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The T315I mutation poses a significant threat to patients with chronic phase chronic myeloid leukemia (CP-CML). This study aimed to establish a nomogram to predict the risk of T315I mutation in CP-CML patients. The training cohort included 1,466 patients from 24 hematology centers, and the validation cohort included 820 patients from an additional 20 centers. Peripheral blood blast (PBB), additional chromosomal abnormality (ACA), dasatinib use, non-EMR at 3 months, and BCR::ABLIS > 1% at 6 months were identified as independent risk factors through multivariate Cox regression analysis. The performance of the nomogram was assessed via receiver operating characteristic (ROC) curves, calibration curves, and decision curve analysis (DCA). The area under the ROC curve (AUC) values at 5, 10, and 15 years were 0.874, 0.925, and 0.930 for the training cohort, and 0.864, 0.814, and 0.803 for the validation cohort, respectively. The calibration curves for both cohorts were close to the ideal diagonal, and the decision curves indicated clinical net benefit. In conclusion, we developed a nomogram to predict the 5-year, 10-year, and 15-year T315I-free survival probabilities of CP-CML patients. This tool can aid clinicians in the early prediction and timely management of high-risk CP-CML patients with the T315I mutation. [ABSTRACT FROM AUTHOR]

Objective: To investigate the inhibitive effects of chimeric oncolytic adenovirus SG235 on leukemia cells in vitro., Methods: The ability of SG235 to infect leukemia cells and the expression of CD46 on blasts from the patient with leukemia were detected by flow cytometry (FACS). The cytotoxicity of the virus was evaluated by MTT assay. Apoptosis induced by SG235 was detected with Annexin-V/PI staining and TUNEL assay followed by FACS analysis., Result: The majority of leukemia cells from the patient with acute leukemia was CD46-positive. GFP-positive cells were 45.1%, 35.7%, 54.2%, 37.0%, 30.1%, %67.1, 17.2% and 33.1% in Mutz-1, Kasumi-1, K562, HL60, Molt- 4, RPMI8226, L428, and Jurkat cell lines treated with SG235-EGFP vector at MOI (multiplicity of infection) of 50 for 48 h.SG235 treatment resulted in marked growth inhibition and apoptosis of Kassumi-1 cells, and also significantly inhibited expression of p-Akt., Conclusion: The chimeric oncolytic adenovirus SG235 can infect leukemia cell effectively and results in the growth inhibition and apoptosis of Kasumi-1 cells in vitro.