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Early diagnosis and treatment initiation of chronic myeloid leukemia (CML) are considered to increase the rate of deep molecular response. However, the early diagnosis of CML is challenging due to the absence of clinical symptoms and peripheral blood test anomaly, especially at the timing of peripheral white blood cell count is within a normal range. This study explored the possibility of artificial intelligence (AI)-based quantitative detection of CML cells using ghost cytometry (GC) technology. We created pre-trained AI models, using the morphological information data of the peripheral blood leukocytes obtained from patients newly diagnosed with CML and healthy individuals. We applied these models to peripheral blood samples from CML patients after initiating tyrosine kinase inhibitor treatment at various time points, which contains smaller amounts of tumor cells. The AI model accurately detected CML cells and a strong correlation between AI-detected CML cells and actual BCR::ABL1 mRNA levels was observed. We concluded that the multidimensional morphological information of single cells obtained using GC, combined with machine learning algorithms, enables the quantitative detection of label-free CML cells. Our finding may enable the development of a screening test that can identify early-stage patients with CML before numerical abnormalities appear in blood tests.
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http://dx.doi.org/10.1038/s41598-025-06664-9 | DOI Listing |
Arch Pharm Res
September 2025
Department of Biosciences, JIS University, 81, Nilgunj Road, Agarpara, Kolkata, West Bengal, 700109, India.
Bacoside A (BCA), a triterpenoid saponin isolated from Bacopa monnieri, exhibits diverse pharmacological properties, including neuroprotective, hepatoprotective, anti-stress, anti-inflammatory, and anti-ulcer effects. In the present study, BCA demonstrates pronounced anticancer activity against K562 chronic myelogenous leukemia (CML) cells by modulating autophagy-apoptosis dynamics. BCA induces dose- and time-dependent cytotoxicity in K562 cells while sparing normal human peripheral blood mononuclear cells (hPBMCs) and Vero cells, indicating therapeutic selectivity.
View Article and Find Full Text PDFBr J Haematol
September 2025
Department of Pediatrics, Stanford University, Stanford, California, USA.
Chronic myeloid leukaemia (CML) accounts for 2% of leukaemias in children and 9% in adolescents. While the BCR::ABL1 fusion gene remains a hallmark across all age groups, emerging evidence suggests that paediatric CML exhibits unique biological and clinical characteristics compared to its adult counterpart. Children often present with more aggressive clinical features and show distinct treatment response patterns.
View Article and Find Full Text PDFBackground: Chronic myeloid leukemia (CML) is a clonal malignancy propelled by the fusion gene originating from the Philadelphia chromosome. This gene activates ABL tyrosine kinase, which enhances the survival of leukemic cells. Although tyrosine kinase inhibitors (TKIs) have significantly advanced the treatment of CML, resistance to these inhibitors presents a substantial hurdle.
View Article and Find Full Text PDFFuture Sci OA
December 2025
Department of Pediatrics, the Seventh Affiliated Hospital, Sun Yat-sen University, Shenzhen, China.
Background: Leukemia is driven by metabolic reprogramming, yet the specific causal roles of plasma metabolites in distinct leukemia subtypes remain unclear.
Methods: This study employed Mendelian randomization (MR) to explore potential causal links between 690 plasma metabolites (and 143 metabolite ratios) and four leukemia subtypes: ALL, AML, CLL, and CML. Genetic variants from genome-wide association studies served as instrumental variables.
PLoS One
August 2025
Faculty of Medical Technology, Prince of Songkla University, Hat Yai, Songkhla, Thailand.
Chronic myeloid leukemia (CML) is a hematologic malignancy originating from hematopoietic stem cells and driven by the BCR-ABL fusion oncogene. Imatinib (IM), a tyrosine kinase inhibitor, is commonly used as a frontline therapy for CML. However, some patients exhibit primary resistance or show persistent molecular evidence of disease despite treatment.
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