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Amadeo Mark Parissenti

Affiliate Scientist and Principal Investigator, Health Sciences North Research Institute
Tenured Full Professor, Department of Chemistry and Biochemistry at Laurentian University 
Tenured Full Professor, Division of Medical Sciences, Northern Ontario School of Medicine 
Chief Scientific Officer, RNA Diagnostics, Inc.

Dr. Parissenti completed a Bachelor of Science in Biochemistry at the University of Guelph in 1983. In 1989 he received his Ph.D. in Biochemistry at York University in Toronto, Ontario. He conducted postdoctoral studies from 1989 to 1991 at Harvard Medical School in Boston and from 1992 to 1995 at the Banting and Best Department of Medical Research at the University of Toronto.

Currently, Dr. Parissenti is an Affiliate Scientist and Principal Investigator at the Health Sciences North Research Institute (HSNRI), as well as a full professor at Laurentian University and the Northern Ontario School of Medicine.

  • 1999-Present American Association for Cancer Research, Active Member
  • 2000-Present Member, Tumour Banking and Correlative Science Committee, Canadian Cancer Trials Group
  • 2003-Present Member, Breast Correlative Sciences Committee, Canadian Cancer Trials Group
  • 2008-2012 Member, Cancer Progression and Therapeutics Grants Review Panel, Canadian Institutes for Health Research (CIHR)
  • 2009-Present Member, Student Appeals Committee, Department of Chemistry and Biochemistry, Laurentian University
  • 2009-2011 Member, Faculty Development Committee and Faculty Retreat Working Group, Northern Ontario School of Medicine
  • 2009-Present Ad Hoc Reviewer, Breast Cancer Research and Treatment, Biochimica Biophysica Acta, Biochemical Journal, BMC Cancer, PLoS ONE, Gene, Future
  • Medicine, Experimental Cell Research, Springer PLUS, Molecular Cancer Therapeutics, British Journal of Cancer
  • 2008 Member, Innovation and Commercialization Group, NORCAT, Sudbury
  • 2010 Member, International Editorial Advisory Board, Current
  • Pharmacogenomics and Personalized Medicine – Journal

  • 2011 Best Intellectual Property Award, TiE Quest Business Competition, Toronto, Ontario
  • 2011 Merit Salary Increment for Research Performance, Laurentian University
  • 2008 Ontario Partnership for Innovation and Commercialization - Proposal "Method of Using RNA Integrity to Measure Patient Response to Chemotherapy"
  • 2003 Merit Salary Increment for Research Performance, Laurentian University
  • 2002 Premier's Research Excellence Award Value: $150,000
  • 1992-95 Canadian Cystic Fibrosis Foundation Postdoctoral Fellowship 
  • 1989-91 Harvard Medical School Fellowship Value: $21,000 US

  • US Patent Application No: 2016/0077,051*
  • US Patent Application No: 2015/0315,656*
  • Methods and Kits for Monitoring Response to Radiation Therapies in Cancer
  • US Patent Application No: 2015/0154,350*
  • US Patent Application No: 2014/0287,063*
    US Patent Application No: 2014/0274,927*
  • TNF-Related Biomarkers For Assessing Cancer Cell Response To Treatment With Taxane And/Or Anthracycline Drugs
  • WO Patent No: 2015048887*
  • WIPO Patent Application WO/2005/052184*
  • US Patent No: 7,371,780*
  • Use of calphostin C to treat drug-resistant tumor cells

*Only unique patents are listed. In several instances the above patents were submitted and granted in many jurisdictions.


Dr. Parissenti’s research specializes in monitoring the effectiveness of cancer treatments in cancer patients by measuring the ability of chemotherapy regimens or radiation therapy to induce the degradation of ribosomal RNA in patient tumours. The phenomenon is called RNA disruption and the test that he and his colleagues have developed is called the RNA Disruption Assay or RDA. His research findings suggest that patients with tumours exhibiting a high RNA disruption score are strong responders to chemotherapy and experience high disease-free survival after treatment. In contrast, patients with a low tumour RNA disruption score are non-responders, often with progression of their disease. Dr. Parissenti and the company now bringing the test to cancer treatment hospitals worldwide (RNA Diagnostics, Inc.) believe that non-responder identified by RDA early in treatment can be spared the toxic side effects of the ineffective treatment regimen and quickly switched to alternate treatments, such as surgery, radiation therapy, or other drugs. This is improving patient’s experiences through their cancer journeys. 

