Objectives: To determine both erythrocyte pyruvate kinase activity (ePKA) at the time of diagnosis of patients with acute leukemia or lymphoma and the differences in the ePKA profiles during the malignant disease and its chemotherapy.
Methods: A prospective, longitudinal clinical study was performed involving 57 patients, 10 were the ones with relapse of acute lymphoblastic leukemia, 32 were the ones with acute lymphoblastic leukemia (ALL) and 15 were the ones with lymphoma. None of the subjects in this study group received treatment or blood transfusion before the study, except the ones diagnosed with relapse of ALL. Forty two healthy children were also selected to form the control group. In order to measure ePKA, blood samples were taken for five times, with 1.5 months apart between each other during the study. Statistical analysis were done by using Wilcoxon's signed rank test, Kruskall-Wallis with Mann-Whitney U Test and Spearman rank correlation coefficient test.
Results: The ePKA of the patients with relapse of ALL, and ALL, but not the patients with lymphoma, at the time of diagnosis were found to be lower compared to the one's in the control group (respectively p = 0.001, p = 0.003). The comparison between the first ePKA samples and the third ePKA samples of the patients with both ALL and lymphoma showed a significant increase (respectively p = 0.006, and p = 0.047).
Conclusion: The measurement of ePKA can be considered for follow-up the neoplastic treatment due to the fact that it is detected to be low in leukemia and relapse of ALL and in normal values after chemotherapy. However, more long-term studies, including more number of cases, are required to be carried out in order to prove the accuracy of this hypothesis. (Tab. 2, Fig. 1, Ref. 28.)
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J Hematol Oncol
January 2025
Bavarian Cancer Research Center (BZKF), R/R ALL Study Group, Bavaria, Germany.
Anti-CD19 chimeric antigen receptor T cells (CAR) are a well-established treatment option for children and young adults suffering from relapsed/refractory B-lineage acute lymphoblastic leukemia. Bridging therapy is used to control disease prior to start of lymphodepletion before CAR infusion and thereby improve efficacy of CAR therapy. However, the effect of different bridging strategies on outcome, side effects and response to CAR therapy is still poorly understood.
View Article and Find Full Text PDFClin Case Rep
January 2025
Pediatric Neurology Department, Pediatric Neurology Research Center Shahid Beheshti University of Medical Sciences Tehran Iran.
Intrathecal methotrexate can cause cauda equina syndrome in pediatric ALL patients, as demonstrated in this rare case of an 8-year-old boy. Symptoms included progressive limb weakness and urinary retention. Early recognition, prompt discontinuation of the offending agent, and multidisciplinary management are crucial.
View Article and Find Full Text PDFMol Biol Rep
January 2025
Hematology and Oncology Research Center, Non-communicable Diseases Research Institute, Shahid Sadoughi University of Medical Sciences, Yazd, Iran.
Background: Recent genomic research has identified several genetic factors contributing to B-cell acute lymphoblastic leukemia (B-ALL). However, the exact cause of the disease is still not fully understood. It is known that mutations in the TAL2 gene play important roles in the development of acute lymphoblastic leukemia.
View Article and Find Full Text PDFCancer Chemother Pharmacol
January 2025
Massey Comprehensive Cancer Center, Virginia Commonwealth University, Richmond, VA, USA.
Purpose: Relapsed and/or refractory acute myeloid leukemia and high-risk myelodysplastic syndrome continue to have a poor prognosis with limited treatment options despite advancements in rational combination and targeted therapies. Belinostat (an HDAC inhibitor) and Pevonedistat (a NEDD8 inhibitor) have each been independently studied in hematologic malignancies and have tolerable safety profiles with limited single-agent activity. Preclinical studies in AML cell lines and primary AML cells show the combination to be highly synergistic, particularly in high-risk phenotypes such as p53 mutant and FLT-3-ITD positive cells.
View Article and Find Full Text PDFJ Hematol Oncol
January 2025
Sylvester Comprehensive Cancer Center, University of Miami, Miami, FL, USA.
Background: Olutasidenib is a potent, selective, oral, small molecule inhibitor of mutant IDH1 (mIDH1) which induced durable remissions in high-risk, relapsed/refractory (R/R) mIDH1 AML patients in a phase 1/2 trial. We present a pooled analysis from multiple cohorts of the phase 1/2 trial of patients with R/R AML who received combination olutasidenib and azacitidine therapy.
Methods: Adult patients with mIDH1 AML received 150 mg olutasidenib twice daily plus standard-of-care azacitidine (OLU + AZA) and were evaluated for response and safety.
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