Breast cancer focus for new fellowship
Breast cancer focus for new fellowship
11 November 2016
Drug resistance in breast cancer will be the focus of cutting-edge genetics and the latest DNA sequencing technologies, in research funded by a new fellowship this week.
University of Auckland research fellow, Dr Francis Hunter who works at the University’s Auckland Cancer Society Research Centre, was awarded a two-year Rutherford Foundation Fellowship.
In this study, Dr Hunter will use cutting-edge genome engineering and next-generation DNA sequencing technologies to identify genes that control and predict the sensitivity and resistance to trastuzumab emtansine (T-DM1) and other HER2-targeting drugs in breast cancer.
“The ultimate goal of this research is to understand the mechanisms of resistance to T-DM1 and develop diagnostic tools to predict sensitivity,” says Dr Hunter. “This will aid in the optimal clinical use of this drug and allow for improved treatment outcomes of these high-risk breast cancers.”
He says the fellowship will allow him the freedom and security to focus on this research project and the delivery of an important new understanding of the mechanisms of resistance and sensitivity to trastuzumab emtansine in breast cancer.
“These funds will enable me to appoint a very skilled laboratory technician (Aziza Khan) to work alongside me on this project,” he says.
“As the most prestigious fellowship that I could receive at this stage of my career, I am also extremely honoured to carry the identity of the Rutherford Foundation as I develop towards full independence as a researcher.”
Breast cancer is one of the most common malignancies in New Zealand with 3000 new diagnoses and 600 deaths each year.
Tragically, this cancer especially affects women in the prime of their life (64 percent of cases are diagnosed below age 65).
“About one quarter of breast cancers are driven by amplification (increased numbers of copies) of a gene known as HER2, which stimulates the growth of tumour cells,” says Dr Hunter.
Breast cancers that test positive for HER2 amplification grow more rapidly and are more likely to metastasise (spread) and recur after treatment.
The drug trastuzumab (commonly known by its commercial name, Herceptin), works by inhibiting HER2 and hence halt the growths and spread of HER2-positive breast cancer.
“Unfortunately, a significant fraction of breast cancer eventually recurs or progresses despite being treated with trastuzumab, leading to very aggressive disease and poor prognosis,” says Dr Hunter.
In 2013, a new drug, trastuzumab emtansine (also known as T-DM1 or Kadcyla), was approved for the treatment of HER2-positive, metastatic breast cancer that has progressed after prior treatment with trastuzumab.
T-DM1 is a member of a new class of pharmaceuticals known as “antibody-drug conjugates” and is comprised of trastuzumab (which is an antibody) chemically attached to a potent cancer-killing toxin, mertansine (DM1).
The result of clinical trials demonstrates that, while T-DM1 is effective as a second-line treatment for metastatic breast cancer, some patients do not respond to the drug at all and, for others, the emergence of resistance to T-DM1 results in temporary medical benefit.
ENDS