Project 170562
Regulatory polymorphisms in apoptosis genes and susceptibility to childhood leukemia
Regulatory polymorphisms in apoptosis genes and susceptibility to childhood leukemia
Project Information
| Study Type: | Observational Case_Control |
| Therapeutic Area: | Oncology |
| Research Theme: | Biomedical |
| Disease Area: | acute lymphoblastic leukemia |
| Data Type: | Canadian |
Institution & Funding
| Principal Investigator(s): | Sinnett, Daniel |
| Co-Investigator(s): | Roy-Gagnon, Marie-Hélène |
| Institution: | Centre hospitalier universitaire Sainte-Justine (Montréal, Québec) |
| CIHR Institute: | Genetics |
| Program: | |
| Peer Review Committee: | Cancer Progression & Therapeutics |
| Competition Year: | 2008 |
| Term: | 3 yrs 0 mth |
Abstract Summary
Acute lymphoblastic leukemia (ALL) is the most common pediatric cancer, but little is known about the cause(s) of this disease. We have shown that the origin of childhood ALL could be explained by the interaction between genetic factors and environmental exposures. Here we propose that the susceptibility (or resistance) to childhood ALL is modified by functional variations in the sequences regulating the expression (promoter) of genes coding for programmed cell death (apoptosis). This hypothesis will be tested by performing genetic studies in ALL children (cases) and healthy individuals (controls). The expected results will provide new knowledge on how genes and the mechanisms of gene regulation lead to disease susceptibility or resistance. In the long term, these findings will allow the development of ALL prevention programs for the population.
Research Characteristics
This project includes the following research characteristics:
Study Justification
"performing genetic studies in ALL children (cases) and healthy individuals (controls)"
Novelty Statement
"provide new knowledge on how genes and the mechanisms of gene regulation lead to disease susceptibility or resistance"
Methodology Innovation
investigating gene-environment interactions in childhood leukemia through regulatory polymorphism analysis