Amira webinar

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Miroslava Cuperlovic-Culf is a Research Officer with National Research Council of Canada and Adjunct Professor of Chemistry at Mount Allison University and University of New Brunswick as well as Adjunct Researcher at Atlantic Cancer Research Institute in Moncton Canada. Miroslava has worked for number of years in the application of metabolomics and transcriptomics in life sciences. She has been actively involved in the bioinformatics, computational biology and computational chemistry however she has also extensive experience and training in experimental methodologies for high throughput analysis of biological systems. Her primary interest is in the exploitation of metabolic changes in cancer for treatment and diagnostics. Miroslava authored many articles, book chapters and several patents as well as the book entitled NMR Metabolomics in Cancer Research. She lives and works in Moncton, New Brunswick, Canada.

In this webinar, Dr. Miroslava’s will talk about cancer metabolic phenotype, analysis of metabolism in cancers and the research work with her collaborators on the investigation of metabolic changes in cancer subtypes.

The session will be moderated by Dr. Amira Djebbari. Dr. Djebbari trained at The Institute for Genomic Research. She completed her post-doctoral experience at the Dana Farber Cancer Institute and Harvard School of Public Health. Dr. Djebbari is currently a scientific project manager in the Ontario Cancer Institute, Princess Margaret Hospital at the University of Toronto.

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Amira webinar

  1. 1. Cancer Metabolism Reinvention of Hallmark of Cancer Miroslava Cuperlovic-Culf, Ph.D.Senior Research Officer, National Research Council of Canada Adjunct Professor, Mount Allison Universityfrom Moncton, NB, Canada22. May, 2012
  2. 2. ALTERED METABOLISM: CAUSE or EFFECT OF CANCERCell Cancer analysis Drug discovery Tissue Diagnostic Cancer analysis Diagnostic Prognostic Organism Treatment assessment Diagnostic Risk assesment
  3. 3. BioenergeticsGenetic changes Cancerof oncogenes and metabolic BiosynthesisOncosuppressors phenotype Oxidative state Tumour microenvironment (pH, hypoxia, nutrient deprivation, autophagy)
  4. 4. CANCER METABOLIC PHENOTYPE Glucose GLUT1 Glucose NUCLEOTIDES PPP SYNTHESIS R5P GLYCOLYSIS G6P Fatty acids Cholesterol AMINO ACID FATTY ACID PEP SYNTHESIS ADP SYNTHESIS Acetyl CoA ATP Pyruvate AcetylH2CO3 CoA Citrate Citrate H+ + CO2 Lactate + H+ aKG Glutamate Amino Acids Lactate +H+ Import Fatty acids
  5. 5. AKT p53EGFR HIF1 MYC STAT3
  6. 6. SNP Alternative splicing Transcription factors Epigenetics Ability Desire miRNA; Translation kinetics Strategy Protein activation/inhibition Protein interactions ActionCuperlovic-Culf, et al. Exp Opin Mol Diagn 2008; Cuperlovic-Culf, et al. DDT 2010;Cuperlovic-Culf, NMR Metabolomics in Cancer Research. Oxford Biosciences, 2013
  7. 7. Glioblastoma multiforme the most common and most aggressive malignant primary brain tumor in humans: LN405 median survival 3months – 2 years (with treatment) BS149 U343 U373 A172 LN319 LN229 LN18 HS683Cuperlovic-Culf, et al. Jour Biol Chem 2012
  8. 8. 1 2 3 4SAM method: Tusher, et al. PNAS, 2001
  9. 9. Group 1: overexpression (red) Increased metabolitesoverexpression in groupIncreased metabolites Microarray data from: Grzmil, et al. Cancer Res, 2001, GSE15824 Wiedemeyer, et al. Cancer Cell 2008, GSE9200
  10. 10. CONCLUSIONS• Metabolic profiling (qualitative and quantitative) leads to information about tumour subtypes;• Metabolic biomarkers for tumour subtypes can be related to gene expression characteristics;
  11. 11. FUTURE• Testing of clinical samples for biomarkers of subtypes discovery and validation;• Development and testing of drug options for glioblastoma subtypes
  12. 12. Rodney Ouellette Adrian Culf Mohamed Touaibia Natalie Lefort Pier Jr. Morin David Ferguson Marc Surette Anissa Belkaid Nabil Belacel Dan Tulpan Jason HinesTHANK YOU/ MERCI
  13. 13. BREAST CANCER METABOLITE CANCER NORMAL L-Valine 73.01(1.36) 110.53(9.12) L-Leucine L-Isoleucine L-Lysine 10.31(1.36) 20.55(2.21) L-Alanine 11.62(1.54) 16.35(1.1) L-Aspartic acid 0.77(0.08) 2.65(0.71) Phenylalanine 6.06(0.96) 11.12(1.88) Tyrosine 0.25(0.12) 0.50(0.14) Glutamine 5.53(0.83) 3.44(0.81) Total Choline 13.93(5.32) 6.58(1.84) UDP-glucose 6.59(0.75) 1.63(1.63) Lactic acid 58.29(13.84) 56.47(18.19) METABOLITE IDC (ER+) AC (ER-) L-Valine 78.05(1.76) 67.98(6.10) L-Leucine L-Isoleucine Glycerol-3-phosphate 50.31(4.56) 38.27(2.12) L-Alanine 12.06(0.59) 11.17(2.05) L-Aspartic acid 0.79(0.07) 0.74(0.09) Phenylalanine 6.82(0.62) 5.23(0.51) Tyrosine 0.26(0.08) 0.24(0.16) Choline 15.02(5.01) 12.84(5.66) Lactic acid 49.2(3.19) 67.39(14.51)Cuperlovic-Culf, et al. Chem Sci (2011)

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