Benjamin K. Tsang, PhD

Telephone: 613-737-8899, Ext. 72926 (Office)
Telephone: 613-737-8899, Ext. 73886 (Laboratory)
Telephone: 613-737-8899, Ext. 72807 (Res. Admin. Assistant)
Fax: 613-761-4403

Senior Scientist, Chronic Disease, Ottawa Hospital Research Institute

Director, Reproductive Biology Unit, Department of Obstetrics and Gynaecology, University of Ottawa

Professor of Obstetrics and Gynaecology (Reproductive Medicine and Gynaecologic Oncology) and Cellular & Molecular Medicine, University of Ottawa

Biographical Sketch
Dr. Ben Tsang is Senior Scientist, Ottawa Hospital Research Institute and Professor of Obstetrics & Gynaecology and Cellular & Molecular Medicine, University of Ottawa. He completed his undergraduate training in chemistry at Bemidji State University, received MSc (Biochemistry) from the University of Iowa, and Ph.D. (Pharmacology) from the University of Ottawa. In 1980, Dr. Tsang joined the University of Ottawa as the Director, Reproductive Biology Unit and initiated a research-intensive academic program in the Department of Obstetrics and Gynaecology. He served as Associate Chair (Research) of the Department, and developed a multi-disciplinary reproductive health research program in Ottawa.  As the Director of Research of the Ottawa Civic Hospital, he played a central role in research development at the Loeb Research Institute, now one of the top health research institutions in Canada and recently named the Ottawa Hospital Research Institute.

Professor Tsang is an internationally recognized ovarian biologist, who has the insight and ability in bringing fundamental research into the clinical context. His team of basic scientists and clinical investigators address important reproductive health issues, including female infertility, ovarian cancer and pregnancy complications. Dr. Tsang’s research program covers the broad area of cell fate regulation in women’s reproductive health. He and his team are examining the cell signaling pathways involved in the regulation of ovarian cell survival and apoptosis and have defined the basic mechanisms governing normal ovarian follicular growth and offered important insights into the pathophysiology of various ovarian disorders associated with infertility, including polycystic ovarian syndrome. In addition, his research on the molecular and cellular basis of chemoresistance in ovarian cancer has provided key information for the development of new therapy for chemoresistant ovarian cancer, a most lethal cancer in women. The success of Professor Tsang’s research program is also reflected by his ability to secure continuous funding from MRC/CIHR during the past 32 years, as well as support from other peer-review funding agencies, government departments, private foundations and industries. To date, he has contributed over 185 full-length original publications and 19 reviews/book chapters and issued 4 US patents. 

Professor Tsang has received many honors and awards, including the Award of Excellence in Reproductive Medicine from the Canadian Fertility and Andrology Society, The OCRI Research Award from the Ottawa Centre for Research and Innovations, Angel Award for cancer research excellence from the Ottawa Regional Cancer Foundation, “Outstanding Alumnus” of Bemidji State University (Minnesota), the J David Grimes Research Career Achievement Award at the Ottawa Hospital Research Institute, the University of Ottawa Faculty of Medicine Award of Excellence (Research) and the Recognition Award (Medical Education). He served as President of the Canadian Fertility and Andrology Society and is a member of the Board of Directors of the Society for the Study of Reproduction. He holds honorary professorship at the Chinese Academy of Sciences, Jinan University, Nanjing Medical University and Taipei Medical University. He is a member of the Advisory Committee of the Cancer Research Institute, Seoul National University. He co-chairs the Canada-Japan Bilateral Program on Women’s Health Research and the Sino-Canada Bilateral Program on Reproductive Health. He is an Editor-in-Chief of the Journal of Ovarian Research, and also serves on the Editorial Board of Endocrinology, Reproduction and Adaptive Medicine.

