NAME
POSITION TITLE
Priya Weerasinghe, MD, MSc, PhD
Assistant Professor
Co-Director, Morphoproteomic Research Laboratory
Department of Pathology and Laboratory Medicine
The University of Texas Houston Medical School
6431 Fannin, MSB 2.408, Houston, TX 77030
Tel: (713) 500 5385
Fax: (713) 500 0730
Email: Priya.Weerasinghe@uth.tmc.edu
EDUCATION/TRAINING
Institution and location
Degree
Year(s) and
Months
Field of study
Vitebsk Medical Institute, Vitebsk, Belarus
University of Toronto, Toronto, Canada
Memorial University of Newfoundland, St. John’s,
NF, Canada
Base Hospital Matale, Matale, Sri Lanka
M.D.
M.Sc.
Ph.D.
6/90
5/96
5/02
Internship
2/91-3/92
Medicine
Pharmacology
Cancer Research/
Tumor Immunology
Medicine and OB GYN
Post
Internship
Postdoctoral
Training
Postdoctoral
Training
Postdoctoral
Training
3/92-9/93
Pediatrics
3/01-1/03
Carcinogenesis
1/03-6/04
Immunology
6/04-3/08
Pharmacology/
Cancer Research
General Hospital Ratnapura, Ratnapura, Sri
Lanka
Harvard University and Massachusetts Institute of
Technology, Boston, MA, USA
National Jewish Medical and Research Center,
Denver, CO, USA
Baylor College of Medicine, Houston, TX, USA
RESEARCH
(1) Signaling pathways of oncosis
It is now known that there are at least two basic patterns of cell injury progressing to death: cell
injury with swelling and karryolysis, known as oncosis, and cell injury with shrinkage and
karryorhexis, known as apoptosis.
Recent studies have explored the relationship of myocardial ischemic injury to the major modes
of cell death, and it appears that myocardial ischemic and reperfusion injury of cardiomyocytes
involves the pathways of apoptosis and oncosis.
Studies pertaining to the relationship between cell injury and death during ischemia indicate that
apoptotic and oncotic mechanisms can proceed together leading to a hybrid form of myocardial
ischemic cell death with oncotic mechanisms and morphology dominating the end stage of
irreversible injury.
We have developed a cell model system, closely resembling this hybrid form of myocardial
ischemic cell death, to unravel the molecular mechanisms of oncosis, in comparison to
apoptosis in murine ventricular cardiomyocytes. Dose-response studies have consistently
shown that cardiomyocytes, when exposed to sanguinarine (a benzophenanthridine alkaloid
biosynthesized from phenylalanine in plants of the papaveraceae family) at lower concentrations
displayed the classic morphology of apoptosis in over 75% of cells and at higher concentrations
displayed the characteristic morphology of oncosis in over 90% of cells.
Tumor cell killing by anticancer agents are also known to involve the major modes of cell death.
Our findings indicate several tumor cell lines including leukemia (K562), lymphoma (CEM-VLB
and CEM-T4), prostate (DU145 and LNCap), breast (MDA-MB-435 and MCF-7), cervical and
neuroblastoma undergo this classic pattern of bimodal cell death, when exposed to
sanguinarine.
Using our cell model system, coupled with a combination of DNA microarray and multiblot
protein detection technics for high throughput screening and siRNA inhibition and forced
expression technics for more targeted analysis of candidate genes, we are studying the kinetics
of the molecular expression profile of oncosis.
This study has the potential to reveal novel oncosis-related molecules that will serve as drug
targets and biomarkers facilitating the design of more effective diagnostic and treatment
strategies.
(2) Non-toxic substances and biological response modifying agents for the prevention
and treatment of disease
Natural products have greatly influenced the development of antitumor agents. Of the nearly
121 prescription drugs in use today for cancer treatment, 90 are derived from plants. Between
1981 and 2002, 48 out of 65 drugs approved for cancer treatment were natural products, based
on natural products, or mimicked natural products in one form or another.
Our laboratory is investigating the molecular signaling mechanisms and immunomodulatory
properties of natural compounds and herbal extracts including sanguinarine, salinomycin,
curcumin and metformin.
