vincristine

P1, N=15, Recruiting, C17 Council | Not yet recruiting --> Recruiting

P2, N=115, Active, not recruiting, St. Jude Children's Research Hospital | Trial primary completion date: Dec 2025 --> Dec 2026

P2, N=18, Recruiting, University of Washington | Not yet recruiting --> Recruiting

P3, N=70, Not yet recruiting, Ain Shams University

Initial chemotherapy with the VAC regimen (vincristine, actinomycin D, and cyclophosphamide) was administered, but the response was poor. To our knowledge, this is the first reported case of infantile fibrosarcoma with RBPMS-NTRK3 fusion in China. Treatment with larotrectinib resulted in marked tumor shrinkage.

Hyperfractionated cyclophosphamide, vincristine, doxorubicin, and dexamethasone (Hyper-CVAD) induction achieved morphological complete remission, but measurable residual disease (MRD) persisted. Consolidation with mini-cyclophosphamide, vincristine, and dexamethasone (mini-CVD) and prednisone, vincristine, methotrexate, and 6-mercaptopurine (POMP) maintenance failed to eradicate MRD, and overt relapse occurred at month 7. Nelarabine salvage was initiated...Early molecular risk stratification and deployment of targeted agents, venetoclax-based combinations, or timely allogeneic transplantation should be considered before irreversible genomic complexity emerges. Prospective studies tailored to high-risk cytogenetic subsets of MPAL are urgently needed.

P1, N=20, Not yet recruiting, City of Hope Medical Center

Non-cytotoxic concentrations of olverembatinib significantly increased the sensitivity of ABCB1-overexpressing cells to paclitaxel and vincristine. Additionally, olverembatinib activated the ATPase activity of ABCB1 in a concentration-dependent manner and exhibited potent binding affinity to ABCB1 in docking simulations. These findings suggest that olverembatinib holds promise as a potent reversal agent for MDR, paving the way for its integration into novel combination chemotherapy regimens to improve cancer treatment outcomes.

In patients with Richter transformation, epcoritamab monotherapy showed clinically meaningful antitumour activity, although the investigator-assessed overall response rate was below the alternative hypothesis of 50%, with a safety profile consistent with previous studies. These findings support further investigation of epcoritamab as a potential treatment option for patients with Richter transformation.

The patient received the first cycle of the chemotherapy regimen of vincristine, doxorubicin, cyclophosphamide, ifosfamide, and etoposide (VAC/IE) and was discharged in a stable condition. This case emphasizes the need to consider EES in the differential diagnosis of nasal masses and highlights the necessity of molecular testing for EWSR1 rearrangements to confirm the diagnosis and guide therapy. Increased awareness and reporting are vital to enhancing diagnosis and management of this rare entity.

This study aimed to determine whether genetic variants in key effector molecules influence treatment outcomes in aggressive B-cell non-Hodgkin lymphoma (B-NHL).We genotyped variants of PRF A91V (rs35947132), GZMB Q48R (rs8192917), and FASL (rs5030772 and rs763110) in 501 patients from the RICOVER-60 trial (NCT0052936/EU-20243), which compared 6 versus 8 cycles of chemotherapy containing cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) with or without rituximab in elderly patients with untreated aggressive B-NHL. Carriers showed significantly better outcomes with CHOP alone but no additional benefit from rituximab. These findings were validated in independent cohorts of aggressive B-NHL but not in CLL, where the PRF1 A91V variant was overrepresented (119/589; 20%) compared to aggressive B-NHL and general population.Our results suggest that PRF A91V is a negative predictive marker for rituximab-mediated cellular cytotoxicity in aggressive B-NHL and may have broader implications for immune effector cell-based therapies.

Comparative analysis with idelalisib revealed similar toxicity profiles to Qona11, distinct from vincristine. In vivo studies in NOD/SCID mice bearing Jurkat xenografts showed that Qona11 (100 mg.kg-1) was well tolerated with no systemic toxicity, although it did not inhibit leukemia cell proliferation in immune-independent models. Overall, Qona11 exhibits promising anticancer activity and low systemic toxicity, warranting further preclinical investigation in solid tumor models and combination therapies.