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Transcriptional profiling of 5T33MM cells treated in vivo with quisinostat, decitabine or the combination.

ChEBI2018-02-26 更新2026-07-12 收录

多发性骨髓瘤药物机制

表观遗传药物转录组学

数据链接：

https://www.ebi.ac.uk/biostudies/ArrayExpress/studies/E-MTAB-3178 数据链接链接失效反馈

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Transcriptional profiling of 5T33MM cells treated in vivo with quisinostat, decitabine or the combination.

应用场景：

创建时间：

2018-02-26

多发性骨髓瘤药物机制

基因表达调控

The PI3K/mTOR pathway is a constitutively active in multiple myeloma. Single inhibition of mTOR usually confers reactivation of the pathway. VS-5584 (SB2343) is a bispecific PI3K/mTOR inhibitor which

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Efficacy of Melflufen in Patients with Relapsed/Refractory Multiple Myeloma and Mutated or Deleted TP53

多发性骨髓瘤药物机制

单细胞转录组学

Clinical challenges remain for patients with relapsed/refractory multiple myeloma (MM), especially for high-risk patients with del(17p) and TP53 mutation who have poor response and significantly short

NIAID Data Ecosystem30

Inhibition of the Aryl Hydrocarbon Receptor - Polyamine Biosynthesis Axis Suppresses Multiple Myeloma and prostate cancer progression

多发性骨髓瘤药物机制

AHR-多胺代谢靶点发现

Polyamine inhibition for cancer therapy is, conceptually, an attractive approach but has yet to meet success in the clinical setting. The aryl hydrocarbon receptor (AHR) is the central transcriptional

NIAID Data Ecosystem20

Gene expression profile of OSSL_325096 treated myeloma cells

多发性骨髓瘤药物机制

转录组差异

OSSL_325096 is a compound that acts as p97/VCP inhibitor and induces apoptosis in myeloma cells. Therefore, we treated KMS12PE and KMS11 myeloma cell lines with OSSL_325096 or DMSO and compare gene ex

NIAID Data Ecosystem40

Gene expression data from multiple myeloma cell lines treated with Novel Anti-B-cell Maturation Antigen α-Amanitin Antibody-drug Conjugate, HDP-101.

多发性骨髓瘤药物机制

抗体药物偶联物转录组学

Deletion (Del) of 17p involving the TP53 tumor suppressor remains an adverse prognostic factor in multiple myeloma, and more effective targeted therapies are needed for these patients. Genomic studie

NIAID Data Ecosystem30

Transcriptional profiling of 5T33MM cells treated in vivo with quisinostat, decitabine or the combination.

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