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Dr Pradeep Tanwar

ARC Future Fellow

School of Biomedical Sciences and Pharmacy (Medical Biochemistry)

Tackling Silent Killers

By investigating the pathogenesis of female reproductive tract cancers, Dr Pradeep Tanwar aims to develop targeted therapies to improve clinical outcomes.

Dr Pradeep Tanwar and colleagues.

Dr Pradeep Tanwar and his team are methodically investigating questions surrounding female reproductive tract cancers from several different angles.

An investigator of the Hunter Cancer Research Alliance, the potential massive impact of Pradeep’s work has been recognized by his appointment as an ARC Future Fellow and a Cancer Institute NSW Career Development Fellow.

“We work on female reproductive tract cancers,” Pradeep explains.

“We mainly focus on two cancers - ovarian cancer, the most deadly of gynecological cancers in women, and endometrial cancer or cancer of the uterus, which is the most common gynecological cancer in females.”

“What we are interested in is how the cancer develops to start with, and once it has developed, how does it progress to a stage where it spreads to other organs,” he says.

“And when it spreads, how can we control it. So we are interested in both how we can control the development or initiation, and how we can control the spread, of these cancers.”

A needle in a haystack

Pradeep explains that genetics, lifestyle factors, and age, are all risk factors for reproductive tract cancers.

“But having a genetic predisposition does not mean these cancers will develop, so lifestyle factors play a role”, Pradeep explains.

“You will find two thousand factors that are different between a patient that has cancer and a patient who does not have cancer, a patient who has metastasis versus a patient who does not have it.”

“So, what are those differences? What combination of factors result in the actual development of the disease? We are looking for a needle in a haystack. But that might be the key.”

Breakdown in cell communication has been identified as a factor in increased incidence of cancers as has been patient’s age, so this communication process is also being studied.

“Cancer is basically excessive production of cell types,” Pradeep says.

“Every day billions of cells are regenerated in the body, and a number of cells need to die to keep everything in perfect harmony. The signals that keep this system in harmony are sometimes disrupted. We hope to discover a way to correct that disruption.”

Working models

With lack of population-wide screening program, symptoms that can mimic other conditions, and diagnostic procedures that are difficult and non-conclusive, cancers of the reproductive tract are notoriously illusive and are most often diagnosed in later stages.

Pradeep’s group use genetically modified animal models, cancer patient-derived xenograft models and primary human tissue samples to define the molecular and cellular events involved in carcinogenesis.

The Hunter Cancer Biobank (HCB) at the Hunter Medical Research Institute (HMRI) collects affected patient tissue, which is then provided to researchers. In this important way, many cancer patients through the Hunter and surrounding areas have contributed to this and other cancer research.

Utilising animal models allows researchers to target early stages of the disease and investigate possible markers that may be identified through existing pathology test processes, ultimately facilitating more timely diagnosis.

Working with these models also allows the team in the lab to bombard tumorous tissue with combinations of off-label medications. Pradeep is hoping to find a medication, already approved and mass produced, or combination of such, that can be repurposed to aid in the fight against these cancers.

Major inroads

Working with a former Harvard colleague, Pradeep has already made a major breakthrough in identifying a protein that can act as a tumour suppressor when treating chemo-resistant ovarian cancer.

He has recently published a paper showing that in animal models and human ovarian cancer cells, progesterone suppresses and oestrogen promotes the growth of cancer cells.

“We were able to find that the initial lesions of ovarian cancers had receptors for oestrogen and progesterone. So if you have too much estrogen, those lesions will develop into cancer.”

As a result of this work, his team including clinicians are exploring the use of hormonal treatments in combination with chemotherapy for reproductive tracts cancers.

“The incidence of cancer in patients is much higher for those who have never used oral contraception than in patients who have used oral contraception,” Pradeep asserts.

“If you take the Pill it suppresses your ovaries and you are less likely to develop ovarian cancer, all reproductive tract cancers.”

“This is vital information for women who may be at high risk due to family history, and women who are postponing pregnancies until later in life.”

The path to here

Pradeep is originally trained in veterinary medicine and animals first ignited his passion for discovering disease prevention strategies.

Frustrated by the amount of animals being put down due to prohibitive treatment costs, Pradeep reasoned that facilitating the maintenance of animal health and worth removed the necessity for large treatment costs, long recovery periods or euthanasia.

“One of the things I also learnt as a veterinarian is that the underlying principle of animal domestication seems to be production. Without reproduction, there is no production. If a cow is not breeding, a farmer is going to get rid of her.”

This principle lead Pradeep to become invested in the study of reproductive systems. A PhD at the University of New England furthered his study of this system in women. A post-doctoral stint at Harvard followed.

“At Harvard, you are embedded in a hospital, so you have oncologists, surgeons, gynecologists, obstetricians, and researchers, all having lunch at the same time,” Pradeep recalls.

“They were discussing their patients and we were discussing our research. I became more and more interested in ovarian and uterine cancers, and learnt a great deal.”

These experiences have resulted in Pradeep establishing a lab environment which comprises of both systemic and specialized approaches in addressing a research problem.  Pradeep’s lab also addresses fundamental questions regarding the normal functioning of the female reproductive tract, such as the cellular dynamics.  Often answers to these questions helps in understanding what is going wrong with the system leading to disease development.