Major Research Programs

1. Ovarian Follicular and Female Infertility.
Ovarian follicular development and atresia is the culmination of complex actions and interactions of gonadotropins and intra-ovarian regulators. Although the importance of FSH, thyroid hormone, epidermal growth factors and transforming growth factor beta family members in the regulation of ovarian function is well established, how these ovarian regulators interact at the subcellular levels in determining the fate of granulosa cells (proliferation differentiation vs. apoptosis) and eventually follicle destiny (continual growth vs. atresia) is poorly understood. In addition, the regulation of preantral follicular growth is distinct from that in antral and preovulatory follicles. As the preantral/early antral development is most susceptible to dysregulation, understanding the molecular and cellular mechanisms controling preantral-early antral growth may provide important insight into ovarian pathophysiology.
Polycystic ovarian Syndrome (PCOS), a multi-factorial heterogeneous syndrome with complex pathologies, affects up to 10% of women of reproductive age and accounts for 75% of anovulatory infertility.  PCOS is associated with follicle growth arrest at the early antral stage, chronic anovulation, minimal granulosa cell proliferation, hyperthecosis and hyper-androgenemia, and insulin resistance. PCOS is a disorder of reproduction and metabolism with potential systemic sequelae such as diabetes and obesity. Obese women often have more severe hyperandrogenism and anovulation than normal weight women with PCOS. In this research program, we examine the crosstalk between death and survival signaling pathways in the regulation of ovarian follicular growth and atresia by endocrine, paracrine and autocrine regulators and/or extracellular matrix protein-receptor activation.

Our research plan will be focused primarily on two aspects: (1) Defining the physiologic actions and interactions of endocrine and intra-ovarian regulators (gonadotropins, the novel adipokine chemerin, GDF9, IGF-I) and their intracellular signalling pathways (prohibitin, PI3K/Akt, MAPK) and mechanisms (microRNAs) in the control of normal follicular growth; and (2) Understanding the complex pathophysiology of PCOS by studying the aberrant regulation of these cellular mechanisms, using an androgenised rat PCOS model and validating these findings by comparing their relative expression in normal and PCOS human follicles. We will also determine if elevated serum chemerin level is indeed associated with obesity and dysregulated steroidogensis, insulin sensitivity and lipid metabolism in PCOS.  
Our research strategies will involve in vivo (eCG- or DES-primed immature rats, mature normal and “PCOS” rats) and in vitro [granulosa cell and follicle cultures coupled to gene manipulation protocols (sense, siRNA, antisense, dominant negatives)] approaches. We will compare the ovarian expression of Chemerin, its receptor CMKLR1, IGF-I receptor, GDF9 and prohibitin in human preantral/early antral follicles and PCOS follicles and serum chemerin levels in normal and obese human subjects w/wo PCOS to validate the results from the rat “PCOS” model. Standard molecular and cellular techniques will be used to assess follicular growth and function (steroidogenesis). The role of microRNAs in the control of key steroidogenic enzymes will also be studied using specific precursors and inhibitors. (Funded by Canadian Institutes of Health Research).

2.  Human Ovarian Cancer Biology and Chemoresistance.

Ovarian cancer (OVCA) is the most lethal gynecological malignancy, which could be attributed primarily to late diagnosis and chemoresistance. Although its initial therapeutic response rate is high, many recur with a resistant phenotype. Chemoresistance is a major hurdle for successful treatment and the mechanism involved is multi-factorial and is partly due to defects in drug-induced apoptosis.  TP53 mutation is a frequent event in human OVCA and is often associated with decreased responsiveness to chemotherapy, suggesting that p53 is required for CDDP sensitivity. It induces apoptosis in a transcription-dependent and -independent manner. p53 is activated by CDDP through a Chk1-mediated phosphorylation of serine residues 15 and 20 which increases its pro-apoptotic properties. Our recent studies indicate that the protein phosphatase magnesium-dependent 1 D (PPMID) is important in the regulation of p53 activation and chemosensitivity in OVCA cells, although its underlying mechanism (s) is unknown. Gelsolin (GSN) is a cytoskeleton-associated protein that regulates actin dynamics and is aberrantly regulated in many tumor types. It also plays an important role in regulating apoptosis. We have shown higher levels of GSN in chemoresistant OVCA and head and neck cell than in their sensitive counterparts  and its level is significantly correlated with recurrent stage IV disease. Mitochondria are highly dynamic organelles, constantly elongating and dividing to form a network, undergo two opposing processes for maintaining mitochondrial function: mitochondrial fission and fusion. Whether and how the mitochondrial dynamics control of chemosensitivity and their dysregulation play a role in the pathobiology of chemoresistance in OVCA, is not known. The PI3K/Akt pathway promotes cell survival and chemoresistance and is frequently amplified/over-expressed in OVCA. If and how p53, GSN and Akt interact in eliciting changes in chemosensitivity is still poorly understood.

