[Impact of TP53 and MYD88 Mutations on Treatment Efficacy in Diffuse Large B-Cell Lymphoma].
To investigate the relationship between TP53 and MYD88 mutations and treatment efficacy in patients with diffuse large B-cell lymphoma (DLBCL) who received rituximab-based standard chemoimmunotherapy.
The clinical data of 92 patients with newly diagnosed DLBCL who were treated in the Department of Hematology of the Huai'an No.1 People's Hospital and Yancheng No.1 People's Hospital from January 1, 2015 to December 30, 2023 were retrospectively analyzed. Chi-square test, univariate and multivariate logistic regression analyses were used to identify risk factors associated with treatment efficacy, and a predictive model was further established. Survival curves were plotted using the Kaplan-Meier method, and differences in survival between groups were compared by the log-rank test.
Among the 92 patients, 71 (77.2%) achieved post-induction remission (remission group) and 21 (22.8%) did not respond to treatment (non-remission group). The proportions of patients with elevated lactate dehydrogenase (LDH) (P =0.022) and those with MYD88 mutation (P =0.021) were significantly higher in the non-remission group than in the remission group. Univariate analysis showed that LDH (OR =3.482, P =0.027) and MYD88 mutation (OR =3.175, P =0.024) were factors influencing treatment efficacy in DLBCL patients receiving chemoimmunotherapy. Multivariate analysis showed that TP53 mutation （P =0.031） and MYD88 mutation （P =0.010） were independent risk factors for poor treatment efficacy in DLBCL patients. A treatment efficacy prediction model for DLBCL was established based on TP53 and MYD88 mutations, with an area under the receiver operating characteristic (ROC) curve of 0.705. According to the novel predictive model, the enrolled patients were divided into high-risk and low-risk groups. Treatment efficacy analysis showed that the objective response rate (ORR) of the low-risk group was significantly higher than that of the high-risk group (92.3% vs. 66.0%, P =0.006), and the progression-free survival (PFS) and overall survival (OS) of patients in the high-risk group were significantly poorer than those in the low-risk group (PFS: P =0.024; OS: P =0.004).
TP53 mutation and MYD88 mutation are independent risk factors for poor efficacy in DLBCL patients receiving first-line immunochemotherapy. The novel predictive model constructed based on these two mutations can identify patients with potential poor response to first-line chemoimmunotherapy, which may provide a reference for optimizing the first-line individualized treatment strategy for DLBCL.
The clinical data of 92 patients with newly diagnosed DLBCL who were treated in the Department of Hematology of the Huai'an No.1 People's Hospital and Yancheng No.1 People's Hospital from January 1, 2015 to December 30, 2023 were retrospectively analyzed. Chi-square test, univariate and multivariate logistic regression analyses were used to identify risk factors associated with treatment efficacy, and a predictive model was further established. Survival curves were plotted using the Kaplan-Meier method, and differences in survival between groups were compared by the log-rank test.
Among the 92 patients, 71 (77.2%) achieved post-induction remission (remission group) and 21 (22.8%) did not respond to treatment (non-remission group). The proportions of patients with elevated lactate dehydrogenase (LDH) (P =0.022) and those with MYD88 mutation (P =0.021) were significantly higher in the non-remission group than in the remission group. Univariate analysis showed that LDH (OR =3.482, P =0.027) and MYD88 mutation (OR =3.175, P =0.024) were factors influencing treatment efficacy in DLBCL patients receiving chemoimmunotherapy. Multivariate analysis showed that TP53 mutation （P =0.031） and MYD88 mutation （P =0.010） were independent risk factors for poor treatment efficacy in DLBCL patients. A treatment efficacy prediction model for DLBCL was established based on TP53 and MYD88 mutations, with an area under the receiver operating characteristic (ROC) curve of 0.705. According to the novel predictive model, the enrolled patients were divided into high-risk and low-risk groups. Treatment efficacy analysis showed that the objective response rate (ORR) of the low-risk group was significantly higher than that of the high-risk group (92.3% vs. 66.0%, P =0.006), and the progression-free survival (PFS) and overall survival (OS) of patients in the high-risk group were significantly poorer than those in the low-risk group (PFS: P =0.024; OS: P =0.004).
TP53 mutation and MYD88 mutation are independent risk factors for poor efficacy in DLBCL patients receiving first-line immunochemotherapy. The novel predictive model constructed based on these two mutations can identify patients with potential poor response to first-line chemoimmunotherapy, which may provide a reference for optimizing the first-line individualized treatment strategy for DLBCL.