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Imatinib versus gastro intestinal stromal tumors

Stiphout, K. J. van (2012) Imatinib versus gastro intestinal stromal tumors. Bachelor's Thesis, Biology.

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Abstract

This thesis is about whether imatinib, a tyrosine kinase inhibitor, is successful enough as a treatment for gastro intestinal stromal tumor (GIST) patients. Of all GISTs 70-80% harbor mutations in the receptor tyrosine kinase KIT, 5-8% in the platelet derived growth factor α tyrosine kinase (PDGFRA) and 12-15% do not harbor any KIT- or PDGFRA mutations (wild-type GISTs). The KIT- or PDGFRA mutations are oncogenic driver mutations, that lead to constant activation of the downstream pathways, which leads to GIST progression. Imatinib inhibits signaling of mutated KIT and mutated PDGFRA in GISTs. Overall imatinib can prevent GIST progression in more than 70% of all GISTs. The problem is that imatinib cannot prevent progression in wild-type GISTs and can only prevent progression in some PDGFRA-mutated GISTs. On top of this imatinib-sensitive GISTs develop drug resistance, probably because imatinib does not actively eradicate all GIST cells. There are many ideas of how to improve treatment of GIST patients, but the most promising for imatinib-resistant GISTs are inhibitors of downstream components of the KIT- or PDGFRA pathway. These promising new drugs do not only prevent GIST progression, but also introduce apoptosis.

Item Type: Thesis (Bachelor's Thesis)
Degree programme: Biology
Thesis type: Bachelor's Thesis
Language: English
Date Deposited: 15 Feb 2018 07:48
Last Modified: 15 Feb 2018 07:48
URI: http://fse.studenttheses.ub.rug.nl/id/eprint/10227

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