The rediscovery of natural compounds in the light of modern molecular medicine is conducted
with a view to identifying the most promising agents for the prevention and treatment of disease
and elucidating critical drug targets and biomarkers.
TEACHING
2014-pres
Lecturer, Pathology, University of Texas Houston (UTH) Medical School.
2012-pres
Facilitator, Problem Based Learning (PBL), UTH Medical School.
2008-2013
Lecturer, Medical Immunology, UTH Medical School.
2008-2009
Lecturer, Histology, UTH Dental School.
.
HONORS
2013-2014
Dean’s Teaching Excellence Award, UTH Medical School.
2013-2014
Curriculum Development Committee, UTH Medical School.
2012-2014
Mentor for the Paul E. Strandjord Young Investigator Award from the Academy of
Clinical Physicians and Scientists (ACLPS).
2010-2011
Teaching Excellence in Medical Immunology, Department of Pathology, UTH
Medical School.
2010-2011
Chair, Committee for the Status of Women (CSW), University of Texas Health
Sciences Center (UTHSC) at Houston.
SELECTED PUBLICATIONS
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Weerasinghe, P., Hallock, S., Brown, R., Loose, D.S., and Buja, L.M., (2013). A Model
for Cardiomyocyte Cell Death: Insights into Mechanisms of Oncosis. Exp. Mol. Pathol.,
94: 289-300.
Weerasinghe, P. and Buja, L.M. (2012). Oncosis: An important nonapoptotic mode of
cell death. Exp. Mol. Pathol. 93: 302-308.
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Chi H., Luo A. Z., Weerasinghe P. and Brown R.E. (2010) Surafenib downregulates
ERK/Akt and STAT3 survival pathways and induces apoptosis in a human
neuroblastoma cell line. Int. J. Clin Exp. Pathol, 3(4): 408-415.
Guan, Y., Ramasamy-Reddy, K., Zhu, Q., Li, Y., Lee, K., Weerasinghe, P., Prchal, J.,
Semenza, G.L. and Jing, N. (2009). G-rich Oligonucleotides Inhibit HIF-1alpha and HIF2alpha and Block Tumor Growth. Mol Ther., 18(1):188-97.
Buja, L.M and Weerasinghe, p. (2009). Unresolved issues in myocardial reperfusion
injury. Cardiovasc Pathol. 19(1):29-35.
Weerasinghe, P., Li, Y., Guan, Y., Zhang, R., Tweardy, D.J. and Jing, N. (2008).
T40214/PEI complex: A potent therapeutics for prostate cancer that targets STAT3
Signaling. Prostate, 68(13):1430-42.
Priya Weerasinghe, Gabriela E. Garcia, Ping Yuan, Lili Feng, Li Mao and Naijie Jing
(2007). STAT3 is a critical therapeutic target for non-small cell lung cancer (NSCLC) and
GQ-ODN, as a STAT3 inhibitor, represents a promising treatment in NSCLC. Int. J.
Oncol., 31(1):129-36.
Aggarwal, B.B., Ichikawa, H., Garodia, P., Weerasinghe, P., Sethi, G., Bhatt, I.D.,
Pandey, M.K., Shishodia, S., Nair, M.G. (2006). From traditional Ayurvedic medicine to
modern medicine: identification of therapeutic targets for suppression of inflammation
and cancer. Expert Opin. Ther. Targets, 10(1): 87-118.
Hallock, S., Tang, S.C., Buja, L.M., Trump, B.F., Liepins, A. and Weerasinghe, P.
(2007). Aurintricarboxylic Acid Inhibits Protein Synthesis Independent, SanguinarineInduced Apoptosis and Oncosis. Toxicol. Pathol., 35(2):300-9.
Weerasinghe, P., Hallock, S., Tang, S.C., Trump, B. and Liepins A. (2006).
Sanguinarine overcomes P-glycoprotein-mediated multidrug-resistance via induction of
apoptosis and oncosis in CEM-VLB 1000 cells. Exp Toxicol. Pathol. 58: 21-30.
Ding, Z., Tang, S.C., Weerasinghe, P., Yang, X., Pater, A. and Liepins, A. (2002). The
alkaloid sanguinarine is effective against multidrug resistance in human cervical cells via
bimodal cell death. Biochem. Pharmacol., 63(8):1415-1421.