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  • Dr. Thomas Pulinilkunnil, PhD


Assistant Professor, Dept. of Biochemistry, Faculty of Medicine, Dalhousie University, Dalhousie Medicine New Brunswick
Operational Director- Dal Med NB Research


Adjunct Professor University of New Brunswick

Research Interests:

Energy metabolism, proteotoxicity, autophagy, lysosome, fatty acids, cardiotoxicity, Anti-cancer drugs

• Lysosomal autophagy and proteotoxicity in cancer biology and therapeutics
• Role of energy metabolism in cancer pathology
• Pathophysiology of anti-cancer therapeutics

Reprogrammed energetics and metabolism is an emerging hallmark of cancer cells. Indeed, altered mitochondrial fuel metabolism contributes to oncogenic mutations which in turn influences cellular signaling and function. Numerous oncogenic processes that are resistant to chemotherapeutics are found to exhibit features of intermittent oxygen and nutrient deprivation, mitochondrial stress, abnormal cell growth and suppressed cellular death. Recent studies have shown that abnormalities in cellular metabolism augment autophagy to facilitate cancer cells to precipitously adapt to environmental stressors by sustaining uninterrupted proliferation thereby evading demise by radiation and/or chemotherapy. Our laboratory is currently elucidating the mechanism by which tumor cell metabolism signals changes in lysosomal autophagy and mechanisms by which this signaling could influence the outcomes of treating cancer. By specifically examining the cross talk between mitochondria and lysosome we hope to uncover novel biochemical pathways that could be targeted selectively to render cancer cells susceptible to first line cancer treatment. Cancer progression is also secondary to interruptions in cancer treatment given the acute and chronic toxicity of chemotherapeutics. The second arm of my research program focuses towards understanding the toxic mechanisms of Anthracycline-containing chemotherapeutics such as doxorubicin (DXR) and its clinical manifestations to improve patient’s ability to regain normalcy following anti-cancer treatment.

Involvement with BHCRI to date:

Dr. Pulinilkunnil is a BHCRI Associate Member.


(506) 636-6973




DMNB, 100 Tucker Park Road, PO Box 5050, Saint John E2L 4L5


PUBLISHED (My current h-index is 22 as assessed by web of science)

Zhang D, Wang F, Lal N, Chiu A, Wan A, Jia J, Bierende D, Flibotte S, Sinha S, Asadi A, Hu X, Taghizadeh F, Pulinilkunnil T, Nislow C, Vlodavsky I, Johnson J, Kieffer T, Hussein B, Rodrigues B. (2017). Heparanase overexpression induces glucagon resistance and protects animals from chemically-induced diabetes. Diabetes. 66(1): 45-57.

Kennedy K, Trivedi P, Pulinilkunnil T. (2017). Revisiting Cardiomyocyte Metabolism in Health and Disease. Inter. J. Cardiol. (Submitted)

D’Souza K, Kershaw E, Pulinilkunnil T, Kienesberger P. (2017). Autotaxin is regulated by glucose and insulin in adipocytes. Endocrinology (Accepted).

Slade L, Cowie A, Martyniuk CJ, Kienesberger PC, Pulinilkunnil T. (2017). Dieldrin augments mTOR signaling and inhibits lysosomal acidification in the adult zebrafish heart (Danio rerio). J. Pharmacol. Exp. Ther. (Submitted)

Trivedi P, Bartlett J, Kienesberger PC, Pulinilkunnil T. (2016). Glucolipotoxicity diminishes cardiomyocyte TFEB and inhibits lysosomal autophagy during obesity and diabetes. BBA-Cell. Mol. Biol. Lipids. 1861(12 Pt A):1893-1910.

Bartlett J, Trivedi P, Pulinilkunnil, T. (2016). Doxorubicin cardiomyopathy and autophagy: Garbage in but no garbage out. J. Mol. Cell. Cardiol. (Accepted).  

Bartlett, J., Trivedi, P., Yueng, P., Kienesberger, P., & Pulinilkunnil, T. (2016). Doxorubicin Impairs Cardiomyocyte Viability by Suppressing Transcription Factor EB Expression and Disrupting Lysosomal Autophagy. Biochem. J. 473(21):3769-3789.

Schoiswohl G, Stefanovic-Racic M, Menke M, Wills R, Surlow B, Basantani M, Sitnick M, Cai L, Yazbeck C, Stolz D, Pulinilkunnil T, O’Doherty R, Kershaw E. (2015). Impact of reduced ATGL-mediated adipocyte lipolysis on obesity-associated insulin resistance and inflammation in male mice. Endocrinology. 156(10): 3610.

O’Neill H, Lally J, Galic S, Pulinilkunnil T, Ford R, Holloway G, Dyck J, van Denderen B, Kemp B, Steinberg G. (2015). Skeletal muscle AMPK and ACC2 S212 phosphorylation is not required for the control of fatty acidoxidation during exercise. Physiol. Rep. 3(7): e12444.

Dube, J., Sitnick, M., Schoiswohl, G., Wills, R., Basantani, M., Cai, L., Pulinilkunnil, T., Kershaw, E. (2015). Adipose triglyceride lipase (ATGL) deletion from adipocytes, but not skeletal myocytes, impairs acute exercise performance in mice. AJP- Endocrinol. Metabol. 308(10):E879-90

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