Overcoming challenges

When reflecting on the many challenges to the diagnosis and treatment of female reproductive cancers, Pradeep cites the increased incidence of obesity amongst women as a major hurdle.

Pradeep and his team have spent four years investigating the role of fat cells in the growth of cancer cells. By providing accessible fuel, fat deposits in the body can accelerate and feed cancers. This process is particularly relevant to ovarian cancer, which metastasizes first to the omentum (a fatty tissue).

“These cancer cells have free food and a free supply of energy,” Pradeep explains.

“But if we can find ways to destruct that communication, then it is possible that cancer cells might be starved to death.”

Another challenge is translating research directly into practice, with Pradeep seeing opportunities for women, and their clinicians, to make informed female reproductive health choices but lacking the information to do so.

“Female reproductive health and fitness is still a taboo topic, although it is a very important part of female biology, and essential to women's health and survival,” Pradeep says.

“So not only do we need to continue searching for answers regarding these cancers, but we need to raise awareness about what we find which translates directly to saving lives.”

Tackling Silent Killers

Dr Pradeep Tanwar and his team are methodically investigating questions surrounding female reproductive tract cancers from several different angles.

Read more

Career Summary

Biography

Dr Pradeep Tanwar is an ARC Future Fellow, a Cancer Institute NSW Career Development Fellow and an investigator of the Hunter Cancer Research Alliance.  Throughout his research career, Dr Tanwar’s research work has focussed on defining molecular footsteps involved in the pathogenesis of the reproductive tract cancers. In the last 5 years, Dr Tanwar’s work resulted in 15 research publications in high impact journals including PNAS x2, Cancer Research, Human Molecular Genetics, PLos Genetics, Nature Genetics and Carcinogenesis x3, and led to invitations to speak at various conferences/symposiums such as Gordon Conference on Reproductive Tract Biology and Reproductive and Endocrine-related Cancer Symposium jointly organised by the Society of Reproductive Biology and the Endocrine Society of Australia.  His group is using genetically modified mouse models, cancer patient-derived xenograft models and primary human tissue samples to define the molecular and cellular events involved in carcinogenesis and then using this knowledge to develop targeted therapies to improve clinical outcomes in human patients.

Research Expertise
1. Role of Microenvironment in Endometrial cancer 2. Wnt-PI3K-mTOR signaling axis, EMT (Epithelial Mesenchymal Transition), and ovarian cancer 3. Cancer stem cells in ovarian cancer 3. Pathogenesis of Genitourinary cancers

Teaching Expertise
Course coordinator for HUBS2107: Mammalian Growth and Development

Collaborations


Keywords

  • Cancer biology
  • Cancer stem cells
  • Endometrial cancer
  • Genetics
  • Genitourinary cancers
  • Gynecologic oncology
  • PCOS
  • ovarian cancer

Languages

  • English (Fluent)

Fields of Research

Code Description Percentage
060403 Developmental Genetics (incl. Sex Determination) 20
111201 Cancer Cell Biology 50
111203 Cancer Genetics 30

Professional Experience

UON Appointment

Title Organisation / Department
Senior Lecturer University of Newcastle
School of Biomedical Sciences and Pharmacy
Australia

Academic appointment

Dates Title Organisation / Department
1/08/2012 - 13/12/2014 Lecturer University of Newcastle
School of Biomedical Sciences and Pharmacy
Australia
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Publications

For publications that are currently unpublished or in-press, details are shown in italics.


Journal article (30 outputs)

Year Citation Altmetrics Link
2017 George JW, Patterson AL, Tanwar PS, Kajdacsy-Balla A, Prins GS, Teixeira JM, 'Specific deletion of LKB1/Stk11 in the Müllerian duct mesenchyme drives hyperplasia of the periurethral stroma and tumorigenesis in male mice.', Proc Natl Acad Sci U S A, 114 3445-3450 (2017)
DOI 10.1073/pnas.1612284114
2017 Goad J, Ko Y-A, Kumar M, Syed SM, Tanwar PS, 'Differential Wnt signaling activity limits epithelial gland development to the anti-mesometrial side of the mouse uterus.', Dev Biol, 423 138-151 (2017)
DOI 10.1016/j.ydbio.2017.01.015
Citations Scopus - 1
Co-authors Manish Jhamb
2017 Kumar M, Tanwar P, 'Organ Culture and Whole Mount Immunofluorescence Staining of Mouse Wolffian Ducts.', J Vis Exp, (2017)
DOI 10.3791/55134
Co-authors Manish Jhamb
2017 Bajwa P, Sahoo SS, Tanwar PS, 'Age-related mTOR in gynaecological cancers.', Aging (Albany NY), 9 301-302 (2017)
DOI 10.18632/aging.101190
2017 Goad J, Ko YA, Syed SM, Crossingham YJ, Tanwar PS, 'Data on the mRNA expression by in situ hybridization of Wnt signaling pathway members in the mouse uterus', Data in Brief, 12 208-212 (2017)

© 2017 The AuthorsWnt signaling plays an important role in uterine organogenesis and oncogenesis. Our mRNA expression data documents the expression of various Wnt pathway members... [more]

