Major Research Interests
One of the major clinical obstacles in the treatment of PDAC is the ability of these tumor cells to metastasize and develop resistance toward standard chemotherapy. Cancer metastasis requires Epithelial-Mesenchymal Transition (EMT), a process accompanied by acquisition of stem cell-like properties in disseminating cells. Of clinical significance, in solid tumors cancer stem cells (CSCs) have been proposed to play a critical role in tumor progression and are considered as a cause of tumor recurrence and resistance to conventional therapy. We have shown that tumor microenvironment influences the transcription factor (TF) networking in the pancreatic cell which determine the aggressive behaviour of tumor cells from non-invasive towards more invasive and metastatic state. Increasing evidence suggests that the tumor microenvironment reconstructs the transcriptional networking which is linked to the squamous or quasi-mesenchymal subtype of PDAC, and is associated with EMT, invasion or stemness properties. The goal of our research work is the identification of novel chromatin regulators and key TFs, which maintain the mesenchymal behaviour, stem cell-like state and drug resistance properties in pancreatic cancer.
Representative images show the mutually exclusive pattern of E-cadherin and Sox2 in murine-PDAC progression.
Model shows that the tumor microenvironment reconstructs the transcriptional network that eventually determine the functional identities of PDAC