Our overall objective is to better understand the mechanisms of chemoresistance in human OVCA by investigating p53, GSN and Akt function in the control of mitochondrial fission and fusion and nuclear function in these cells. Our overall hypothesis is that chemosensitivity is determined by complex interactions of intracellular intermediates which culminate in the regulation of apoptosis at different subcellular levels. Akt confers resistance in part by suppressing CDDP-induced p53 activation and apoptotic pathways.Specifically, in chemosensitive OVCA cells, CDDP treatment leads to I-GSN-Drp1 interaction and mitochondrial import. Activated p53 is translocated from the cytosol to the mitochondria and interacts with I- GSN-Drp1 complex, resulting in displacement of I-GSN. Drp1-p53 complex induces mitochondrial fission, Cytochrome c-AIF release and apoptosis. Secondly, we also hypothesize that the processing of Opa1 by protease Oma1, is necessary for mitochondrial fission and apoptosis. In chemoresistance, I-GSN, Drp1 and p53 are not activated nor targeted to the mitochondria, and Opa1 is not processed, resulting in suppressed mitochondrial fission. PPM1D modulates CDDP sensitivity by decreasing Chk1 and p53 activities, a phenomenon promoted by the PI3K/Akt survival pathway. Akt promotes PPM1D phosphorylation, and nuclear translocation, thereby protecting it from calpain-mediated degradation.

Our specific objectives are: (1) To study the role of GSN and p53 in mitochondrial dynamics and chemoresistance; (2) To define the nuclear action of GSN: role in AIF-induced apoptosis;  (3) To examine the mechanism of p53 activation: PPM1D and modulation by Akt;  (4) To assess the role and regulation of PPM1D and Gelsolin in chemosensitivity in vivo (ovarian xenografts and tumour screening), (5) To examine the effectiveness of functional food compounds and natural products in sensitizing chemoresistant ovarian cancer cells to traditional chemotherapeutic agents. The program integrates in vitro, in vivo, and clinical approaches to dissect the mechanisms of chemoresistance in OVCA. The studies will demonstrate, for the first time, (i) role of GSN in the regulation of chemosensitivity, (ii) possible dysregulated mitochondrial fission/fusion in chemoresistance, (iii) regulation of PPMID by Akt in the control of p53 activation and CDDP sensitivity, and (iv) the complex interaction of GSN, p53, PPMID and Akt during CDDP-induced apoptosis. It will provide novel insights into the pathobiology of and possible new therapy for chemoresistant OVCA.  (Supported by Canadian Institutes of Health Research, National Cancer Institute of Canada, and National Research Foundation of Korea).

3.  Role and Regulation of Placental Apoptosis in Health and Diseases

The understanding of the regulatory mechanisms responsible for placental growth is crucial to further our knowledge of what controls fetal growth. Indeed, placental growth is directly correlated with fetal growth as the placenta is essential to provide adequate nutrient, blood and oxygen supply to ensure adequate fetal growth and development. Despite advances in perinatal care, fetal growth restriction, often seen in pre-eclampsia, remains a leading cause of perinatal morbidity and mortality. Infants from these pregnancies often suffer multiple complications such as asphyxia, respiratory distress syndrome, prematurity and metabolic disturbances. In collaboration with Drs. Andrée Gruslin and Ajoy Basak, we are testing the hypothesis that soluble Fas ligand is involved in the regulation of placental apoptosis and is dependent on expression and/or processing of mFasL as regulated by MMP-7 and its inhibitor, TIMP-3. The processing of mFasL is dysregulated in abnormal placental conditions such as pre-eclampsia and fetal growth restriction, which are characterized by hypoxia.

The overall objective of this research program is to examine the role and regulation of soluble Fas ligand in the control of apoptosis in normal and pathological conditions of the human placenta. Specifically, we will: (a) determine the expression of the precursor protein of sFasL (mFasL) throughout placental development and its relationship to placental apoptosis, (b) assess the processing of mFasL and its significance in initiation of placental apoptosis throughout development by examining the expression and activities of MMP-7 and, TIMP-3, (c) examine the influence of hypoxia on mFasL expression and processing and assess the significance of the above mFasL-related changes in pathological placental development, (d) the interaction of EGF and Leptin in the regulation of trophoblast invasion; and (e) the role of proprotein convertase-4 and IGF-II terminal maturation in the pathophysiology of preeclampsia and intrauterine growth restriction.

