Editorial Expression of Concern: Activation of NF-κB and upregulation of intracellular anti-apoptotic proteins via the IGF-1/Akt signaling in human multiple myeloma cells: therapeutic implications.

IF 6.9 1区 医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Oncogene Pub Date : 2024-11-11 DOI:10.1038/s41388-024-03217-8
Constantine S Mitsiades, Nicholas Mitsiades, Vassiliki Poulaki, Robert Schlossman, Masaharu Akiyama, Dharminder Chauhan, Teru Hideshima, Steven P Treon, Nikhil C Munshi, Paul G Richardson, Kenneth C Anderson
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社论表达关注:通过 IGF-1/Akt 信号在人类多发性骨髓瘤细胞中激活 NF-κB 和上调细胞内抗凋亡蛋白:治疗意义。
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来源期刊
Oncogene
Oncogene 医学-生化与分子生物学
CiteScore
15.30
自引率
1.20%
发文量
404
审稿时长
1 months
期刊介绍: Oncogene is dedicated to advancing our understanding of cancer processes through the publication of exceptional research. The journal seeks to disseminate work that challenges conventional theories and contributes to establishing new paradigms in the etio-pathogenesis, diagnosis, treatment, or prevention of cancers. Emphasis is placed on research shedding light on processes driving metastatic spread and providing crucial insights into cancer biology beyond existing knowledge. Areas covered include the cellular and molecular biology of cancer, resistance to cancer therapies, and the development of improved approaches to enhance survival. Oncogene spans the spectrum of cancer biology, from fundamental and theoretical work to translational, applied, and clinical research, including early and late Phase clinical trials, particularly those with biologic and translational endpoints.
期刊最新文献
Lfng-expressing centroacinar cell is a unique cell-of-origin for p53 deficient pancreatic cancer. Unveiling RACK1: a key regulator of the PI3K/AKT pathway in prostate cancer development. Correction: Regucalcin promotes dormancy of prostate cancer. Editorial Expression of Concern: Activation of NF-κB and upregulation of intracellular anti-apoptotic proteins via the IGF-1/Akt signaling in human multiple myeloma cells: therapeutic implications. RBM15 facilitates osimertinib resistance of lung adenocarcinoma through m6A-dependent epigenetic silencing of SPOCK1.
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