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Targeting cell cycle and apoptosis mediators in ALK+ lung cancer

A postgraduate research opportunity at the University of Otago.

Details

Close date
Wednesday, 15 January 2020
Academic background
Sciences, Health Sciences
Host campus
Dunedin
Location
On-campus
Qualifications
PhD, Master’s
Department
Pharmacology and Toxicology
Supervisor
Associate Professor John Ashton

Overview

In recent decades dramatic advances have been made in treating “oncogene dominant” cancers. These are cancers where a particular protein drives the cancer, where blocking the protein can kill the cancer cells. Cancers of this type are now treated with specific inhibitors across a range of different cancers, from breast cancer to melanoma. A recent advance has come in lung cancer, where the mutated ALK receptor has been found to drive the cancer in up to 8% of cases, i.e., over 100 people in NZ a year alone. ALK inhibitors can now give such patients dramatic responses, regressing the tumour and allowing quality of life previously unattainable. However, the effect is temporary, as within several years the cancer evolves resistance to the drugs. Our research has identified over-activation of the ERK pathway as a mechanism of ALK inhibitor resistance, which in turn regulates apoptosis and DNA synthesis. We have further identified BIM and cyclin D1 as mediators of this ERK effect. Both of these are “druggable targets” and student projects would involve investigating whether drugs that modulate BIM and/or cyclin D1 for their ability to overcome ALK inhibitor resistance in lung cancer cells. This work ultimately aims to find drug combination strategies that could help prolong the lives of patients with oncogene dominant cancer of all types.

Contact

Associate Professor John Ashton
Tel   +64 3 479 3040
Email   john.ashton@otago.ac.nz