Research Projects

Understanding the molecular functions of Neat1 in pancreatic cancer progression

ncRNAs have been shown to play a role in tumor suppression and tumor initiation in different types of cancer. During my postdoctoral research, I leveraged p53 ChIP-seq and RNA-seq datasets to identify a new p53-regulated ncRNA named Neat1. In this study, I demonstrated that Neat1 blocks transformation of pancreatic acinar and ductal cells into premalignant lesions. We are now investigating the mechanisms by which Neat1 controls the fate of pancreatic cells.

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The impact of p53 loss and Kras mutation on coding and non-coding genes associated with pancreatic cancer development

Pancreatic cancer is a deadly disease with a less than 5-year survival rate. In pancreatic ductal adenocarcinoma (PDAC), an activating mutation in the Kras proto-oncogene drives the formation preneoplastic lesions named pancreatic intraepithelial neoplasias (PanINs). Subsequently, the progression from PanINs to metastatic PDAC is linked to the loss of p53. We are studying the impact of early mutations in the biology of pancreatic cells, aiming to identify key steps involved in tumor initiation.

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