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KU Leuven (5)


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dissertation (5)


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Dutch (5)


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Dissertation
Moleculaire mechanismen die leiden naar apoptose in UVB bestraalde keratinocyten : rol van ASK-1 in de activatie van het pro-apoptotische p38 MAPK.
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Year: 2005 Publisher: Leuven K.U.Leuven. Faculteit Geneeskunde

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Evaluatie van de rol van autofagie in humane kankercellen na fotodynamische therapie met hypericine.
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Year: 2007 Publisher: Leuven K.U.Leuven. Faculteit Geneeskunde

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Farmacologische en endogene inhibitie van het arachidonzuurmetabolisme tijdens fotodynamische therapie met hypericine.
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Year: 2005 Publisher: Leuven K.U.Leuven. Faculteit Geneeskunde

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Heroriëntatie van chloroquine en hydroxychloroquine als antikankermiddelen. Overzicht van de literatuur.

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Chloroquine (CQ) and hydroxychloroquine (HCQ), both well-known 4-aminoquinoline drugs, have been used in the treatment of malaria for more than 70 years and are now of particular interest in the treatment of cancer. Although the anticancer properties of CQ and HCQ have been widely described in literature, there is still uncertainty about the therapeutic efficacy and the exact mechanisms of action of these drugs in anticancer therapy. This master thesis is designed to provide a complete literature overview of the preclinical and clinical data on CQ and HCQ use in anticancer therapy. Based on this exercise some conclusions can be drawn; first, preclinical studies are generally in favour of CQ and HCQ use in anticancer therapy, especially in combination with conventional anticancer therapies as both drugs sensitize tumour cells to a variety of anticancer agents, potentiating their therapeutic activity. Secondly, most completed clinical trials have reported positive or partial therapeutic responses in patients, however, the majority of clinical trials are phase 1 or 2. Thirdly, CQ and HCQ have recently been found to exert effects both on cancer cells and on the tumour stroma. In cancer cells, CQ and HCQ inhibit the autophagic flux, which is their most widely studied anticancer effect, but they also affect the Toll-like receptor 9, p53, and CXCR4-CXCL12 pathway. In the tumour stroma, CQ and HCQ affect the tumour vasculature, cancer-associated fibroblasts, and the immune system. In conclusion, repurposing CQ and HCQ for anticancer therapy is a promising strategy, deserving further investigations.

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Dissertation
De rol van endotheel-specifieke autofagie in het vormen van melanoma micro-omgeving

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The interest in autophagy as a modulator of tumor microenvironment (TME) has increased over the years, however very little is known on whether and how autophagy regulates key stromal cells, such as tumor-associated endothelial cells (ECs). In previous research, mice harboring an EC-specific knockout (KO) (eliminating Atg5 from blood ECs (BEC) and lymphatic ECs (LEC)) of Atg5 displayed delayed melanoma growth, but increased vessel number. Interestingly, this Atg5-EC defect was associated with increased infiltration of CD8+ T cells. The aim of this study was to determine the contribution of autophagy in the vascular and lymphatic endothelial system to these outcomes. We found that specific BEC-associated autophagy, but not LEC-associated autophagy, phenocopied the effects of Atg5 deletion in both BEC and LEC. On cellular level, we observed that ATG5 knockdown (KD) in human umbilical vein ECs (HUVEC) changed the composition of surface molecules, including increased VCAM-1 expression, which was phenotypically associated to increased T cell adhesion in a co-culture assay. Furthermore, ATG5 KD in HUVEC or LEC changed the expression and secretion of chemokines involved in recruitment of T cells and cancer cells, respectively. Finally, whereas previous results showed that ATG5KD did not affect Notch1 signaling in BEC, preliminary data indicate that ATG5KD in LEC inhibits Notch1 signaling and reduced protein expression of key lymphatic markers through a Notch1-independent mechanism. Combined, these preliminary results indicate a role of EC-specific autophagy in shaping melanoma microenvironment. They also support future studies to our understanding of how autophagy modulates the EC-melanoma cell interface and the development of autophagy modulators in future anticancer treatment.

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