© 2017 The AuthorsWnt signaling plays an important role in uterine organogenesis and oncogenesis. Our mRNA expression data documents the expression of various Wnt pathway members during the key stages of uterine epithelial gland development. Our data illustrates the expression of Wnt signaling inhibitors (Axin2, Sfrp2, Sfrp4, Dkk1 and Dkk3) in mice uteri at postnatal day 6 (PND 6) and day 15 (PND 15). They also describe the expression pattern of the Wnt ligands (Wnt1, Wnt2, Wnt2b, Wnt3, Wnt3a, Wnt5b, Wnt7b, Wnt8a, Wnt8b, Wnt9a, Wnt9b, Wnt10a and Wnt10b) in mice uteri with or without progesterone treatment. Detailed interpretation and discussion of these data is presented in the research article entitled ¿Differential Wnt signaling activity limits epithelial gland development to the anti-mesometrial side of the mouse uterus¿ [1].

DOI 10.1016/j.dib.2017.03.047
2017 Bajwa P, Nielsen S, Lombard JM, Rassam L, Nahar P, Rueda BR, et al., 'Overactive mTOR signaling leads to endometrial hyperplasia in aged women and mice', ONCOTARGET, 8 7265-7275 (2017)
DOI 10.18632/oncotarget.13919
Citations Scopus - 1Web of Science - 1
2016 Kumar M, Atkins J, Cairns M, Ali A, Tanwar PS, 'Germ cell-specific sustained activation of Wnt signalling perturbs spermatogenesis in aged mice, Possibly through non-coding RNAs', Oncotarget, 7 85709-85727 (2016) [C1]

Dysregulated Wnt signalling is associated with human infertility and testicular cancer. However, the role of Wnt signalling in male germ cells remains poorly understood. In this s... [more]

Dysregulated Wnt signalling is associated with human infertility and testicular cancer. However, the role of Wnt signalling in male germ cells remains poorly understood. In this study, we first confirmed the activity of Wnt signalling in mouse, dog and human testes. To determine the physiological importance of the Wnt pathway, we developed a mouse model with germ cell-specific constitutive activation of ßcatenin. In young mutants, similar to controls, germ cell development was normal. However, with age, mutant testes showed defective spermatogenesis, progressive germ cell loss, and flawed meiotic entry of spermatogonial cells. Flow sorting confirmed reduced germ cell populations at the leptotene/zygotene stages of meiosis in mutant group. Using thymidine analogues-based DNA double labelling technique, we further established decline in germ cell proliferation and differentiation. Overactivation of Wnt/ßcatenin signalling in a spermatogonial cell line resulted in reduced cell proliferation, viability and colony formation. RNA sequencing analysis of testes revealed significant alterations in the non-coding regions of mutant mouse genome. One of the novel non-coding RNAs was switched on in mutant testes compared to controls. QPCR analysis confirmed upregulation of this unique noncoding RNA in mutant testis. In summary, our results highlight the significance of Wnt signalling in male germ cells.

Co-authors Murray Cairns, Manish Jhamb
2016 Bajwa P, Nagendra PB, Nielsen S, Sahoo SS, Bielanowicz A, Lombard JM, et al., 'Age related increase in mTOR activity contributes to the pathological changes in ovarian surface epithelium', Oncotarget, 7 19214-19227 (2016) [C1]

Ovarian cancer is a disease of older women. However, the molecular mechanisms of ovarian aging and their contribution to the pathogenesis of ovarian cancer are currently unclear. ... [more]

Ovarian cancer is a disease of older women. However, the molecular mechanisms of ovarian aging and their contribution to the pathogenesis of ovarian cancer are currently unclear. mTOR signalling is a major regulator of aging as suppression of this pathway extends lifespan in model organisms. Overactive mTOR signalling is present in up to 80% of ovarian cancer samples and is associated with poor prognosis. This study examined the role of mTOR signalling in age-associated changes in ovarian surface epithelium (OSE). Histological examination of ovaries from both aged mice and women revealed OSE cell hyperplasia, papillary growth and inclusion cysts. These pathological lesions expressed bonafide markers of ovarian cancer precursor lesions, Pax8 and Stathmin 1, and were presented with elevated mTOR signalling. To understand whether overactive mTOR signalling is responsible for the development of these pathological changes, we analysed ovaries of the Pten trangenic mice and found significant reduction in OSE lesions compared to controls. Furthermore, pharmacological suppression of mTOR signalling significantly decreased OSE hyperplasia in aged mice. Treatment with mTOR inhibitors reduced human ovarian cancer cell viability, proliferation and colony forming ability. Collectively, we have established the role of mTOR signalling in age-related OSE pathologies and initiation of ovarian cancer.

