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Centrosome amplification is sufficient to promote spontaneous tumorigenesis in mammals

ChEBI2017-02-04 更新2026-07-12 收录

中心体扩增

肿瘤发生机制

数据链接：

https://www.ebi.ac.uk/biostudies/ArrayExpress/studies/E-MTAB-5043 数据链接链接失效反馈

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资源简介：

Centrosome amplification is sufficient to promote spontaneous tumorigenesis in mammals

应用场景：

创建时间：

2017-02-04

肿瘤发生机制

细胞衰老调控

Six1 is a developmental transcriptional regulator frequently overexpressed in human tumors. Recent results also show that SIX1 acts as a repressor of cell senescence, an antiproliferative response wit

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p53 amyloid formation induced cellular transformation and tumor formation in xenograft model

p53

肿瘤发生机制

p53 mutation and its subsequent loss of function along with gain of oncogenic functions is associated with cancer. However, the exact mechanism of how altered p53 acts as an oncogene is not clear yet.

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Identification of a novel TINCR-EGFR signaling pathway loop which initiates receptor tyrosine kinases cascade and confers tumorigenesis in human cancer

癌症信号通路

肿瘤发生机制

RNA sequencing was performed to investigate the potential crosstalk between TINCR and microRNAs. Overall design: microRNA profiles of T47D with TINCR knockdown and scramble were generated by deep sequ

NIAID Data Ecosystem50

NGS-mRNA in lung tissues in RAG1-/- and in RAG1-/- Sgo1-/+ mice

基因表达分析

肿瘤发生机制

We compared lung mRNA expression profiles between RAG1-/- control and RAG1-/- Sgo1-/+ chromosome instability model mice. RAG1-/-Sgo1-/+ mice developed significantly more spontaneous lung tumors. Char

NIAID Data Ecosystem80

YAP1 and PRDM14 converge to regulate cell survival and tumorigenesis

肿瘤发生机制

疾病靶点发现

The transcriptional co-activator YAP1 oncogene is the downstream effector of the Hippo pathway, which regulates tissue homeostasis, organ size, regeneration and tumorigenesis. Multiple cancers are dep

NIAID Data Ecosystem50

Centrosome amplification is sufficient to promote spontaneous tumorigenesis in mammals

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