Honours and Awards
2012   Angel Award for ovarian cancer research excellence, Angels in Action and Ottawa Regional Cancer Foundation
2011    OCRI Research Award, Ottawa Centre for Research and Innovations
2008    Award of Excellence in Reproductive Medicine, Canadian Fertility and Andrology Society, Canada.
2008    Outstanding Alumnus, Bemidji State University, Minnesota, USA
2005    J. David Grimes Research Career Achievement Award, Ottawa Health Research Institute
2003    JSPS Visiting Professorship, Kobe University School of Medicine, Kobe, Japan
2002    University of Ottawa Faculty of Medicine Recognition Award for Contributions in Medical Education
1996    Award of Excellence, Faculty of Medicine, University of Ottawa, in recognition of outstanding achievement or contribution to the Faculty in research, scholarship, education, or other contributions to the life of the Faculty.
2005    Co-Founder and Co-Chair, Sino-Canada Bilateral Program in Reproductive Health Research
2004    Co-Founder and Co-Chair, Canada-Japan Bilateral Exchange Program in Reproductive Biology and Human Reproduction
2004    Program Director, CIHR-funded, Strategic Training Initiative in Research in Reproductive Health Sciences


2012 - present Board of Directors, Society for the Study of Reproduction
2009 - present  World Class University Professor, Biomodulation Major, Department of Agricultural Biotechnology, Seoul National University, Republic of Korea
2008 - Present  Taipei Medical University, Taipei, Taiwan
2006 - Present Honorary Professor, Nanjing Medical University, China
2004 - Present Honorary Professor, State Key Laboratory in Reproductive Biology, Institute of Zoology, Chinese Academy of Sciences, Beijing, China
1998 - Present Honorary Professor, Jinan University, Guangzhou, China
1998 - Present Director, Reproductive Biology Unit, Department of Obstetrics and Gynaecology, The Ottawa Hospital (Civic Campus)
2008 - Present Editor-in-Chief (2012-present), Associate Editor (2008-2012), Journal of Ovarian Research
2006 - Present Editorial Board, Reproduction
2009 - Present Editorial Board, Adaptive Medicine
2005 - Present Editorial Advisory Board, Journal of Obstetrics and Gynaecology Canada
2002 – 2008    Chair (2005-2008) and Board of Directors (2002-2004), Ovarian Workshop.
2007                Cancer Research Society Grants Panel
2005 - 2006     President, Canadian Fertility and Andrology Society
2001 - 2005     Associate Editor, Journal of Obstetrics and Gynaecology Canada
2002 - 2006     Editorial Board, Biology of Reproduction
1999 - 2003     Associate Chair, Research, Department of Obstetrics & Gynaecology, University of Ottawa
1984 - 1986     Director of Research, Ottawa Civic Hospital
Current Funding

Research Operation Support 

2007 - 2018Canadian Institutes of Health Research for project entitled “Molecular and Cellular Mechanisms of chemoresistance in ovarian cancer” - Operating Grant
2007-2012: $ 630,615 (with Drs. A. Basak and E. Carmona)
2013-2018: $ 807,445
2012 - 2017Canadian Institutes of Health Research for project entitled “Regulation of Ovarian Follicular Development: Mechanisms of Dysregulation in PCOS” - Operating Grant:    $670,610
2011 - 2014 CIHR-NSFC China-Canada Joint Health Research Initiative “Thyroid Hormone and Ovarian Follicular Growth and Steroidogenesis” - Operating Grant [Principal Applicants: BK Tsang (Canada) and GL Xia (China)]. $150,000 + 700,000 RMB (~$250,000)
2007 - 2018Canadian Institutes of Health Research for project entitled “Molecular and Cellular Mechanisms of chemoresistance in ovarian cancer” - Operating Grant
2007-2012: $630,615 (with Drs. A. Basak and E. Carmona)
2013-2018: Funding pending approval (Application ranked # 1 in Sept 2012 Competition – recommended funding by Grant Committee: $1,062,425
2009 – 2015Korean Ministry of Education, Science and Technology (MEST) for World Class University Program on “Biomodulation” – Set-up and Operating Team Grant (Principal Applicant: JY Han; $25,000,000) with allocation of $1,200,000 to BK Tsang (2009-2013)
2009 - 2015CIHR Institute of Human Development, Child and Youth Health “Training Program in Reproduction, Early Development, and the Impact on Health (REDIH)” – Team Grant - (Principal Applicant: JM Baltz): $1,790,000
2009 – 2015CIHR Institute of Human Development, Child and Youth Health “Quebec Training Network in Perinatal Research (QTNPR)” – Team grant – (Principal Applicant: W. Fraser): $1,790,000
2008 – 2013Natural Science and Engineering Research Council for program entitled “EmbryoGene Research Network” for Strategic Network Grant (Drs. M-A Sirard et al): $4,895,000

