, Active, not recruiting, PETHEMA Foundation | Recruiting --> Active, not recruiting | Trial completion date: Aug 2023 --> Aug 2026 | Trial primary completion date: Aug 2023 --> Aug 2026

TRIM28 is critical in promoting BTZ resistance in GC cells. Targeting TRIM28 could potentiate BTZ treatment outcomes and offer a promising therapeutic strategy for overcoming drug resistance in GC treatment.

Compared with standard chemoimmunotherapy, PD-L1 blockade combined with BTZ had greater antitumor effects because of the inability of cisplatin (CDDP) and pemetrexed (PEM) to regulate IFNGR1 expression. Notably, compared with BTZ treatment alone, anti-PD-L1 therapy increased BTZ tumor accumulation by promoting microvascular maturation, potentially addressing a major obstacle to the use of BTZ in solid tumors. Taken together, these results suggest that BTZ, when combined with immunotherapy, holds great promise for treating lung cancer.