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dc.rights.licenseCC-BY-NC-ND
dc.contributor.advisorExterne beoordelaar - External assesor,
dc.contributor.authorZee, Ivar van der
dc.date.accessioned2023-04-20T09:22:58Z
dc.date.available2023-04-20T09:22:58Z
dc.date.issued2023
dc.identifier.urihttps://studenttheses.uu.nl/handle/20.500.12932/43810
dc.description.abstractObjectives: Identify biomolecular mechanisms responsible for acral lentiginous melanoma (ALM) ulceration and its associated worsened clinical outcomes. Methods: Transcriptomes of 59 Mexican ALM patients with varying ulceration status were analysed through the Feature-Engine Python library, which ranked genes based on how much their expression differs between ulcerated and non-ulcerated tumours. This ranking was analysed through gene set enrichment analysis to identify biological components. Results: Multiple proteins that make up desmosomes (a cell-cell adhesion complex) appear downregulated in ulcerated tumours. The genes PERP and TP63, which are thought to be essential to desmosome formation, also appear downregulated. Conclusion: Given the role desmosomes play in both skin integrity and tumour suppression, we hypothesize them to be the link between ulceration and the associated worsened clinical outcomes. PERP could be involved in causing their dysregulation.
dc.description.sponsorshipUtrecht University
dc.language.isoEN
dc.subjectThe study aimed to identify biomolecular mechanisms responsible for acral lentiginous melanoma (ALM) ulceration and its associated worsened clinical outcomes using the transcriptomes of 59 Mexican ALM patients.
dc.titleUlceration in Mexican Acral Lentiginous Melanoma patients
dc.type.contentMaster Thesis
dc.rights.accessrightsOpen Access
dc.subject.courseuuDrug Innovation
dc.thesis.id15373


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