DOI 10.18632/oncotarget.8468
Citations Scopus - 3Web of Science - 3
2016 Nagendra PB, Goad J, Nielsen S, Rassam L, Lombard JM, Nahar P, Tanwar PS, 'Ovarian hormones through Wnt signalling regulate the growth of human and mouse ovarian cancer initiating lesions.', Oncotarget, 7 64836-64853 (2016) [C1]
DOI 10.18632/oncotarget.11711
2016 Kumar M, Syed SM, Taketo MM, Tanwar PS, 'Epithelial Wnt/ßcatenin signalling is essential for epididymal coiling', Developmental Biology, 412 234-249 (2016) [C1]

© 2016 Elsevier Inc.Organ shape and size are important determinants of their physiological functions. Epithelial tubes are anlagen of many complex organs. How these tubes acquire... [more]

© 2016 Elsevier Inc.Organ shape and size are important determinants of their physiological functions. Epithelial tubes are anlagen of many complex organs. How these tubes acquire their complex shape and size is a fundamental question in biology. In male mice, the Wolffian duct (WD; postnatally known as epididymis) undergoes an astonishing transformation, where a straight tube only a few millimetres long elongates to over 1000 times its original length and fits into a very small space, due to extensive coiling of epithelium, to perform the highly specialized function of sperm maturation. Defective coiling disrupts sperm maturation and leads to male infertility. Recent work has shown that epithelial cell proliferation is a major driver of WD coiling. Still, very little is known about the molecular signals involved in this process. Testicular androgens are known regulators of WD development. However, epithelial androgen receptor signalling is dispensable for WD coiling. In this study, we have shown that Wnt signalling is highly active in the entire WD epithelium during its coiling, and is limited to only a few segments of the epididymis in later life. Pharmacological and genetic suppression of Wnt signalling inhibited WD coiling by decreasing cell proliferation and promoting apoptosis. Comparative gene expression analysis identified Fibroblast growth factor 7 (Fgf7) as a prime Wnt target gene involved in WD coiling and in vitro treatment with Fgf7 protein increased coiling of WDs. In summary, our work has established that epithelial canonical Wnt signalling is a critical regulator of WD coiling and its precise regulation is essential for WD/epididymal differentiation.

DOI 10.1016/j.ydbio.2016.02.025
Citations Scopus - 4Web of Science - 4
Co-authors Manish Jhamb
2016 Kumar M, Camlin NJ, Holt JE, Teixeira JM, McLaughlin EA, Tanwar PS, 'Germ cell specific overactivation of WNT/beta catenin signalling has no effect on folliculogenesis but causes fertility defects due to abnormal foetal development', SCIENTIFIC REPORTS, 6 (2016) [C1]
DOI 10.1038/srep27273
Citations Scopus - 1Web of Science - 1
Co-authors Manish Jhamb, Eileen Mclaughlin, Janet Holt
2014 Kumar M, Sahoo S, Tanwar PS, 'MTOR: A NOVEL TARGET FOR TESTICULAR CANCER', Asia-Pacific Journal of Clinical Oncology, 10 2-3 (2014)
Co-authors Manish Jhamb
2014 Tanwar PS, Mohapatra G, Chiang S, Engler DA, Zhang L, Kaneko-Tarui T, et al., 'Loss of LKB1 and PTEN tumor suppressor genes in the ovarian surface epithelium induces papillary serous ovarian cancer', CARCINOGENESIS, 35 546-553 (2014) [C1]
DOI 10.1093/carcin/bgt357
Citations Scopus - 16Web of Science - 13
2013 Tanwar PS, Kaneko-Tarui T, Lee HJ, Zhang L, Teixeira JM, 'PTEN loss and HOXA10 expression are associated with ovarian endometrioid adenocarcinoma differentiation and progression', Carcinogenesis, 34 893-901 (2013) [C1]

Epithelial ovarian cancer is a heterogeneous disease that is subdivided into five major histotypes but the mechanisms driving their differentiation are not clear. Mutations in ade... [more]

Epithelial ovarian cancer is a heterogeneous disease that is subdivided into five major histotypes but the mechanisms driving their differentiation are not clear. Mutations in adenomatous polyposis coli (APC) and ß-catenin are commonly observed in the human ovarian endometrioid adenocarcinoma (OEA) patients. However, the mechanisms subsequent to APC deletion in ovarian tumorigenesis have not been well characterized. We have conditionally deleted APC in the murine ovarian surface epithelium (OSE) and showed that its loss leads to development of epithelial inclusion cysts. High-grade OEAs with tightly packed villoglandular histology were observed in older APC-deleted mice. Phosphatase and tensin homolog (PTEN) expression was elevated in the early lesions but lost after progression to the more advanced tumors. Knockdown of APC or expression of a gain-of-function ß-catenin similarly induced human OSE cells to develop tumors with endometrioid histology in xenografts. Expression of HOXA10 was induced in both the advanced APC-deleted murine tumors and in the tumor xenografts of human OSE cells with knocked-down APC. These results show that reduced APC activity is sufficient to induce formation of epithelial inclusion cysts and support OEA development and suggest that induced HOXA10 expression and loss of PTEN are key mechanisms driving endometrioid histotype differentiation and progression. © The Author 2012.Published by Oxford University Press. All rights reserved.

