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Population-based Genetics of Non-Hodgkin Lymphoma

The focus of this research is to discover the inherited genetic factors that influence susceptibility to Non-Hodkin Lymphoma and other related Lymphoid Cancers within families.

Project Leaders Angela Brooks-Wilson
Project Co-Investigators Joseph Connors , Randy Gascoyne , John J. Spinelli
Involved Organizations
Canada's Michael Smith Genome Science Centre
British Columbia Cancer Agency
Simon Fraser University
Funding Agencies
Canadian Institutes of Health Research

Example family tree with Lymphoid cancers indicated as solid shading.

Overview

Cancer is now responsible for 1 million potential years of life lost in Canada, and costs Canadians 14.2 billion dollars/year in direct and indirect costs. The incidence of non-Hodgkin lymphoma (NHL) has nearly doubled in the last 35 years, and it is now the 5th most common malignancy in Canada. NHL cases likely arise in a genetically susceptible part of the population, potentially in individuals who have faulty DNA repair mechanisms. Methods to prevent and avoid NHL and other cancers, for example by means of screening for at-risk individuals, will be of increasing importance for the Canadian healthcare system.

Programmed cell death, or apoptosis, is a natural mechanism used to remove damaged cells from the body before they can become cancerous. This process of detection and repair of DNA damage carried out by our bodies is intimately connected with the cellular controls that trigger apoptosis. If cells that sustain DNA damage fail to undergo apoptosis, they may incur additional mutations that take them along the road to becoming cancerous. Non-Hodgkin lymphoma (NHL) includes a group of tumours of immune cells. They have in common a tendency to show a type of DNA damage called a translocation, in which two chromosomes become abnormally fused together. Translocations are generally found next to specific genes related to development of lymphoma, and result in altered gene expression and aberrant lymphoid cell growth. We reason that two types of failure are likely to have happened in such cells: 1) failure to repair DNA damage properly, and 2) failure to flag the cell as damaged and trigger apoptosis. Previously, we studied the relationship between genetic variation in six key DNA repair genes and NHL. In this work, we will focus on one DNA repair gene we found to be associated with NHL, and will also assess whether genetic variation in any of 15 apoptosis genes contributes to NHL risk. We will be working with an international consortium for lymphoma research to further confirm our findings. The identification of genetic factors that predispose individuals to NHL may be useful in the development of diagnostic tests to help identify those at-risk for this cancer, leading to early diagnosis and treatment, as well as the identification of new drugs.

Recent Publications

 

Contact Information

For all project related inquires please contact us.

Stephanie McInnis, Project Coordinator
Genome Sciences Centre, BC Cancer Agency
Email: smcinnis@bcgsc.ca
Phone: 604-675-8000 ext. 7965
Fax: 604-675-8178