Research Personnel Support 

2012 – 2013             CIHR- REDIH Scholarship for Qi Wang: $ 17,800
2012 – 2013              CIHR- REDIH Scholarship for Dr. Ji Young Kim: $ 41,000
2011 – 2012              CIHR- REDIH Scholarship for Cheng Zhang: $ 17,800
2010 – 2012              CIHR- QTNPR Postdoctoral Fellowship for Dr. Ji Young Kim: $ 75,000
2010 – 2012              CIHR- QTNPR Scholarship for Qi Wang: $ 35,600
2011 – 2012              CIHR- REDIH Scholarship for Mr. Kai Xue: $ 17,800
2010 – 2012              China Scholarship Council Graduate Scholarship for Ms. Ying Ying Han: $28,800
2009 – 2013              China Scholarship Council Graduate Scholarship for Mr. Bao Kong: $57,600
2008 – 2010                  China Scholarship Council Graduate Scholarship for Mr. Cheng Zhang: $28,800

Current Research Group Members
Benjamin Tsang, PhD (Senior Scientist)
Ji Young Kim (Postdoctoral Fellow)
Ahmed Ali, MSc (PhD Candidate)
Bao Kong, MSc  (PhD Candidate)
Lee Farrand, MSc (PhD Candidate)
Qi Wang, MSc (PhD Candidate)
Xue Kai, MSc (PhD Candidate)
Akechai Im-Aram, DVM (MSc candidate)


Selected Key Publications

Wang Q, Kim JY, Xue K, Liu JY, Leader A and Tsang BK. Chemerin, a novel regulator of follicular growth and steroidogenesis and its potential involvement in the pathogenesis of PCOS. Endocrinology 153: 5600-5611 (2012).

Xue K, Liu JY, Murphy BR and Tsang BK. Orphan nuclear receptor NR4A1 is a negative regulator of DHT-induced rat preantral follicular growth. Molecular Endocrinology 26:2004-2015 (2012).

Wang Q, Leader A and Tsang BK. Inhibitory role of chemerin and prohibitin on FSH-induced steroidogenesis. Endocrinology(2012, In Press).

Woo MG, Xue K, Liu J, McBride H, Tsang BK.  Calpain-mediated processing of p53-associated, Parkin-like cytoplasmic protein (PARC) affects chemosensitivity of human ovarian cancel cells by promoting p53 subcellular trafficking.  J Biol Chem 287: 3963–3975 (2012)

Ali AY, Abedini MR, Tsang BK.  The oncogenic phosphatase PPM1D confers cisplatin resistance in ovarian carcinoma cells by attenuating checkpoint kinase 1 and p53 activation. Oncogene 31: 2175-2186 (2012)

Leung EL, Wong JC, Johlfs MG, Tsang BK, Fiscus RR.  Protein kinase G type 1alpha activity in human ovarian cancer cells significantly contributes to enhanced Src activation and DNA synthesis/cell proliferation. Molec. Cancer Res 8: 578-591 (2010). 

Abedini MR, Muller EJ, Brun J, Bergeron R, Gray DA and Tsang, BK. Cisplatin induces p53-dependent FLICE-like inhibitory protein (FLIP) ubiquitination in ovarian cancer cells. Cancer Research 68: 4511-4517 (2008).

Yang X, Fraser M, Moll U. Basak A, and Tsang, BK. Akt-mediated Cisplatin resistance in Ovarian Cancer: Modulation of p53 Action on Caspase-dependent Mitochondrial Death Pathway. Cancer Research 66:3126-3136 (2006).

Wang HM, Jiang JY, Zhu C, Peng C and Tsang, BK. Role and Regulation of Nodal/ALK7 Signalling pathway in the control of ovarian follicular development and atresia. Molec. Endocr. 20: 2469-2482 (2006)

Fraser M, Chan SL, Chan SSL, Fiscus RR and. Tsang, BK. Regulation of p53 and suppression of apoptosis by the soluble guanylyl cyclase/cGMP pathway in human ovarian cancer cells. Oncogene 25:2203-2212 (2006).

Orisaka M, Orisaka S, Jiang J-Y, Craig J, Wang Y, Kotsuji F and Tsang, BK. Growth Differentiation Factor-9 is anti-apoptotic during follicular development from preantral to early antral stage. Molec. Endocr. 20: 2456-2468 (2006).

