My interest started because I wanted to understand why different patients respond differently to chemotherapy, and why chemotherapy works but then the tumour grows back. Ovarian cancer is a great example of this–most patients respond initially to treatment but, after 6 months, the tumour grows back. I wanted to study why these patients respond differently and what we can do to make treatment work better.
At the time that I started my PhD, leukemias were thought to be unique because they featured a type of mutation called a “chromosomal translocation”. This is when two chromosomes break and reattach to the other broken chromosome. This affects the genes at the breakpoints, and by identifying these genes you could often pinpoint a new mechanism of leukemia. Nowadays, this is redundant because there are much more efficient means of finding new mutations (because of advances in technology), and also because chromosomal translocations have since been discovered in other cancers. But at the time I liked the idea of using the breakpoint as a “signpost” to the disease-causing genes, and that’s why I picked leukemia as a disease to research.
My interest started because I wanted to understand why different patients respond differently to chemotherapy, and why chemotherapy works but then the tumour grows back. Ovarian cancer is a great example of this–most patients respond initially to treatment but, after 6 months, the tumour grows back. I wanted to study why these patients respond differently and what we can do to make treatment work better.
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At the time that I started my PhD, leukemias were thought to be unique because they featured a type of mutation called a “chromosomal translocation”. This is when two chromosomes break and reattach to the other broken chromosome. This affects the genes at the breakpoints, and by identifying these genes you could often pinpoint a new mechanism of leukemia. Nowadays, this is redundant because there are much more efficient means of finding new mutations (because of advances in technology), and also because chromosomal translocations have since been discovered in other cancers. But at the time I liked the idea of using the breakpoint as a “signpost” to the disease-causing genes, and that’s why I picked leukemia as a disease to research.
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