Microarray analysis to identify the molecular mechanisms whereby pDCs confer growth and drug resistance in MM cells

ChEBI2009-07-31 更新2026-07-21 收录

肿瘤耐药机制

微阵列生物信息学

数据链接：

https://www.ebi.ac.uk/biostudies/ArrayExpress/studies/E-GEOD-17407 数据链接链接失效反馈

官方服务：

资源简介：

Microarray analysis to identify the molecular mechanisms whereby pDCs confer growth and drug resistance in MM cells

创建时间：

2009-07-31

Targeting tumor-macrophage interaction via the Notch2-Jag1 axis reverses tumor resistance to paclitaxel

肿瘤耐药机制

信号通路靶向治疗

Taxanes are widely used in chemotherapy, but intrinsic and acquired resistance limit the clinical outcomes. Studies showed tumor interaction with suppressive macrophages plays a key role in taxane res

NIAID Data Ecosystem80

YAP activation mediates acquired resistance to ALK inhibitor in ALK rearranged non–small cell lung cancer

肿瘤耐药机制

ALK靶向治疗

To investigate a possible candidate for overcoming the acquired resistance to ALK-TKI, we established an in vitro model of acquired resistance to crizotinib (H3122-CR) by exposing EML4-ALK–positive H3

NIAID Data Ecosystem40

SAKE (Single-cell RNA-Seq Analysis and Klustering Evaluation) Identifies Markers of Resistance to Targeted BRAF Inhibitors in Melanoma Cell Populations. Homo sapiens isolate:451Lu is a selected xenograft aggressive metastatic sub-line of WM164. WM164 is a metastatic human melanoma cell line established from a metastatic site (right upper arm) in a 22-year-old male with stage IV superficial spreading melanoma. 451Lu cell line features the specific V600E (Val600Glu) mutation at codon 600 in the BRAF gene.

单细胞转录组学

肿瘤耐药机制

The goal of this study is to apply the SAKE algorithms to identify drug-resistant cellular populations as human melanoma cells respond to targeted BRAF inhibitors. Single-cell RNA-Seq data from 10x Ge

NIAID Data Ecosystem20

Suppression of adaptive responses to targeted cancer therapy by transcriptional repression [RNA-seq]. Homo sapiens

肿瘤耐药机制

转录组药物响应

Large-scale genomic profiling efforts have facilitated the characterization of molecular alterations in cancers and aided the development of targeted kinase inhibitors for a wide array of cancer types

NIAID Data Ecosystem50

Divergent BRAF Inhibitor Resistance Mechanisms Revealed through Epigenetic Mapping. Divergent BRAF Inhibitor Resistance Mechanisms Revealed through Epigenetic Mapping

肿瘤耐药机制

表观遗传学分析

In this report, we generated eight matched pairs of vemurafenib sensitive/resistant melanoma lines and subjected these to concurrent RNA-seq and H3K27Ac ChIP-seq analysis. Globally, we identified two

NIAID Data Ecosystem30

Microarray analysis to identify the molecular mechanisms whereby pDCs confer growth and drug resistance in MM cells

资源简介：

相关数据集