vincristine

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.

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.

Together, the HGBLs may present with aggressive features; respond poorly to R-CHOP, ie, rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone; and may benefit from intensified induction regimens. In the relapsed and refractory setting, chimeric antigen receptor T-cell therapy has demonstrated significant efficacy, and there is much expectation for other novel therapeutic approaches, including bispecific antibodies. By understanding the biology and a commitment to collaborative prospective evaluation, their high diagnostic and treatment challenges may be resolved.

We report the case of a 38-year-old male with unresectable intra-abdominal DSRCT treated with the VAC-IE regimen (vincristine, doxorubicin, and cyclophosphamide, alternating with ifosfamide and etoposide) as first-line therapy...As second-line therapy, he received gemcitabine and docetaxel...Alternative regimens include temozolomide plus irinotecan or gemcitabine plus doxorubicin. In patients with androgen receptor positivity, hormonal blockade with leuprolide and bicalutamide may be a therapeutic option, particularly in frail patients...DSRCT is a challenging and aggressive malignancy requiring a multidisciplinary and individualized approach. The combination of systemic therapy and local control measures remains critical for improving patient outcomes.

A HB patient-derived xenograft (PDX) model was treated with placebo, vincristine + irinotecan (VI), dinaciclib, or VI + dinaciclib to evaluate tumor growth and response to therapy. In our PDX model, treatment with VI + dinaciclib resulted in decreased tumor volume, viability and HB cell proliferation. Given these findings, combination treatment with VI and dinaciclib should be investigated further as a treatment for chemoresistant HB.

CD5+ diffuse large B-cell lymphoma (DLBCL) is aggressive, and Rituximab-Cyclophosphamide Hydroxydaunorubicin Vincristine Prednisone (R-CHOP) combined with radiotherapy is recommended, but prognosis is affected by age, Lactate Dehydrogenase (LDH) levels, and molecular characteristics such as TP53 mutations. Radiotherapy and chemotherapy are the first choice for treatment. It is very important to formulate a reasonable treatment plan according to the results of pathology and molecular analysis.

P3, N=114, Enrolling by invitation, N.N. Petrov National Medical Research Center of Oncology