Väitös (patologia): MSc Meng Wang
Aika
9.6.2025 klo 15.00 - 19.00
MSc Meng Wang esittää väitöskirjansa ”Novel immune and genetic drivers of melanoma: Integrative and new preclinical models to uncover the impact of new chromosomal and tranomic changes on tumor progression and immunity” julkisesti tarkastettavaksi Turun yliopistossa maanantaina 9.6.2025 klo 15.00 (Turun yliopiston, MEDISIINA C, Osmo Järvi -sali, Kiinamyllynkatu 10, Turku).
Yleisön on mahdollista osallistua väitökseen myös etäyhteyden kautta: https://utu.zoom.us/j/63715470725 (kopioi linkki selaimeen).
Vastaväittäjänä toimii professori Roger Chammas (University of São Paulo, Brasilia) ja kustoksena apulaisprofessori Carlos Rogerio Figueiredo (Turun yliopisto). Tilaisuus on englanninkielinen. Väitöksen alana on patologia.
Väitöskirja yliopiston julkaisuarkistossa: https://www.utupub.fi/handle/10024/181189 (kopioi linkki selaimeen).
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Tiivistelmä väitöstutkimuksesta:
Melanoma is a severe form of cancer that can start in the skin or the eyes. While new treatments that activate the immune system, called immunotherapies, have improved the survival of many patients, not all respond well, and we still don’t fully understand why. My research explored the reasons behind this resistance and sought new ways to improve treatment.
To achieve this, I studied two major types of melanomas: cutaneous melanoma (on the skin) and uveal melanoma (in the eye). Using large patient datasets and an approach called integrative analysis, I investigated the genes and immune-related changes that drive tumor progression and resistance. In skin melanoma, I found that low levels of the gene ß2M and changes in CD1D, which help activate key immune cells, were linked to poor response to immunotherapy. These findings reveal how some tumors manage to escape immune detection.
In uveal melanoma, I focused on the gene BAP1, which is consistently lost in patients with the most aggressive disease. Despite its importance, no effective therapies or immune-based models exist to study BAP1’s role. To address this, I developed a new laboratory model using CRISPR gene-editing technology. This model allows us to study BAP1 loss in a system with an intact immune system and provides a much-needed tool to explore how BAP1 loss drives tumor growth and immune evasion.
By combining clinical data with experimental models, my research bridges real-world patient observations with lab-based discoveries. It lays the groundwork for more effective and personalized treatments, especially for patients with aggressive or treatment-resistant forms of melanoma.
Yleisön on mahdollista osallistua väitökseen myös etäyhteyden kautta: https://utu.zoom.us/j/63715470725 (kopioi linkki selaimeen).
Vastaväittäjänä toimii professori Roger Chammas (University of São Paulo, Brasilia) ja kustoksena apulaisprofessori Carlos Rogerio Figueiredo (Turun yliopisto). Tilaisuus on englanninkielinen. Väitöksen alana on patologia.
Väitöskirja yliopiston julkaisuarkistossa: https://www.utupub.fi/handle/10024/181189 (kopioi linkki selaimeen).
***
Tiivistelmä väitöstutkimuksesta:
Melanoma is a severe form of cancer that can start in the skin or the eyes. While new treatments that activate the immune system, called immunotherapies, have improved the survival of many patients, not all respond well, and we still don’t fully understand why. My research explored the reasons behind this resistance and sought new ways to improve treatment.
To achieve this, I studied two major types of melanomas: cutaneous melanoma (on the skin) and uveal melanoma (in the eye). Using large patient datasets and an approach called integrative analysis, I investigated the genes and immune-related changes that drive tumor progression and resistance. In skin melanoma, I found that low levels of the gene ß2M and changes in CD1D, which help activate key immune cells, were linked to poor response to immunotherapy. These findings reveal how some tumors manage to escape immune detection.
In uveal melanoma, I focused on the gene BAP1, which is consistently lost in patients with the most aggressive disease. Despite its importance, no effective therapies or immune-based models exist to study BAP1’s role. To address this, I developed a new laboratory model using CRISPR gene-editing technology. This model allows us to study BAP1 loss in a system with an intact immune system and provides a much-needed tool to explore how BAP1 loss drives tumor growth and immune evasion.
By combining clinical data with experimental models, my research bridges real-world patient observations with lab-based discoveries. It lays the groundwork for more effective and personalized treatments, especially for patients with aggressive or treatment-resistant forms of melanoma.
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