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David W Hedley, MD

Senior Scientist
Division of Applied Molecular Oncology
Ontario Cancer Institute (OCI)

Clinical Studies Resource Centre Member
Ontario Cancer Institute (OCI)

Keywords: signal transduction, drug resistance, pancreatic cancer, fluorescence microscopy, flow cytometry, molecular therapeutics, hypoxia 

Research Interests
Our main goal is to develop effective cancer treatments based on a deeper understanding of the molecular processes occurring in human cancers. The laboratory seeks to close the gap between basic cancer research and the early clinical trials programs at Princess Margaret Hospital. To this end, we have access to a wide range of exciting new anticancer agents that are just entering early human clinical trials. Areas of emphasis include the use of xenograft models including primary orthotopic implants from human cancers, and the development of analytical methods for studying complex molecular interactions at the single cell level.

We have particular expertise in the development and application of advanced methodology based on the use of flow cytometry and digital fluorescence microscopy. This technology development is done in close collaboration with members of the Physics Division, the Department of Pathology, and the STTARR Program. Areas of current interest include the effects of tumour hypoxia on survival signaling in solid tumours; the analysis of complex signaling interactions in hematological malignancies based on multiparametric flow cytometry; and the role of aberrant signaling pathways in the growth of pancreatic cancers.

In addition to using model systems based on tissue culture and human tumour xenografts, the laboratory is also involved in the analysis of samples obtained from patients on clinical trials involving molecular cancer therapeutics.

Pubmed Publications
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Selected Publications

  • Iakovlev, V., Pintilie, M., Morrison, A., Fyles, A., Hill, R.P., and Hedley, D.W. Effect of distributional heterogeneity on the analysis of tumor hypoxia based on carbonic anhydrase IX. Laboratory Investigation 87:1206-1217, 2007.

  • Pham, N-A., Tsao, M-S, Cao, P. and Hedley, DW. Dissociation of gemcitabine sensitivity and protein kinase B signaling in pancreatic ductal adenocarcinoma models. Pancreas 2007; 35:e16-26.

  • Birle, D. and Hedley DW. Suppression of the Hypoxia-Inducible Factor-1 Response in Cervical Carcinoma Xenografts by Proteasome Inhibitors. Cancer Research 2007; 67:1735-43.

  • Birle DC and Hedley DW. Signaling interactions of rapamycin combined with erlotinib in cervical carcinoma xenografts. Molecular Cancer Therapeutics 2006; 5:2494-2502.

  • Tong FK. Chow S, Hedley DW. Pharmacodynamic Monitoring of BAY 43-9006 (Sorafenib) in Phase I Clinical Trials Involving Solid Tumor and AML/MDS Patients, using Flow Cytometry to Monitor Activation of the ERK Pathway in Peripheral Blood Cells. Cytometry B 2006; 70:107-114.

  • Hedley, D.W., Nicklee, T., Moreno-Merlo, F., Pintilie, M., Fyles, A., Milosevic, M., and Hill, R. Relations Between Non-Protein Sulfydryl Levels In The Nucleus And Cytoplasm, Tumor Oxygenation, And Clinical Outcome Of Patients With Uterine Cervical Carcinoma. International Journal of Radiation Oncology, Biology, and Physics 61:137-144, 2005.

  • Yau,C.Y.F., Wheeler,J., Sutton, K., and Hedley, D.W. Inhibition of Integrin-Linked Kinase (ILK) by QLT0254 Inhibits Akt-Dependent Signaling Pathways and is Growth Inhibitory in Orthotopic Primary Pancreatic Cancer Xenografts. Cancer Research 65:1497-1504, 2005.
 
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  David  W Hedley
Mailing Address
Primary Lab
Princess Margaret Hospital
7th Floor Rm 7-111
610 University Ave
Toronto, Ontario
Canada M5G 2M9

 
Email

Phone Numbers
416.946.4501 x2911(Primary)

 
Staff and Trainees
Sue Chow
Lina Alam
Trudey Nicklee
Trevor Do
May Cheung
Mary Cao
Neesha Dhani
Jorg Schwock
Shadi Mamaghani
Joao Magalhaes
Qing Chang

   
 
 
 
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