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Apoptosis, autophagy and senescence protect BRAFV600E nevi from malignant transformation

ChEBI2016-06-30 更新2026-07-12 收录

黑色素瘤发生机制

细胞防御通路

数据链接：

https://www.ebi.ac.uk/biostudies/ArrayExpress/studies/E-GEOD-23976 数据链接链接失效反馈

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资源简介：

Apoptosis, autophagy and senescence protect BRAFV600E nevi from malignant transformation

应用场景：

创建时间：

2016-06-30

黑色素瘤发生机制

表观遗传学分析

The “cancerized field” concept posits that cells of a given tissue share a potentially oncogenic mutation or insult and are thus cancer-prone, yet only discreet clones within the field initiate tumor

NIAID Data Ecosystem60

Transcriptionally inactive ATF2 variant drives melanomagenesis. Transcriptionally inactive ATF2 variant drives melanomagenesis

黑色素瘤发生机制

ATF2转录因子功能

This SuperSeries is composed of the SubSeries listed below. Overall design: Refer to individual Series

NIAID Data Ecosystem50

mTORC1 activation blocks BrafV600E-induced growth-arrest but is insufficient for melanoma formation. Mus musculus

黑色素瘤发生机制

小鼠模型转录组分析

Expression profiling was performed using uncultured melanocytes and melanoma cell from various mouse models of BrafV600E induced melanocytic proliferation Various genotypes were analyzed at different

NIAID Data Ecosystem30

RNA-seq analysis of MPCs treated with FGF1 variants. RNA-seq analysis of MPCs treated with FGF1 variants

基因表达分析

细胞防御通路

RNA-seq is a powerful tool to analyze differential expression of cellular pathways under different conditions. The goal of this study is to analyze the potential pathways involved in cellular defense

NIAID Data Ecosystem50

Emergence of neural crest identity is a key early step in melanoma formation [ChIP-Seq]

黑色素瘤发生机制

表观遗传调控

The âcancerized fieldâ concept posits that cells of a given tissue share a potentially oncogenic mutation or insult and are thus cancer-prone, yet only discreet clones within the field initiate tu

NIAID Data Ecosystem40

Apoptosis, autophagy and senescence protect BRAFV600E nevi from malignant transformation

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