Majority of human cancers upregulate insulin-like growth factor receptor 1 (IGF1R), a tyrosine kinase receptor, upon chemotherapy or radiotherapy and is predicated to have poor outcome of treatment modality. Resistance to current line of therapy is major cause for failure of treatment and disease recurrence. Signalling through IGF1R has strong proliferative and anti-apoptotic effect, which argues for its importance in tumorigenesis; however understanding the significance of IGF1R upregulation during development of chemoresistance will be important. Recent study from our lab using isogenic models of chemoresistant ovarian cancer cells showed that expression of IGF1R is increased at both transcript and protein level during onset of chemoresistance. In the present study I aim to identify the transcriptional regulators for IGF1R which modulate its expression during course of chemoresistance development and investigate the role of IGF-1R signalling in maintenance of chemoresistance and pathogenesis.
Junior Research Fellow