Research Assistant

Job Description

Triple-negative breast cancer (TNBC) is a heterogeneous type of breast cancer lacking estrogen receptor (ER), progesterone receptor (PR), and human epithelial growth factor receptor 2 (HER2) expression. The high heterogeneity of TNBC has been widely suggested as the reason for poor responses to targeted therapies. While changes in the coding and regulatory genome have been studied in detail, how 40% of the genome comprising the retrotransposable elements (REs) might impact the biology of TNBC is unknown. The aberrant activation of REs and their contribution to oncogenesis of solid tumours have been recently investigated. However, studying the oncogenic and immunogenic roles of REs in TNBC is lagging mainly because of the heterogeneity of this disorder. 

Our central hypothesis is that ectopic transcriptional activation of REs in different subtypes of TNBC leads to significant changes in expression of specific genes, a subset of which may play a direct role in tumorigenesis of this malignancy. To address this hypothesis, We need to functionally validate predicted oncogenic and immunogenic REs through the specific aims:

1) Validation of prioritized oncogenic RE-derived chimeric transcripts 

2) Immunopeptidome validation of high-affinity scoring RE peptides

BSc
MSc

Triple-negative breast cancer (TNBC) is a heterogeneous type of breast cancer lacking estrogen receptor (ER), progesterone receptor (PR), and human epithelial growth factor receptor 2 (HER2) expression. The high heterogeneity of TNBC has been widely suggested as the reason for poor responses to targeted therapies. While changes in the coding and regulatory genome have been studied in detail, how 40% of the genome comprising the retrotransposable elements (REs) might impact the biology of TNBC is unknown. The aberrant activation of REs and their contribution to oncogenesis of solid tumours have been recently investigated. However, studying the oncogenic and immunogenic roles of REs in TNBC is lagging mainly because of the heterogeneity of this disorder. 

Our central hypothesis is that ectopic transcriptional activation of REs in different subtypes of TNBC leads to significant changes in expression of specific genes, a subset of which may play a direct role in tumorigenesis of this malignancy. To address this hypothesis, We need to functionally validate predicted oncogenic and immunogenic REs through the specific aims:

1) Validation of prioritized oncogenic RE-derived chimeric transcripts 

2) Immunopeptidome validation of high-affinity scoring RE peptides