Research
Neuroblastoma is an “orphan disease,” meaning that no pharmaceutical has adopted it to find a cure. There simply aren’t enough kids with the disease to make it profitable for them to spend the roughly $1 billion required to get new treatment to the marketplace.
So it’s left to neuroblastoma families to save their own kids.
In 2001, the Birrell family started The James Fund For Neuroblastoma Research to raise money for research which would find treatment to save 7 year old James. Because they were in a race against the clock, they created a system to “fast track” their discoveries.
They raised funds for one year “seed grants”, to test new ideas about neuroblastoma which had never been explored before. Those funds were immediately put to use, with the researcher on the job within weeks. At the end of the year, any promising results were taken to big granting agencies which often funded development of those ideas over the next few years.
Meanwhile, James Fund supporters were raising funds for the next seed grant.
Since 2001, The James Fund has raised $4.5 Million dollars and “leveraged” another $5 Million in matching funds from granting agencies. We have funded 46 projects in 8 countries. Our fast-track research model has contributed an impressive amount of data to the world’s knowledge about neuroblastoma.
And it has created a model that is now emulated throughout Canada and the world.
It is this innovative approach which has awarded James Fund researchers the top neuroblastoma research awarded in the world, for their discovery of the neuroblastoma stem cell. It is why James’ own doctor is representing Canada on several prestigious international committees on neuroblastoma treatment.
The James Fund has empowered neuroblastoma families across Canada to join hands under our umbrella. We are one of the best hopes neuroblastoma families have of saving their child.
We have worked extremely hard and have an impressive track record. We have made huge personal sacrifices, and have overcome some difficult obstacles.
And we’re not giving up. But we need your help.
Below are some select studies of research. Please note that we are updating this part of the site, and newer studies will be added shortly.
Some of the following are PDF documents and all will open in a new window.
Published Works
2005:
- Das, Bikul, Yeger, Herman, Tsuchida, Rika, Torkin, Risa, Gee, Matthew F.W., Thorner, Paul S., Shibuya, Masabumi,
Malkin, David, Baruchel, Sylvain. A
Hypoxia-Driven Vascular Endothelial Growth Factor/Flt1 Autocrine Loop Interacts
with Hypoxia-Inducible Factor-1{alpha} through Mitogen-Activated Protein Kinase/Extracellular Signal-Regulated
Kinase 1/2 Pathway in Neuroblastoma. Cancer Res 2005 65: 7267-7275. - Lavoie, JF, LeSauteur, L., Kohn, J., Wong, J., Furtoss, O., Thiele, C.J., Miller, F.D., and Kapaln, D.R.
TrkA Induces Apoptosis of Neuroblastoma
Cells and Does So via a p53-dependent Mechanism. J. Biol. Chem. 2005 280: 29199-29207. - Henry K. Teng, Kenneth K. Teng, Ramee Lee, Saundrene Wright, Seema Tevar, Ramiro D. Almeida, Pouneh
Kermani, Risa Torkin, Zhe-Yu Chen, Francis S. Lee, Rosemary T. Kraemer, Anders Nykjaer, and Barbara
L. Hempstead. ProBDNF
Induces Neuronal Apoptosis via Activation of a Receptor Complex of p75NTR and Sortilin. J. Neurosci. 25:
5455-5463; doi:10.1523/JNEUROSCI.5123-04.2005. - Torkin, R., Lavoie, JF., Kaplan, D.R., and Yeger, H. Induction
of caspase-dependent, p53-mediated apoptosis by apigenin in human neuroblastoma. Molecular Cancer
Therapeutics. January 2005 4:1-11.
2004:
- He, Ying; Das, Bikul; Baruchel, Sylvain; Kumar, Piyush; Wiebe, Leonard; Reilly, Raymond M.
Meta-[123I]iodobenzylguanidine
is selectively radiotoxic to neuroblastoma cells at concentrations that spare cells of haematopoietic lineage. Nuclear
Medicine Communications: November 2004 – Volume 25 – Issue 11 – pp 1125-1130.
2003:
- Beheshti B, Braude I, Marrano P, Thorner P, Zielenska M, Squire JA. Chromosomal
localization of DNA amplifications in neuroblastoma tumors using cDNA microarray comparative genomic
hybridization. Neoplasia. 2003 January; 5(1): 53–62.
