The name of possible thesis directors can be found in the list of participating laboratories on our website: http://www.unil.ch/cancer-immunology/home/menuinst/research-groups.html
For students interested in applying through the Track 2 procedure, they are encouraged to make a list of up to 5 choices, with the understanding that not all laboratories have open positions at a given time, and they may be considered by other faculty members with similar interests.
The applications have to be sent to : firstname.lastname@example.org
Next Selection : Winter 2019-2020
Deadline for application December 10th
Interviews : end of january 2020
Open positions for the winter 2019-2020 session:
- Dr. François Kuonen/Prof. Michel Gilliet
Immunodermatology - CHUV
1 Open position
Epigenetic landscape and master regulators of non-melanoma skin cancers progression
Using high-throughput sequencing techniques (RNA-, ATAC- and CHIP-sequencing) and computational modelling, we attempt to identify the transcription factors/epigenetic regulators of non-melanoma skin cancer progression. Our main interest is the study of the epigenetic mechanisms implicated in tumor plasticity and resistance to targeted therapy, with an emphasis on translational validation in both preclinical (mouse genetic models) and clinical (human samples) models.
Immunodermatology - CHUV
1 Open position - track 2
“Dysregulation of immune pathways during targeted treatments of autoimmune diseases”
Biologic therapeutics targeting TNF and other cytokines such as IL-6, IL-17, or IL-23 have been an immense scientific and clinical advancement and revolutionized the treatment of many debilitating chronic inflammatory disorders, such as rheumatoid arthritis, inflammatory bowel disease, or psoriasis. To date, more than 2.5 million patients have been treated with anti-TNFs and three different anti-TNF agents are currently among the top 10 best-selling drugs worldwide. Nevertheless, TNF blockade has its limitations and increases susceptibility to infections and skin cancer. Surprisingly, anti-TNF agents, which are normally extremely effective in treatment of chronic inflammatory diseases, can induce also new autoimmune diseases, including lupus erythematosus (0.5% of all anti-TNF treated patients) and paradoxical psoriasis (2-5%). Anti-IL-17s can induce Crohns disease and eczema. They represent extremely important side effects in the treatment of major chronic autoimmune diseases as they potentially necessitate treatment cessation. Supported by funding from the Swiss National Science Foundation (project # 310030_156173), we have recently elucidated the underlying pathogenic mechanisms and identified that anti-TNF induced overexpression of type I interferon (IFN) drives these side effects (yin-yang of TNF and type-I IFN). Yet the exact mechanisms by which type-I IFN mediates the phenotype of paradoxical psoriasis and other autoimmune diseases remain elusive. Likewise, it remains unknown how effective anti-IL17 treatment can induce eczema in psoriasis patients.
Our laboratory has numerous in-vitro techniques and in-vivo models at hand, we have established our own mouse models and have easy access to human samples to functionally analyze the underlying pathomechanisms of these treatment side effects and the dysregulation of the various pathways induced by targeted therapies.