My PhD thesis investigated the environmental and epigenetic etiologies in driving liver neoplasias in several model systems. In the model of chronic mitochondrial defect, I found that mitochondrial dysfunction stimulates Kupffer cells, resulting into cholangiolar neoplastic growth. In another model of HDAC2 deficiency, the aged knockout mice developed steatohepatitic HCC, indicative of the role of lipogenesis in tumor development. In the last model, I proved that the inflammatory micro-niche promotes malignant transformation of hepatocytes through LTbR signaling.
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My PhD thesis investigated the environmental and epigenetic etiologies in driving liver neoplasias in several model systems. In the model of chronic mitochondrial defect, I found that mitochondrial dysfunction stimulates Kupffer cells, resulting into cholangiolar neoplastic growth. In another model of HDAC2 deficiency, the aged knockout mice developed steatohepatitic HCC, indicative of the role of lipogenesis in tumor development. In the last model, I proved that the inflammatory micro-niche pro...
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