PDF(Pubmed)
Abstract：
UNASSIGNED: Bruton tyrosine kinase inhibitor (BTKi) resistance is an unsolved problem in the treatment of relapse/recurrence (R/R) mantle cell lymphoma (MCL). Although salvage therapy following ibrutinib resistance has been attempted in recent years, the survival of resistant patients was significantly reduced. Once ibrutinib-treated patients relapse, the 1-year survival rate is only 22%. Acquired drug resistance and primary drug resistance were found to relate closely to genetic mutations. The hub genes identification and clinical data analysis of patients resistant to BTKi based on the Chinese MCL gene mutation profile are worthy of exploration.
UNASSIGNED: Based on 28 MCL patients\' mutation data and clinical data, 6 hub genes were screened by a gene panel of 69 genes and univariate Cox prognostic analysis. Prognosis and responses to salvage therapy regimen were analyzed.
UNASSIGNED: Patients with BTKi had less favorable clinical features at baseline. Chimeric antigen receptor T-cell (CAR-T) therapy yielded the best response among salvage treatments. The 6 hub genes were screened by a gene panel of 69 genes (GP79) which might be a potential predictor for MCL patients with BTKi resistance.
UNASSIGNED: The clinical characteristics of BTKi resistance in MCL patients were summarized, and 6 hub genes were identified to provide ideas and suggestions for further research.
UNASSIGNED: Based on 28 MCL patients\' mutation data and clinical data, 6 hub genes were screened by a gene panel of 69 genes and univariate Cox prognostic analysis. Prognosis and responses to salvage therapy regimen were analyzed.
UNASSIGNED: Patients with BTKi had less favorable clinical features at baseline. Chimeric antigen receptor T-cell (CAR-T) therapy yielded the best response among salvage treatments. The 6 hub genes were screened by a gene panel of 69 genes (GP79) which might be a potential predictor for MCL patients with BTKi resistance.
UNASSIGNED: The clinical characteristics of BTKi resistance in MCL patients were summarized, and 6 hub genes were identified to provide ideas and suggestions for further research.
摘要：
UNASSIGNED：布鲁顿酪氨酸激酶抑制剂（BTKi）耐药性是治疗复发/复发（R/R）套细胞淋巴瘤（MCL）的一个尚未解决的问题。尽管近年来已经尝试了依鲁替尼耐药后的挽救治疗，耐药患者的生存率显著降低.一旦伊布鲁替尼治疗的患者复发，1年生存率仅为22%。发现获得性耐药和原发性耐药与基因突变密切相关。基于中国MCL基因突变谱的BTKi耐药患者的hub基因鉴定和临床数据分析值得探索。
未经证实：基于28名MCL患者的突变数据和临床数据，通过69个基因的基因小组和单变量Cox预后分析筛选了6个hub基因。分析预后和对抢救治疗方案的反应。
未经证实：BTKi患者在基线时具有较差的临床特征。嵌合抗原受体T细胞（CAR-T）疗法在抢救治疗中产生了最好的反应。通过69个基因（GP79）的基因组筛选了6个hub基因，这可能是BTKi耐药MCL患者的潜在预测指标。
UNASSIGNED:总结MCL患者BTKi耐药的临床特点,并鉴定出6个hub基因，为进一步研究提供思路和建议。
未经证实：基于28名MCL患者的突变数据和临床数据，通过69个基因的基因小组和单变量Cox预后分析筛选了6个hub基因。分析预后和对抢救治疗方案的反应。
未经证实：BTKi患者在基线时具有较差的临床特征。嵌合抗原受体T细胞（CAR-T）疗法在抢救治疗中产生了最好的反应。通过69个基因（GP79）的基因组筛选了6个hub基因，这可能是BTKi耐药MCL患者的潜在预测指标。
UNASSIGNED:总结MCL患者BTKi耐药的临床特点,并鉴定出6个hub基因，为进一步研究提供思路和建议。