DOI 10.1093/carcin/bgs405
Citations Scopus - 15Web of Science - 11
2012 Tanaka Y, Park JH, Tanwar PS, Kaneko-Tarui T, Mittal S, Lee H-J, Teixeira JM, 'Deletion of Tuberous Sclerosis 1 in Somatic Cells of the Murine Reproductive Tract Causes Female Infertility', ENDOCRINOLOGY, 153 404-416 (2012) [C1]
DOI 10.1210/en.2011-1191
Citations Scopus - 20Web of Science - 20
2012 Meirelles K, Benedict LA, Dombkowski D, Pepin D, Preffer FI, Teixeira J, et al., 'Human ovarian cancer stem/progenitor cells are stimulated by doxorubicin but inhibited by Mullerian inhibiting substance', PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 109 2358-2363 (2012) [C1]
DOI 10.1073/pnas.1120733109
Citations Scopus - 51Web of Science - 45
2012 Tanwar PS, Commandeur AE, Zhang L, Taketo MM, Teixeira JM, 'The Mullerian inhibiting substance type 2 receptor suppresses tumorigenesis in testes with sustained beta-catenin signaling', CARCINOGENESIS, 33 2351-2361 (2012) [C1]
DOI 10.1093/carcin/bgs281
Citations Scopus - 6Web of Science - 6
2012 Tanwar PS, Kaneko-Tarui T, Zhang L, Teixeira JM, 'Altered LKB1/AMPK/TSC1/TSC2/mTOR signaling causes disruption of sertoli cell polarity and spermatogenesis', Human Molecular Genetics, 21 4394-4405 (2012) [C1]
Citations Scopus - 31Web of Science - 29
2012 Tanwar PS, Kaneko-Tarui T, Zhang L, Tanaka Y, Crum CP, Teixeira JM, 'Stromal liver kinase B1 STK11 signaling loss induces oviductal adenomas and endometrial cancer by activating mammalian target of Rapamycin Complex 1', PLOS Genetics, 8 1-14 (2012) [C1]
Citations Scopus - 25Web of Science - 20
2011 Tanwar PS, Zhang L, Kaneko-Tarui T, Curley MD, Taketo MM, Rani P, et al., 'Mammalian Target of Rapamycin Is a Therapeutic Target for Murine Ovarian Endometrioid Adenocarcinomas with Dysregulated Wnt/beta-Catenin and PTEN', PLOS ONE, 6 (2011) [C1]
DOI 10.1371/journal.pone.0020715
Citations Scopus - 30Web of Science - 29
2011 Tanwar PS, Zhang L, Roberts DJ, Teixeira JM, 'Stromal Deletion of the APC Tumor Suppressor in Mice Triggers Development of Endometrial Cancer', CANCER RESEARCH, 71 1584-1596 (2011) [C1]
DOI 10.1158/0008-5472.CAN-10-3166
Citations Scopus - 32Web of Science - 29
2011 Tanwar PS, Zhang L, Teixeira JM, 'Adenomatous Polyposis Coli (APC) Is Essential for Maintaining the Integrity of the Seminiferous Epithelium', MOLECULAR ENDOCRINOLOGY, 25 1725-1739 (2011) [C1]
DOI 10.1210/me.2011-0057
Citations Scopus - 19Web of Science - 19
2011 Tanwar PS, McFarlane JR, 'Dynamic expression of bone morphogenetic protein 4 in reproductive organs of female mice', REPRODUCTION, 142 573-579 (2011) [C1]
DOI 10.1530/REP-10-0299
Citations Scopus - 11Web of Science - 11
2010 Tanwar PS, Kaneko-Tarui T, Zhang L, Rani P, Taketo MM, Teixeira J, 'Constitutive WNT/Beta-Catenin Signaling in Murine Sertoli Cells Disrupts Their Differentiation and Ability to Support Spermatogenesis', BIOLOGY OF REPRODUCTION, 82 422-432 (2010) [C1]
DOI 10.1095/biolreprod.109.079335
Citations Scopus - 60Web of Science - 60
2010 Tanwar PS, Zhang L, Tanaka Y, Taketo MM, Donahoe PK, Teixeira JM, 'Focal Mullerian duct retention in male mice with constitutively activated beta-catenin expression in the Mullerian duct mesenchyme', PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 107 16142-16147 (2010) [C1]
DOI 10.1073/pnas.1011606107
Citations Scopus - 17Web of Science - 17
2009 Tanwar PS, Lee H-J, Zhang L, Zukerberg LR, Taketo MM, Rueda BR, Teixeira JM, 'Constitutive Activation of Beta-Catenin in Uterine Stroma and Smooth Muscle Leads to the Development of Mesenchymal Tumors in Mice', BIOLOGY OF REPRODUCTION, 81 545-552 (2009) [C1]
DOI 10.1095/biolreprod.108.075648
Citations Scopus - 60Web of Science - 57
2009 Viswanathan SR, Powers JT, Einhorn W, Hoshida Y, Ng TL, Toffanin S, et al., 'Lin28 promotes transformation and is associated with advanced human malignancies', NATURE GENETICS, 41 843-U109 (2009) [C1]
DOI 10.1038/ng.392
Citations Scopus - 442Web of Science - 419
2008 Wu X, Tanwar PS, Raftery LA, 'Drosophila follicle cells: Morphogenesis in an eggshell', SEMINARS IN CELL & DEVELOPMENTAL BIOLOGY, 19 271-282 (2008) [C1]
DOI 10.1016/j.semcdb.2008.01.004
Citations Scopus - 65Web of Science - 57
2008 Tanwar PS, O'Shea T, McFarlane JR, 'In vivo evidence of role of bone morphogenetic protein-4 in the mouse ovary', Animal Reproduction Science, 106 232-240 (2008)

The transition of a primordial follicle to a primary follicle is an early step in folliculogenesis. All female mammals are born with a fixed stock of primordial follicles, and exh... [more]