Dr. Parissenti and his team are also looking at how the human body and tumours within it modify and inactivate chemotherapy drugs. Other researchers have found that a certain class of chemotherapy drugs called anthracyclines are modified and inactivated by protein molecules in the liver called “aldoketoreductases” (AKRs), which add a “hydroxyl group” to anthracyclines.  Interestingly, this modification of anthracyclines makes it much more toxic to the heart. Dr. Parissenti’s research group has discovered that tumour cells resistant to anthracyclines exhibit high AKR levels. Interestingly, the group has also found that a naturally occurring AKR inhibitory compound (beta-cholanic acid) restores anthracycline toxicity in anthracycline-resistant cells. They are currently examining the mechanism for this and whether this may have utility in cancer patients.

Dr. Parissenti and his research group have also discovered that a variety of chemotherapy agents induce the production of a cytokine hormone called tumour necrosis factor alpha (or TNF alpha).   This factor when produced in tumour cells causes them to die by a process called “apoptosis”. Interestingly, tumour cells resistant to chemotherapy drugs called taxanes exhibit a reduced ability to produce TNF alpha. Recent data from Dr. Parissenti’s lab indicate that as tumour cells acquire resistance to chemotherapy drugs, they also produce a variety of other cytokines which help circumvent chemotherapy drug action. The goal in the future is to uncover mechanisms to re-establish TNF alpha production in order to induce the death of drug-resistant tumour cells.


  • 2016-2017 Mitacs Accelerate Program (Federal Government)
  • 2015-2017 Northern Cancer Foundation (Local Foundation)
  • 2015-2017 Northern Ontario Heritage Fund Corporation
  • 2015-2017 Industrial Research Assistance Program (Federal)
  • 2015-2018 MaRS EXCITE Program (Provincial)

  • Narendrula R, MIspel-Beyer K, Guo B, Parissenti AM, Pritzker LB, Pritzker K, Masilamani T, Wang X, and Lanner C. (2016) RNA disruption is associated with response to multiple classes of chemotherapy drugs in tumor cells. BMC Cancer. 16(1): 146
  • Trudeau ME, Chapman JA, Guo B, Clemons MJ, Dent RA, Jong RA, Kahn HJ, Pritchard KI, Han L, O'Brien P, Shepherd LE, and Parissenti AM. (2015). A phase I/II trial of epirubicin and docetaxel in locally advanced breast cancer (LABC) on 2-weekly or 3-weekly schedules: NCIC CTG MA.22.SpringerPlus. 4:631.
  • Edwardson DW, Narendrula R, Chewchuk S, Mispel-Beyer K, Mapletoft JPJ, and Parissenti AM. (2015). Role of Drug Metabolism in the Cytotoxicity and Clinical Efficacy of Anthracyclines.Current Drug Metabolism. 16(6): 412-426.
  • Parissenti, AM, Guo B, Pritzker LB, Pritzker KPH, Wang X, Zhu M, Shepherd LE, and Trudeau ME. (2015). Tumor RNA disruption predicts survival benefit from breast cancer chemotherapy.Breast Cancer Research and Treatment. 153(1): 135-144.
  • Pritzker K, Pritzker L, Generali D, Bottini A, Cappelletti MR, Guo B, Parissenti, AM, and Trudeau M. (2015). RNA Disruption and Drug Response in Breast Cancer Primary Systemic Therapy.Journal of the National Cancer Institute Monographs. 2015(51): 76-80.
  • Sprowl JA, Reed K, Armstrong SR, Lanner C, Guo B, Kalatskaya I, Stein L, Hembruff SL, Tam A, and Parissenti AM. (2012). Alterations in tumor necrosis factor signaling pathways are associated with cytotoxicity and resistance to taxanes: a study in isogenic resistant tumor cells. Breast Cancer Research. 14(1): 1-18.
  • Holleman A, Chung I, Olsen RR, Kwak B, Mizokami A, Saijo N, Parissenti A, Duan Z, Voest EE, and Zetter BR.(2011). Mir-135a contributes to paclitaxel resistance in tumor cells both in vitro and in vivo. Oncogene. 30(43): 4386-4398.
  • Reed K, Hembruff SL, Sprowl JA, and Parissenti AM.(2010). The temporal relationship between ABCB1 promoter hypomethylation, ABCB1 expression and acquisition of drug resistance. The Pharmacogenomics Journal. 10(6): 489-504.
  • Parissenti AM, Chapman JA, Kahn HJ, Guo B, Han L, O'Brien P, Clemons MP, Jong R, Dent R, Fitzgerald B, Pritchard KI, Shepherd LE, and Trudeau ME. (2010). Association of low tumor RNA integrity with response to chemotherapy in breast cancer patients. Breast Cancer Research and Treatment. 119(2): 347-56.
  • Veitch ZW, Guo B, Hembruff SL, Bewick AJ, Heibein AD, Eng J, Cull S, Maclean DA, and Parissenti A. (2009). Induction of 1C aldoketoreductases and other drug dose-dependent genes upon acquisition of anthracycline resistance. Pharmacogenetics and Genomics. 19(6): 477-488.
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