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Functional Genomics in Human Cells for Drivers of Lethal Metastatic Human Cancers

Status: 
Active
Competition: 
2015 Disruptive Innovation in Genomics Competition
Sector: 
Health
Genome Centre(s):
Ontario Genomics
Project Leader(s):
Michael Taylor (The Hospital for Sick Children (SickKids)), Rama Khokha (Princess Margaret Cancer Centre)
Fiscal Year Project Launched: 
2016-2017
Project Description: 

Phase 1 Project

Often in cancer it’s not the primary tumour that kills patients, but the spread of the cancer to other areas of the body, in a process called metastasis. This is particularly the case with two highly lethal types of cancer, medulloblastoma (MB), the most common malignant brain tumour in children, and pancreatic adenocarcinoma, the fourth leading cause of cancer deaths in Canadians. Almost 100% of children who die from medulloblastoma die from the metastases, as the primary tumour almost never comes back following therapy. Pancreatic cancer spreads very early, while lack of symptoms means many patients are not diagnosed until after metastasis has taken place. Because of this, surgery to remove the tumour is seldom a cure, while the cancer has proved relatively resistant to systemic therapies and there has been limited benefit from the use of the newer targeted agents.

Recent results from the lab of Dr. Michael Taylor of The Hospital for Sick Children have shown that the biology of the metastases is extremely different from the primary tumour. Thus it is unlikely that treatments developed to treat the primary tumour will work on the metastases. On top of this, more than 95% of current model systems focus on the primary tumour, making it very difficult to study metastatic cancer. For this project Dr. Taylor has teamed with Dr. Rama Khokha (Princess Margaret Cancer Centre) to use forward genetic screening of human cells to develop and deploy unique tools for the discovery of the drivers of metastasis. Their work is the best, and perhaps the only way to improve survival rates of Canadians with these deadly human cancers.