The transition of a primordial follicle to a primary follicle is an early step in folliculogenesis. All female mammals are born with a fixed stock of primordial follicles, and exhaustion of that stock leads to menopause or infertility. Recently, several in vitro studies have indicated that BMP-4, BMP-7, and several other growth factors affect the transition of primordial to primary follicles. The aim of our present study was to investigate role of BMP-4 in this process using passive immunization to investigate the role of BMP-4 in a prepubertal mouse model. After seven days of treatment, the weight of antiBMP-4 treated ovaries was significantly lower than the ovaries from mice treated with nonimmune Ig. The number of primary follicles was lower, and the numbers of primordial follicles were higher in antiBMP-4 treated ovaries compared to control ovaries. Treatment with equine chorionic gonadotrophin (eCG) showed no influence on the effects of antiBMP-4 in the mouse ovary. Thus, the results of our study indicate that in vivo BMP-4 acts as transition factor in transition of primordial to primary follicle. © 2007 Elsevier B.V. All rights reserved.

DOI 10.1016/j.anireprosci.2007.04.015
Citations Scopus - 17
2008 Wu X, Yamada-Mabuchi M, Morris EJ, Tanwar PS, Dobens L, Gluderer S, et al., 'The Drosophila homolog of human tumor suppressor TSC-22 promotes cellular growth, proliferation, and survival', PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 105 5414-5419 (2008) [C1]
DOI 10.1073/pnas.0800945105
Citations Scopus - 15Web of Science - 13
Show 27 more journal articles

Conference (27 outputs)

Year Citation Altmetrics Link
2016 Bajwa P, Tanwar PS, 'Targeting mTOR signalling in serous ovarian cancer', ANZGOG (2016)
2016 kumar M, Tanwar PS, 'Wnt signalling actions in spermatogenesis are mediated by non-coding RNAs' (2016)
2016 sahoo S, Tanwar PS, 'Mechanical control of human endometrium: Role of ECM-mediated TGFß signalling in uterine epithelium' (2016)
2016 Bangaraswamaiah Nagendra, goad J, Nielsen S, rassam L, Lombard JM, Nahar P, Tanwar PS, 'Pill to prevent ovarian cancer' (2016)
2016 Tanwar PS, sahoo S, 'Extracellular matrix mediated TGFß signalling supports endometrial cancer metastasis' (2016)
2016 goad J, kumar M, Syed SM, Tanwar PS, 'Molecular mechanisms of endometrial gland development' (2016)
2016 Goad J, Bangaraswamaiah Nagendra P, Tanwar PS, 'A pill a day keeps ovarian cancer at bay: a link between reproductive health and predisposition to cancer' (2016)
2016 bajwa P, Tanwar PS, 'mTOR and endometrial aging: Hyperactivation of mTOR signalling contributes to the age-associated changes in uterine epithelium' (2016)
2016 Tanwar PS, 'Stromal-epithelial communications in endometrial functions and diseases' (2016)
2016 Sercombe L, bajwa P, Tanwar PS, 'mTORC1 is an essential regulator of granulosa cell proliferation and viability: important insights for infertility in PCOS' (2016)
2015 Kumar M, Goad J, Syed S, Tanwar PS, 'Twists and Turns: Balanced Wnt signalling is essential for epididymal coiling' (2015) [E3]
2015 Bajwa P, Tanwar PS, 'Age related increase in mTOR activity contributes to the pathogenesis of ovarian cancer' (2015) [E3]
2015 Tanwar PS, Sahoo S, 'Extracellular matrix mediated TGFß signalling supports endometrial cancer metastasis' (2015) [E3]
2015 Goad J, Kumar M, Syed S, Tanwar PS, 'Gone with the Wnt: Unopposed oestrogen leads to endometrial cancer by regulating Wnt signaling' (2015) [E3]
2015 Sercombe L, Sahoo S, Tanwar PS, 'mTORC1 hyperactivation induces the ovarian phenotype of PCOS' (2015) [E3]
2015 Goad J, Syed S, Tanwar PS, 'Synergistic effect of unopposed oestrogen and overactive Wnt signalling in endometrial cancer' (2015) [E3]
2015 Syed S, Goad J, Sahoo S, Cardona J, Kumar J, Tanwar P, 'Endometrial hyperplasia and cancer: Side effects of miscommunication' (2015) [E3]
2015 Syed S, Goad J, Sahoo S, Cardona J, Tanwar PS, 'Influence of bad neighborhood: Stromal contribution to endometrial cancer development' (2015) [E3]
2014 Kumar M, Sahoo SS, Tanwar P, 'MTOR: A NOVEL TARGET FOR TESTICULAR CANCER', ASIA-PACIFIC JOURNAL OF CLINICAL ONCOLOGY (2014) [E3]
2014 Tanwar PS, Kaneko-Tarui T, Teixeira JM, 'Constitutive Wnt/B-Catenin Signaling in Mice in the Absence of Mullerian Inhibiting Substance/AntiMulleiran Hormone Signaling Leads to the Development of a Polycystic Ovary Phenotype', REPRODUCTIVE SCIENCES (2014) [E3]
2013 Tanwar PS, 'Frequent alterations in mTOR signaling in human ovarian serous carcinomas', 25th Lorne Cancer Conference (2013) [E3]
2013 Tanwar PS, 'The Müllerian Inhibiting Substance type 2 receptor is an endogenous tumor suppressor and its loss phenocopies PTEN loss or activation of Kras in testes with sustained ßcatenin signaling', Society of Reproductive Biology Endocrine Society of Australia Annual Scientific Meeting (2013) [E3]
2013 Tanwar PS, 'Preclinical models of ovarian cancer: PI3K-mTOR signalling axis', Translational Cancer Research Conference (2013) [E3]
2011 Tanwar PS, Zhang L, Teixeira J, 'APC (Adenomatous Polyposis Coli), a Tumor Suppressor Gene, Is Required for Maintenance of Sertoli Cell Polarity and Microtubules Integrity.', BIOLOGY OF REPRODUCTION (2011) [E3]
2010 Tanwar PS, Zhang L, Tanaka Y, Taketo MM, Donahoe PK, Teixeira J, 'Mullerian Mesenchyme-Specific Activation of Wnt/Beta-Catenin Signaling Inhibits Mullerian Duct Regression and Contributes to Male Infertility', BIOLOGY OF REPRODUCTION (2010) [E3]
2010 Tanaka Y, Park JH, Tanwar PS, Kaneko-Tarui T, Mittal S, Teixeira J, 'DELETION OF TSC1 IN OVARIAN SOMATIC CELLS OF THE FEMALE REPRODUCTIVE TRACT CAUSES INFERTILITY.', FERTILITY AND STERILITY (2010) [E3]
2009 Tanwar PS, Kaneko-Tarui T, Zhang L, Rani P, Taketo MM, Teixeira J, 'Progressive Spermatogonial Stem Cell Loss in Mice with Constitutively Activated Beta-Catenin in Postpubertal Sertoli Cells is Associated with Persistent Expression or GDNF and MIS.', BIOLOGY OF REPRODUCTION (2009) [E3]
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Grants and Funding

