dc.rights.license | CC-BY-NC-ND | |
dc.contributor.advisor | Externe beoordelaar - External assesor, | |
dc.contributor.author | Nijs, Nathalie | |
dc.date.accessioned | 2021-11-30T00:00:16Z | |
dc.date.available | 2021-11-30T00:00:16Z | |
dc.date.issued | 2021 | |
dc.identifier.uri | https://studenttheses.uu.nl/handle/20.500.12932/252 | |
dc.description.abstract | When you have cancer, you get treated with a drug, but this treatment is not always fully effective. There is a chance that you get resistant against this drug, with other words the drug won’t work anymore. This resistance can occur when you get mutations in your DNA, here we focus on the copy number alterations (CNAs). CNAs are mutations that result in the gain (amplification) of loss (deletion) in copies of sections of DNA. When we know which genes play a role in these resistance mechanisms, the future treatment decision making, which drug the patient gets, may be improved. We used HMF and PCAWG datasets, which contains samples from treated and untreated patients. With this approach, we were able to detect already known CNAs that are linked with resistance, but we also find some potential resistance candidates that require further validation analysis. | |
dc.description.sponsorship | Utrecht University | |
dc.language.iso | EN | |
dc.subject | Identify and characterize genomic features that underwent positive selection during treatment by comparing whole genome sequencing data of treated cancer patients against treated naive cancer patients. | |
dc.title | Somatic copy number alterations reveal insight in drivers of resistance as a response to specific treatments | |
dc.type.content | Master Thesis | |
dc.rights.accessrights | Open Access | |
dc.subject.keywords | Cancer; resistance; GISTIC; PCAWG; HMF; CNVs | |
dc.subject.courseuu | Bioinformatics and Biocomplexity | |
dc.thesis.id | 865 | |