Genes & Diseases最新文献_第10页

MDM2 inhibitors in cancer immunotherapy: Current status and perspective 癌症免疫疗法中的 MDM2 抑制剂：现状与展望

IF 6.9 2区医学

Genes & Diseases Pub Date : 2024-03-28 DOI: 10.1016/j.gendis.2024.101279

{"title":"MDM2 inhibitors in cancer immunotherapy: Current status and perspective","authors":"","doi":"10.1016/j.gendis.2024.101279","DOIUrl":"10.1016/j.gendis.2024.101279","url":null,"abstract":"<div><p>Murine double minute 2 (MDM2) plays an essential role in the cell cycle, apoptosis, DNA repair, and oncogene activation through p53-dependent and p53-independent signaling pathways. Several preclinical studies have shown that MDM2 is involved in tumor immune evasion. Therefore, MDM2-based regulation of tumor cell-intrinsic immunoregulation and the immune microenvironment has attracted increasing research attention. In recent years, immune checkpoint inhibitors targeting PD-1/PD-L1 have been widely used in the clinic. However, the effectiveness of a single agent is only approximately 20%–40%, which may be related to primary and secondary drug resistance caused by the dysregulation of oncoproteins. Here, we reviewed the role of MDM2 in regulating the immune microenvironment, tumor immune evasion, and hyperprogression during immunotherapy. In addition, we summarized preclinical and clinical findings on the use of MDM2 inhibitors in combination with immunotherapy in tumors with MDM2 overexpression or amplification. The results reveal that the inhibition of MDM2 could be a promising strategy for enhancing immunotherapy.</p></div>","PeriodicalId":12689,"journal":{"name":"Genes & Diseases","volume":"11 6","pages":"Article 101279"},"PeriodicalIF":6.9,"publicationDate":"2024-03-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S235230422400076X/pdfft?md5=e8193d8f3cf4de801a721c4c34ffe215&pid=1-s2.0-S235230422400076X-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140402376","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

STIM1 promotes acquired resistance to sorafenib by attenuating ferroptosis in hepatocellular carcinoma STIM1 通过减弱肝细胞癌中的铁变态反应，促进对索拉非尼的获得性耐药性

IF 6.9 2区医学

Genes & Diseases Pub Date : 2024-03-28 DOI: 10.1016/j.gendis.2024.101281

{"title":"STIM1 promotes acquired resistance to sorafenib by attenuating ferroptosis in hepatocellular carcinoma","authors":"","doi":"10.1016/j.gendis.2024.101281","DOIUrl":"10.1016/j.gendis.2024.101281","url":null,"abstract":"<div><p>Dysregulated calcium (Ca<sup>2+</sup>) signaling pathways are associated with tumor cell death and drug resistance. In non-excitable cells, such as hepatocellular carcinoma (HCC) cells, the primary pathway for Ca<sup>2+</sup> influx is through stromal interaction molecule 1 (STIM1)-mediated store-operated calcium entry (SOCE). Previous studies have demonstrated the involvement of STIM1-mediated SOCE in processes such as genesis, metastasis, and stem cell self-renewal of HCC. However, it remains unclear whether STIM1-mediated SOCE plays a role in developing acquired resistance to sorafenib in HCC patients. In this study, we established acquired sorafenib-resistant (SR) HCC cell lines by intermittently exposing them to increasing concentrations of sorafenib. Our results showed higher levels of STIM1 and stronger SOCE in SR cells compared with parental cells. Deleting STIM1 significantly enhanced sensitivity to sorafenib in SR cells, while overexpressing STIM1 promoted SR by activating SOCE. Mechanistically, STIM1 increased the transcription of SLC7A11 through the SOCE-CaN-NFAT pathway. Subsequently, up-regulated SLC7A11 increased glutathione synthesis, resulting in ferroptosis insensitivity and SR. Furthermore, combining the SOCE inhibitor SKF96365 with sorafenib significantly improved the sensitivity of SR cells to sorafenib both <em>in vitro</em> and <em>in vivo</em>. These findings suggest a potential strategy to overcome acquired resistance to sorafenib in HCC cells.</p></div>","PeriodicalId":12689,"journal":{"name":"Genes & Diseases","volume":"11 6","pages":"Article 101281"},"PeriodicalIF":6.9,"publicationDate":"2024-03-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2352304224000783/pdfft?md5=24271de70c9addc8ffbf4b8c9b7a8bd7&pid=1-s2.0-S2352304224000783-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140398428","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Expanding the spectrum of novel candidate genes using trio exome sequencing and identification of monogenic cause in 27.5% of 320 families with steroid-resistant nephrotic syndrome 利用三组外显子测序扩展新型候选基因谱，在 320 个类固醇耐受性肾病综合征家族中确定 27.5% 的单基因病因

