Copy number alterations are the most commonly observed genome alteration. I sought to find an amplified target for collateral lethality-based treatment that is “hyperactivated” and expressed at a higher rate than expected. Using a list of previously identified hyperactivated genes, I filtered the targets based on function and location, amplification status of various cancer types, and targetability. Oncogenes that were present in the final phase of selection were investigated using data from DepMap to see if their sensitivity to inhibitors increased with expression and copy number. Mouse double minute 2 homolog (MDM2) had a strong correlation increasing sensitivity with both expression and copy number whereas Kirsten rat sarcoma virus (KRAS) had no correlation. The pair were then used as positive and negative controls to see if other genes with low molecular weight inhibitors had the same profile. Lysine Demethylase 5B (KDM5B) and ribosomal protein S6 kinase B1 (RPS6KB1) were identified as possible targets for their correlations in breast cancer and pan-cancer respectively.
| Identifer | oai:union.ndltd.org:UPSALLA1/oai:DiVA.org:uu-532338 |
| Date | January 2024 |
| Creators | Giffin, Victoria |
| Publisher | Uppsala universitet, Institutionen för biologisk grundutbildning |
| Source Sets | DiVA Archive at Upsalla University |
| Language | English |
| Detected Language | English |
| Type | Student thesis, info:eu-repo/semantics/bachelorThesis, text |
| Format | application/pdf |
| Rights | info:eu-repo/semantics/openAccess |
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