Frontiers in oncology · 2025
A viral infection prediction model for patients with r/r B-cell malignancies after CAR-T therapy: a retrospective analysis.
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Guo Shujing, Liu Jile, Wang Bing, Zhang Xiaomei, Zhao Yifan, Xu Jianmei, Cao Xinping, Zhao Mohan, Xiao Xia, Zhao Mingfeng
Аннотация
BACKGROUND: Chimeric antigen receptor T cell (CAR-T) therapy for relapsed/refractory (r/r) B cell acute lymphoblastic leukemia (B-ALL) and B cell non-Hodgkin lymphoma (B-NHL) patients has shown promising effects, but side effects such as viral infections have been observed.
METHODS: A total of 45 patients with r/r B-ALL and r/r B-NHL were included in this retrospective study. Patient demographics were recorded, with the primary endpoint being viral infection within 3 months post CAR-T treatment. Univariate and multivariate logistic regression analyses and least absolute shrinkage and selection operator (LASSO) regression analysis were used to analyze independent factors. The patients were divided into a training cohort of 28 and a validation cohort of 17 to construct a prediction model based on determined independent factors. The model's discrimination and calibration were assessed using the receiver operating characteristic curve (ROC), calibration plot, and decision curve analysis (DCA curve).
RESULTS: The univariate and multivariate logistic regression analyses of the 43 patients showed that low baseline lymphocyte ratio was an independent risk factor and using granulocyte colony-stimulating factor (G-CSF) early was a protective factor for viral infection after CAR-T therapy in patients with B-ALL and B-NHL. Based on that, the area under the ROC curve (AUC) of the training cohort and validation cohort was 0.935 (95% CI 0.837-1.000) and 0.869 (95%CI 0.696-1.000), respectively, showing excellent predictive value.
CONCLUSIONS: We established a nomogram to predict the factors' influence on viral infection after CAR-T therapy and found that the ratio of baseline lymphocytes and using G-CSF early or lately were able to predict viral infection after CAR-T therapy in r/r B-ALL and B-NHL.
METHODS: A total of 45 patients with r/r B-ALL and r/r B-NHL were included in this retrospective study. Patient demographics were recorded, with the primary endpoint being viral infection within 3 months post CAR-T treatment. Univariate and multivariate logistic regression analyses and least absolute shrinkage and selection operator (LASSO) regression analysis were used to analyze independent factors. The patients were divided into a training cohort of 28 and a validation cohort of 17 to construct a prediction model based on determined independent factors. The model's discrimination and calibration were assessed using the receiver operating characteristic curve (ROC), calibration plot, and decision curve analysis (DCA curve).
RESULTS: The univariate and multivariate logistic regression analyses of the 43 patients showed that low baseline lymphocyte ratio was an independent risk factor and using granulocyte colony-stimulating factor (G-CSF) early was a protective factor for viral infection after CAR-T therapy in patients with B-ALL and B-NHL. Based on that, the area under the ROC curve (AUC) of the training cohort and validation cohort was 0.935 (95% CI 0.837-1.000) and 0.869 (95%CI 0.696-1.000), respectively, showing excellent predictive value.
CONCLUSIONS: We established a nomogram to predict the factors' influence on viral infection after CAR-T therapy and found that the ratio of baseline lymphocytes and using G-CSF early or lately were able to predict viral infection after CAR-T therapy in r/r B-ALL and B-NHL.