Summary

Number of grants 21
Total funding $3,451,401

Click on a grant title below to expand the full details for that specific grant.


20171 grants / $20,000

Mediator complex subunit 12 (MED12) gene in pathogenesis of uterine smooth muscle tumours$20,000

Funding body: John Hunter Hospital Charitable Trust

Funding body John Hunter Hospital Charitable Trust
Project Team Doctor Muhammad Jamaluddin, Doctor Pradeep Tanwar, Doctor Pravin Nahar
Scheme Research Grant
Role Investigator
Funding Start 2017
Funding Finish 2017
GNo G1700368
Type Of Funding Other Public Sector - State
Category 2OPS
UON Y

20161 grants / $21,745

Uterine smooth muscle cells as a cell of origin for lymphangioleiomyomatosis (LAM)$21,745

Funding body: John Hunter Hospital Charitable Trust

Funding body John Hunter Hospital Charitable Trust
Project Team Doctor Pradeep Tanwar, Doctor Pravin Nahar
Scheme Research Grant
Role Lead
Funding Start 2016
Funding Finish 2016
GNo G1600379
Type Of Funding Other Public Sector - State
Category 2OPS
UON Y

201511 grants / $2,414,195

Targeting chemoresistant ovarian cancer cells$508,396

Funding body: Cancer Institute NSW

Funding body Cancer Institute NSW
Project Team Doctor Pradeep Tanwar
Scheme Career Development Fellowship
Role Lead
Funding Start 2015
Funding Finish 2017
GNo G1400754
Type Of Funding Other Public Sector - State
Category 2OPS
UON Y

High resolution fourier transform mass spectrometry platform for the discovery of novel cancer biomarkers and drug targets using label-free and isobaric-tagged approaches for quantitative proteomics.$500,000

Funding body: Cancer Institute NSW

Funding body Cancer Institute NSW
Project Team Professor Xu Dong Zhang, Doctor Matt Dun, Professor Jennifer Martin, Professor Hubert Hondermarck, Laureate Professor John Aitken, Doctor Nikki Verrills, Doctor Pradeep Tanwar, Laureate Professor Rodney Scott, Professor Maria Kavallaris, Dr Darren Saunders
Scheme Research Equipment Grant
Role Investigator
Funding Start 2015
Funding Finish 2016
GNo G1500599
Type Of Funding Other Public Sector - State
Category 2OPS
UON Y

Contribution of ovarian cancer stem cells to chemoresistance and recurrent disease.$378,941

Funding body: NHMRC (National Health & Medical Research Council)

Funding body NHMRC (National Health & Medical Research Council)
Project Team Doctor Pradeep Tanwar
Scheme Project Grant
Role Lead
Funding Start 2015
Funding Finish 2017
GNo G1400046
Type Of Funding Aust Competitive - Commonwealth
Category 1CS
UON Y

Advanced Technical Support for Oncology Single Cell Analysis Technologies$300,000

Funding body: Cancer Institute NSW

Funding body Cancer Institute NSW
Project Team Laureate Professor Rodney Scott, Professor Xu Dong Zhang, Professor Hubert Hondermarck, Conjoint Professor Stephen Ackland, Doctor Craig Gedye, Doctor Pradeep Tanwar, Doctor Chen Chen Jiang, Doctor Matt Dun, Professor Paul de Souza, Associate Professor Kevin Spring, Dr Tao Liu
Scheme Research Infrastructure Grants
Role Investigator
Funding Start 2015
Funding Finish 2018
GNo G1500824
Type Of Funding Other Public Sector - State
Category 2OPS
UON Y

