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Homoharringtonine in Relapsed/Refractory Paediatric T-Cell Acute Lymphoblastic Leukaemia-A Case Series and a Report on the Use of In Vitro Drug Profiling.
Pediatr Blood Cancer
January 2025
Hong Kong Children's Hospital, Kowloon, Hong Kong SAR, China.
Paediatric relapse/refractory T-cell acute lymphoblastic leukaemia (T-ALL) is notoriously difficult to treat. This group of heavily pre-treated patients needs effective agents that can rapidly control the disease while not having significant toxicity. Homoharringtonine (HHT) has been widely used in children with acute myeloid leukaemia, but there is little information on T-ALL.
View Article and Find Full Text PDFApigenin facilitates apoptosis of acute lymphoblastic leukemia cells via AMP-activated protein kinase-mediated ferroptosis.
Oncol Res
January 2025
Department of Microbiology, College of Preclinical Medicine, Zunyi Medical University, Zunyi, 563003, China.
Background: The outcomes of pediatric patients with acute lymphoblastic leukemia (ALL) remain far less than favorable. While apigenin is an anti-cancer agent, studies on the mechanism by which it regulates ALL cell cycle progression are inadequate. Ferroptosis and AMP-activated protein kinase (AMPK) signaling are important processes for ALL patients.
View Article and Find Full Text PDFCpG island methylator phenotype classification improves risk assessment in pediatric T-cell Acute Lymphoblastic Leukemia.
Blood
January 2025
Umeå University, Department of Medical Biosciensces, Department of Clinical Microbiology, Umeå, Sweden.
Current intensive treatment of pediatric T-cell acute lymphoblastic leukemia (T-ALL) has substantial side-effects, highlighting a need for novel biomarkers to improve risk stratification. Canonical biomarkers such as genetics and immunophenotype are largely not used in pediatric T-ALL stratification. This study aimed to validate the prognostic relevance of DNA methylation CpG island methylator phenotype (CIMP) risk stratification in two pediatric T-ALL patient cohorts: the Nordic NOPHO ALL2008 T-ALL study cohort (n=192) and the Dutch DCOG ALL-10/ALL-11 validation cohorts (n=156).
View Article and Find Full Text PDFTLE4 is a repressor of the oncogenic activity of TLX3 in T-cell acute lymphoblastic leukemia.
Leukemia
January 2025
Department of Human Genetics, KU Leuven, Leuven, Belgium.
T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive hematological disease originating from the malignant transformation of T-cell progenitors, caused by the accumulation of genetic aberrations. One-fifth of T-ALL patients are characterized by ectopic expression of the homeobox transcription factor TLX3. However, the role of TLX3 in T-ALL remains elusive, partly due to the lack of suitable study models.
View Article and Find Full Text PDFVariations in the TP53 and KRAS genes indicate a particularly adverse prognosis in relapsed pediatric T-ALL. We hypothesized that these variations might be subclonally present at disease onset and contribute to relapse risk. To test this, we examined two cohorts of children diagnosed with T-ALL: one with 81 patients who relapsed and 79 matched non-relapsing controls, and another with 226 consecutive patients, 30 of whom relapsed.
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