https://github.com/mschubert/mad2-transposon

Analysis code for "Cancer tolerance to chromosomal instability is driven by Stat1 inactivation in vivo"
https://github.com/mschubert/mad2-transposon

Last synced: 11 days ago
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Analysis code for "Cancer tolerance to chromosomal instability is driven by Stat1 inactivation in vivo"

• Host: GitHub
• URL: https://github.com/mschubert/mad2-transposon
• Owner: mschubert
• Created: 2017-10-25T12:00:06.000Z (over 7 years ago)
• Default Branch: master
• Last Pushed: 2024-02-04T19:01:18.000Z (12 months ago)
• Last Synced: 2024-09-17T17:42:50.676Z (5 months ago)
• Language: R
• Homepage: https://www.biorxiv.org/content/10.1101/2021.12.03.471107v2
• Size: 1.71 MB
• Stars: 0
• Watchers: 3
• Forks: 0
• Open Issues: 11
• Metadata Files:
  • Readme: README.md

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README

        
# Analysis code for "Cancer tolerance to chromosomal instability is driven by Stat1 inactivation _in vivo_"

> Chromosomal instability is a hallmark of cancer, but also an instigator of

> aneuploidy-induced stress, reducing cellular fitness. To better understand

> how cells with CIN adjust to aneuploidy and adopt a malignant fate in vivo,

> we performed a genome-wide mutagenesis screen in mice. We find that

> specifically aneuploid tumors inactivate Stat1 signaling in combination with

> increased Myc activity. By contrast, loss of p53 is common, but not enriched

> in CIN tumors. Validation in another tissue type confirmed that CIN promotes

> immune cell infiltration, which is alleviated by Stat1 loss combined with Myc

> activation, but not with p53 inactivation, or Myc activation alone.

> Importantly, we find that this mechanism is preserved in human aneuploid

> cancers. We conclude that aneuploid cancers inactivate Stat1 signaling to

> circumvent immune surveillance.

https://www.biorxiv.org/content/10.1101/2021.12.03.471107v2

This repository contains all analysis code, but we are still in the process of

cleaning it up and properly documenting it.