Background: This study aimed to assess the significance of combined expression of interleukin-2 receptor (CD25) and the interleukin-3 receptor (CD123) in acute myeloid leukemia (AML) patients.
Methods: The expression of CD25 and CD123 on blast cells in bone marrow samples were identified by flowcytometry in 94 patients (⩽ 60 years old) with de novo acute myeloid leukemia (AML) treated at the Mansoura University Oncology Center (MUOC).
Results: Of the 94 samples at diagnosis there were 17 (18.1%) CD25+/CD123+ (double positive) cases; 25 (26.6%) CD25+/CD123- (single positive); 32 (34.0%) CD25-/CD123+ (single positive) cases; 20 (21.3%). CD25-/CD123- (double negative). Most of the AML patients have double CD25+/CD123+ were significantly associated with poor and intermediate risk as compared to those associated with those in the good risk group (P= 0.005). The lowest induction of remission was recorded in AML patients have double CD25+/CD123+ expression as compared to the remaining AML patient group. Study the effect of these biomarkers on the overall survival reveal that AML patients exhibited double CD25+/CD123+ expression had significantly shorter overall survival as compared to negative ones.
Conclusion: Double CD25+/CD123+ co-expression in AML patients is a dismal prognostic marker and could be used as novel biomarker for risk stratification for AML patients.
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http://dx.doi.org/10.3233/CBM-201519 | DOI Listing |
Cancers (Basel)
January 2025
Medigene Immunotherapies GmbH, 82152 Planegg-Martinsried, Germany.
Background/objectives: MDG1011 is an autologous TCR-T therapy developed as a treatment option for patients with myeloid malignancies, including acute myeloid leukemia (AML), myelodysplastic syndrome (MDS), and multiple myeloma (MM). It is specific for the target antigen PReferentially expressed Antigen in MElanoma (PRAME). The recombinant TCR used in MDG1011 recognizes PRAME VLD-peptide presented by HLA-A*02:01-encoded surface molecules.
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January 2025
Princess Maxima Center for Pediatric Oncology, 3584 CS Utrecht, The Netherlands.
Background: Proteolysis targeting chimeras (PROTACs) are heterobifunctional small molecules that utilize the ubiquitin-proteasome system to selectively degrade target proteins. This innovative technology has shown remarkable efficacy and specificity in degrading oncogenic proteins and has progressed through various stages of preclinical and clinical development for hematologic malignancies, including adult acute myeloid leukemia (AML). However, the application of PROTACs in pediatric AML remains largely unexplored.
View Article and Find Full Text PDFBiomedicines
January 2025
Biobank of Research, IRCCS Azienda Ospedaliera, Universitaria di Bologna, Policlinico di S. Orsola, 40138 Bologna, Italy.
Acute myeloid leukemias (AMLs) comprise a group of genetically heterogeneous hematological malignancies that result in the abnormal growth of leukemic cells and halt the maturation process of normal hematopoietic stem cells. Despite using molecular and cytogenetic risk classification to guide treatment decisions, most AML patients survive for less than five years. A deeper comprehension of the disease's biology and the use of new, targeted therapy approaches could potentially increase cure rates.
View Article and Find Full Text PDFBiomedicines
January 2025
Clinical Research Center, Jiangnan University Medical Center, 68 Zhongshan Road, Wuxi 214002, China.
Acute myeloid leukemia (AML) is an aggressive cancer with variable treatment responses. While clinical factors such as age and genetic mutations contribute to prognosis, recent studies suggest that CT attenuation scores may also predict treatment outcomes. This study aims to develop a nomogram combining clinical and CT-based factors to predict treatment response and guide personalized therapy for AML patients.
View Article and Find Full Text PDFBiomedicines
January 2025
Department of Hematology and Oncology, University Cancer Center Schleswig-Holstein (UCCSH), University Hospital Schleswig-Holstein, 23562 Lübeck, Germany.
: GFI1-36N represents a single-nucleotide polymorphism (SNP) of the zinc finger protein Growth Factor Independence 1 (GFI1), in which the amino acid serine (S) is replaced by asparagine (N). The presence of the gene variant is associated with a reduced DNA repair capacity favoring myeloid leukemogenesis and leads to an inferior prognosis of acute myeloid leukemia (AML) patients. However, the underlying reasons for the reduced DNA repair capacity in leukemic cells are largely unknown.
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