IF 6.9 2区医学

Genes & Diseases Pub Date : 2024-03-28 DOI: 10.1016/j.gendis.2024.101280

Ronen Schneider , Shirlee Shril , Florian Buerger , Konstantin Deutsch , Kirollos Yousef , Camille N. Frank , Ana C. Onuchic-Whitford , Thomas M. Kitzler , Youying Mao , Verena Klämbt , Muhammad Y. Zahoor , Katharina Lemberg , Amar J. Majmundar , Bshara Mansour , Ken Saida , Steve Seltzsam , Caroline M. Kolvenbach , Lea Maria Merz , Nils D. Mertens , Tobias Hermle , Friedhelm Hildebrandt

引用次数: 0

Transcriptional programs associated with luminal play a vital role in invasive mucinous lung adenocarcinoma 与管腔相关的转录程序在浸润性黏液肺腺癌中发挥着重要作用

IF 6.9 2区医学

Genes & Diseases Pub Date : 2024-03-26 DOI: 10.1016/j.gendis.2024.101278

Shufan Zhang , Rong Jiang , Changguo Wang , Manqiu Yang , Tao Wang , Jianzhou Cui , Guangbin Li , Shaomu Chen , Moli Huang

引用次数: 0

CD147 facilitates cisplatin resistance in ovarian cancer through FOXM1 degradation inhibition CD147 通过抑制 FOXM1 降解促进卵巢癌的顺铂耐药性

IF 6.8 2区医学

Genes & Diseases Pub Date : 2024-03-24 DOI: 10.1016/j.gendis.2024.101277

Miao Wang , Lin Chen , Yu Wang , Tian Fan , Chunyu Zhu , Zhixian Li , Lei Mou , Hong Yang , Airong Qian , Yu Li

引用次数: 0

Reduction of Atp5b protects mice from diet-induced obesity 减少 Atp5b 可保护小鼠免于饮食诱发的肥胖症

IF 6.9 2区医学

Genes & Diseases Pub Date : 2024-03-22 DOI: 10.1016/j.gendis.2024.101276

Xiaohua Huang , Binting Qin , Zhengfeng Fang , Lianqiang Che , Yan Lin , Shengyu Xu , Yong Zhuo , Lun Hua , Xuemei Jiang , Mengmeng Sun , Hairui Wang , De Wu , Qingqiang Long , Bin Feng

引用次数: 0

Predicting anti-cancer drug sensitivity through WRE-XGBoost algorithm with weighted feature selection 通过带有加权特征选择的 WRE-XGBoost 算法预测抗癌药物敏感性

IF 6.9 2区医学

Genes & Diseases Pub Date : 2024-03-22 DOI: 10.1016/j.gendis.2024.101275

Yiyao Jiang , Ming Chen , Zhongmin Xiong , Yufang Qin

引用次数: 0

The important role and core marker gene of tumor-infiltrating plasma cells in the microenvironment of lung adenocarcinoma 肿瘤浸润浆细胞在肺腺癌微环境中的重要作用及核心标记基因

IF 6.9 2区医学

Genes & Diseases Pub Date : 2024-03-22 DOI: 10.1016/j.gendis.2024.101274

Jianhong Zhang , Chengyang Song , Xiuqin Feng, Qian Yu, Xueying Yang

引用次数: 0

Corrigendum to “SEMA4D acts as a novel oligogenic pathogenic gene of idiopathic hypogonadotropic hypogonadism through the PlexinB1/MET/RND1/RHOA/RAF1/MAPK signaling axis” [Genes & Diseases 10 (2023) 65–68] 对 "SEMA4D通过PlexinB1/MET/RND1/RHOA/RAF1/MAPK信号轴作为特发性性腺功能减退症的新型寡致病基因 "的更正 [Genes & Diseases 10 (2023) 65-68]