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作 者:Jing Tang Yue Li Jiazhu Wu Haorui Shen Hua Yin Jinhua Liang Li Wang Jianyong Li Yi Xia Wei Xu
机构地区:[1]Department of Hematology,The First Affiliated Hospital of Nanjing Medical University,Jiangsu Province Hospital,Nanjing,Jiangsu 210029,China [2]Key Laboratory of Hematology of Nanjing Medical University,Nanjing,Jiangsu 210029,China [3]Collaborative Innovation Center for Cancer Personalized Medicine,Nanjing,Jiangsu 210029,China
出 处:《Genes & Diseases》2024年第2期550-553,共4页基因与疾病(英文)
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).
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 survival.However,it remains unclear what leads to PRDM1 inactivation and the drug resistance mechanism caused by abnormal inactivation of PRDM1.We 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 inactivation.We first proposed that TP53 could regulate PRDM1 by histone ubiquitination modification at the post-transcriptional level.
关 键 词:PRDM1 TP53 THERAPEUTIC
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