QPCR array-based profiling of primary glioblastoma multiforme tumours
Autophagy is an important homeostatic process, whereby cellular proteins and organelles are digested, and the metabolites recycled to maintain cell viability under conditions of stress (including hypoxia and nutrient deprivation, which feature in solid tumours). The role of autophagy in glioma is yet to be fully explored. We hypothesize that the cytoprotective role of autophagy may be an important mechanism underlying treatment resistance. This study will profile components of the autophagy signalling pathway in primary GBM tumours, with the aim of identifying novel targets to sensitize patients to therapy.
In the context of cancer, autophagy can be regarded as a double-edged sword. Components of this pathway have been shown to act as tumour suppressors. For example, Beclin 1 (an inducer of autophagy) is deleted in 40% of prostate cancers, 50% of breast cancers and 75% of ovarian cancers. In contrast, tumour cells may also exploit autophagy as a survival mechanism. A range of therapies been shown to induce "pro-survival" or cytoprotective autophagy, including radiation, chemotherapy, histone deacetylase inhibitors, TNFα, IFNγ, imatinib, rapamycin and tamoxifen. It has also been shown that severely stressed cancer cells can shrink via autophagy to a state of reversible dormancy. We hypothesize that inhibition of pro-survival autophagy may increase the efficacy of current therapeutic agents.
Want to find out more?
Contact us to find out what’s involved in applying for a PhD.
Contact Research Expert to find out more about participating in this opportunity.
Browse for other opportunities within the North Shore - Kolling Institute of Medical Research .
The opportunity ID for this research opportunity is: 1485
Other opportunities with Dr Nicole Parker