Neopterin is a pteridine molecule released by immune activated monocytes. Monocytic maturation may be induced in acute myeloid leukaemia (AML) blasts and the U937 leukaemic cell line by 1,25-dihydroxyvitamin D3 [1,25(OH)2D3], an effect which is augmented by both gamma interferon (IFN) or granulocyte-macrophage colony stimulating factor (GM-CSF). We have demonstrated that, while 1,25(OH)2D3 and GM-CSF alone have little effect, both IFN and GM-CSF act synergistically with 1,25(OH)2D3 to increase neopterin secretion in the U937 cell line. Neopterin secretion was associated with, but not necessarily dependent on, the degree of phenotypic differentiation achieved by cells. Neopterin secretion was also synergistically enhanced in AML blasts by the action of 1,25(OH)2D3 in combination with IFN but not GM-CSF; secretion was enhanced in AML blasts without concomitant evidence of phenotypic maturation. We have shown that the monocytoid cell line U937, under appropriate conditions, may secrete neopterin in response to stimulatory agents other than IFN. In addition, the distinct difference in the pattern of response to the combination of 1,25(OH)2D3 with GM-CSF compared with that of 1,25(OH)2D3 plus IFN suggests that the augmentation of 1,25(OH)2D3 effect by IFN and GM-CSF is mediated by separate mechanisms.
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http://dx.doi.org/10.1016/0960-0760(94)90255-0 | DOI Listing |
Cell Commun Signal
January 2025
Department of Biosciences and Medical Biology, Paris-Lodron University Salzburg, Hellbrunner Strasse 34, Salzburg, 5020, Austria.
FLT3 mutations occur in approximately 25% of all acute myeloid leukemia (AML) patients. While several FLT3 inhibitors have received FDA approval, their use is currently limited to combination therapies with chemotherapy, as resistance occurs, and efficacy decreases when the inhibitors are used alone. Given the highly heterogeneous nature of AML, there is an urgent need for novel targeted therapies that address the disease from multiple angles.
View Article and Find Full Text PDFFront Oncol
January 2025
The Second Department of General Surgery, the Fourth Hospital of Hebei Medical University, Hebei, Shijiazhuang, China.
Background: Stromal-cell-derived factor 1 (SDF-1) plays a crucial role in hematopoiesis and has been implicated in acute myeloid leukemia (AML) pathogenesis. Understanding its relationship with chemotherapy outcomes could lead to improved therapeutic approaches for elderly AML patients.
Methods: This study retrospectively analyzed the medical records of elderly AML patients (n = 187) and compared serum SDF-1α levels with age-matched controls (n = 120).
Background: Acute myeloid leukemia (AML) with RAM immunophenotype is a newly recognized high-risk AML immunophenotypic subcategory characterized by blasts with bright expression of CD56 and weak to absent expression of CD45, HLA-DR, and CD38, as first described by the Children's Oncology Group (COG). The relationship between AML-RAM and other CD56-positive acute leukemias is unclear. The goal of this study is to characterize the clinicopathological characteristics of AML with RAM phenotype and compare them with other CD56 co-expressing acute leukemias.
View Article and Find Full Text PDFLoss of anticancer NK cell function in AML patients is associated with fatal disease progression and remains poorly understood. Here, we demonstrate that AML-blasts isolated from patients rapidly inhibit NK cell function and escape NK cell-mediated killing. Transcriptome analysis of NK cells exposed to AML-blasts revealed increased CREM expression and transcriptional activity, indicating enhanced cAMP signalling, confirmed by uniform production of the cAMP-inducing prostanoid PGE2 by all AML-blast isolates from patients.
View Article and Find Full Text PDFDrug Resist Updat
January 2025
Loma Linda University Cancer Center, Loma Linda, CA 92354, United States; Department of Basic Sciences, Loma Linda University, Loma Linda, CA 92354, United States. Electronic address:
Chromosomal rearrangements (CR) initiate leukemogenesis in approximately 50 % of acute myeloid leukemia (AML) patients; however, limited targeted therapies exist due to a lack of accurate molecular and genetic biomarkers of refractory mechanisms during treatment. Here, we investigated the pathological landscape of treatment resistance and relapse in 16 CR-AML patients by monitoring cytogenetic, RNAseq, and genome-wide changes among newly diagnosed, refractory, and relapsed AML. First, in FISH-diagnosed KMT2A (MLL gene, 11q23)/AFDN (AF6, 6q27)-rearrangement, RNA-sequencing identified an unknown CCDC32 (15q15.
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