Bortezomib depended on PRDM1 and TP53 to exert therapeutic effect in activated B-cell-like diffuse large B-cell lymphoma
作者机构：Department of HematologyThe First Affiliated Hospital of Nanjing Medical UniversityJiangsu Province HospitalNanjingJiangsu 210029China Key Laboratory of Hematology of Nanjing Medical UniversityNanjingJiangsu 210029China Collaborative Innovation Center for Cancer Personalized MedicineNanjingJiangsu 210029China
出 版 物：《Genes & Diseases》 (基因与疾病（英文）)
年 卷 期：2024年第11卷第2期
页 面：550-553页
核心收录：
学科分类：1002[医学-临床医学] 100214[医学-肿瘤学] 10[医学]
基 金：supported by the National Natural Science Foundation of China(No.81720108002,81700193,82170186) Jiangsu Province's Medical Elite Programme(China)(No.ZDRCA2016022) Project of National Key Clinical Specialty(China),Jiangsu Provincial Special Program of Medical Science(China)(No.BE2017751) National Science and Technology Major F Project(China)(No.2018ZX09734007) Nature Science Foundation for Youths of Jiangsu Province,China(No.BK20220719) China Postdoctoral Science Foundation(No.2021M691336) Jiangsu Post doctoral Science Foundation(China)(No.2021K083A)
主 题：PRDM1 TP53 therapeutic
摘 要：PR/SET domain 1(PRDM1)gene is located on chromosome 6q21,encoding the B lymphocyte-induced maturation protein 1(BLIMP1).1 It is reported that loss of PRDM1 function is exacerbated in activated B-cell-like(ABC)-diffuse large B cell lymphoma(DLBCL)and associated with inferior ***,it remains unclear what leads to PRDM1 inactivation and the drug resistance mechanism caused by abnormal inactivation of *** investigated the contribution of PRDM1 gene as a prognosis and potential therapeutic target for ABC-DLBCL patients and further clarified the possible mechanism of PRDM1 abnormal *** first proposed that TP53 could regulate PRDM1 by histone ubiquitination modification at the post-transcriptional level.
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