Qiu Q, Yang M, Basak A, Mbikay M, Tsang, BK, Gruslin A. ProIGF-II processing in the human placenta: The expression and role of the proprotein convertase PC4. Proc Nat. Acad. Sci. USA 102: 11047-11052 (2005).

Dan HC, Sun M, Kaneko S, Feldman RI., Nicosia SV, Wang HG, Tsang, BK, Cheng JQ. Akt Phosphorylation and Stabilization of XIAP. J. Biol. Chem. 279: 5405-5412 (2004).

Abedini MR., Qiu Q, Yan X and Tsang, BK. Possible Role of FLICE-Like Inhibitory Protein (FLIP) in Chemoresistant Ovarian Cancer Cells in vitro. Oncogene 24: 6977-7004 (2004).

Fraser M, Leung BM, Yan X, Dan HC, Cheng JQ and Tsang, BK. p53 is a determinant in Xiap/Akt-mediated chemoresistance in human ovarian cancer cells. Cancer Research 63: 7081-7088 (2003).

Asselin E, Mills GB and Tsang, BK. Xiap regulates AKT activity and its caspase 3- dependent cleavage during cisplatin-induced apoptosis in human ovarian cancer cells. Cancer Research 61: 1862-1868 (2001).

Sasaki H, Sheng Y, Kotsuji F and Tsang, BK. (2000). Down-regulation of Xiap induces apoptosis in chemoresistant human ovarian cancer cells. Cancer Research 60: 5659-5666.

Recent Publications (2008- Present)

Du MR, Qiu Q, Gruslin A, Gordon J, Li DJ and Tsang BK. SB225002 promotes mitotic catastrophe in chemo-sensitive and –resistant ovarian cancer cells independent of p53 status in vitro. PLOS ONE (2012, In Press)

Ali AY, Farrand L, Kim JY, Byun S, Suh JY, Lee HJ and Tsang BK. Molecular determinants of ovarian cancer chemoresistance: new insights into an old conundrum. Ann NY Acad Sci 1271:58-67 (2012)

 Al-Bahlani S, Fraser M, Wong AY, Sayan BS, Bergeron R, Melino G, Tsang BK. P73 regulates cisplatin-induced apoptosis in ovarian cancer cells via a calcium/calpain-dependent mechanism. Oncogene 30:4219-4230 (2011)

Haider M, Qiu Q, Bani-Yaghoub M, Tsang BK, Gruslin A.  Characterization and role of NUMB in the human extravillous trophopblast.  Placenta 32: 441-449 (2011).

Leung EL, Wong JC, Johlfs MG, Tsang BK, Fiscus RR.  Protein kinase G type 1alpha activity in human ovarian cancer cells significantly contributes to enhanced Src activation and DNA synthesis/cell proliferation. Mol Cancer Res. 8: 578-591 (2010)

Fu J, Lv X, Lin H, Wu L, Wang R,  Zhou Z, Zhang B, Wang YL, Tsang BK, Zhu C, Wang H.  Ubiquitin ligase cullin 7 induces epithelial-mesenchymal transition in human choriocarcinoma cells. J Biol Chem. 285:10870-10879 (2010)

Orisaka M, Jiang J-Y, Orisaka S, Kotsuji F, Tsang BK.   Growth Differentiation Factor-9 promotes rat preantral follicle growth by    up-regulating follicular androgen biosynthesis.  Endocrinology 150: 2740-2748(2009). 

Gregory-Bass RC, Olatinwo M , Xu W, Matthews R, Stiles JK, Thomas K, Liu D, Tsang, BK and Thompson WE. Prohibitin silencing reverses stabilization of mitochondrial integrity and chemoresistance in ovarian cancer cells by increasing their sensitivity to apoptosis. Internat. J. Cancer 122: 1923-1930 (2008)

Leung LH, Fraser M, Fiscus RR and Tsang, BK. Cisplatin alters nitric oxide synthase levels in human ovarian cancer cells: involvement in p53 regulation and cisplatin resistance. Br. J. Cancer 98, 1803 - 1809 (2008)

Fraser M, Bai T and Tsang, BK. Akt promotes cisplatin resistance in human ovarian cancer cells through inhibition of p53 phosphorylation and nuclear function. Internat. J Cancer. 122:534-546 (2008)

Yang X, Fraser M, Abedini MR, Bai T and Tsang, BK. Regulation of AIF-Mediated, Cisplatin-Induced Apoptosis by Akt. Br. J. Cancer 98: 803-808 (2008).