The Hunter Cancer Biobank (HCB): Maximising community value through validation, annotation and distribution throughout NSW$300,000

Funding body: Cancer Institute NSW

Funding body Cancer Institute NSW
Project Team Professor John Forbes, Conjoint Professor Stephen Ackland, Laureate Professor Rodney Scott, Professor Marjorie Walker, Professor Xu Dong Zhang, Doctor Pradeep Tanwar, Doctor Nikola Bowden, Doctor Craig Gedye, Doctor James Lynam, Doctor Kelly Kiejda, Doctor Jennette Sakoff, Mr Loui Rassam, Dr Tara Roberts, Professor Soon Lee, Dr Betty Kan
Scheme Research Infrastructure Grants
Role Investigator
Funding Start 2015
Funding Finish 2018
GNo G1500825
Type Of Funding Other Public Sector - State
Category 2OPS
UON Y

High resolution fourier transform mass spectrometry platform for the discovery of novel cancer biomarkers and drug targets using label-free and isobaric-tagged approaches for quantitative proteomics.$196,250

Funding body: University of Newcastle

Funding body University of Newcastle
Project Team Professor Xu Dong Zhang, Doctor Matt Dun, Professor Jennifer Martin, Professor Hubert Hondermarck, Laureate Professor John Aitken, Doctor Nikki Verrills, Doctor Pradeep Tanwar, Laureate Professor Rodney Scott, Professor Maria Kavallaris, Dr Darren Saunders
Scheme Equipment Grant
Role Investigator
Funding Start 2015
Funding Finish 2015
GNo G1500935
Type Of Funding Internal
Category INTE
UON Y

Live cell imager for enhancement of pre-clinical cancer studies in the Hunter Translational Cancer Research Centre$124,938

Funding body: Cancer Institute NSW

Funding body Cancer Institute NSW
Project Team Conjoint Professor Stephen Ackland, Doctor Kelly Kiejda, Associate Professor Kevin Spring, Professor Xu Dong Zhang, Associate Professor Deborah Marsh, Associate Professor Christopher Scarlett, Doctor Pradeep Tanwar, Doctor Kathryn Skelding, Doctor Rick Thorne, Doctor Nikola Bowden
Scheme Research Equipment Grant
Role Investigator
Funding Start 2015
Funding Finish 2016
GNo G1500598
Type Of Funding Other Public Sector - State
Category 2OPS
UON Y

High throughput automated all-in-one laser scanning FLUOVIEW FV10i microscope$54,698

Funding body: NHMRC (National Health & Medical Research Council)

Funding body NHMRC (National Health & Medical Research Council)
Project Team Professor Xu Dong Zhang, Professor Robert Callister, Laureate Professor John Aitken, Doctor Pradeep Tanwar, Doctor Chen Chen Jiang, Doctor Lei Jin
Scheme Equipment Grant
Role Investigator
Funding Start 2015
Funding Finish 2015
GNo G1501576
Type Of Funding Other Public Sector - Commonwealth
Category 2OPC
UON Y

Uterine fibroids: Molecular basis of pathogenesis of uterine leiomyoma$25,222

Funding body: John Hunter Hospital Charitable Trust

Funding body John Hunter Hospital Charitable Trust
Project Team Doctor Pradeep Tanwar, Doctor Pravin Nahar
Scheme Research Grant
Role Lead
Funding Start 2015
Funding Finish 2015
GNo G1500010
Type Of Funding Other Public Sector - State
Category 2OPS
UON Y

Live cell imager for enhancement of pre-clinical cancer studies in the Hunter Translational Cancer Research Centre$25,000

Funding body: University of Newcastle

Funding body University of Newcastle
Project Team Conjoint Professor Stephen Ackland, Doctor Kelly Kiejda, Associate Professor Kevin Spring, Professor Xu Dong Zhang, Associate Professor Deborah Marsh, Associate Professor Christopher Scarlett, Doctor Pradeep Tanwar, Doctor Kathryn Skelding, Doctor Rick Thorne, Doctor Nikola Bowden
Scheme Equipment Grant
Role Investigator
Funding Start 2015
Funding Finish 2015
GNo G1500953
Type Of Funding Internal
Category INTE
UON Y

The Annual Scientific Meeting of the Endocrine Society of Australia and the Society of Reproductive Biology, Adelaide Australia, 23-26 August 2015$750

Funding body: University of Newcastle - Faculty of Health and Medicine

Funding body University of Newcastle - Faculty of Health and Medicine
Project Team Doctor Pradeep Tanwar
Scheme Travel Grant
Role Lead
Funding Start 2015
Funding Finish 2015
GNo G1501056
Type Of Funding Internal
Category INTE
UON Y

20143 grants / $116,081

JuLI Stage $71,674

Funding body: NHMRC (National Health & Medical Research Council)

DVC(R) Research Support for Future Fellow (FT13)$42,907

Funding body: University of Newcastle

Funding body University of Newcastle
Project Team Doctor Pradeep Tanwar
Scheme Future Fellowship Support
Role Lead
Funding Start 2014
Funding Finish 2017
GNo G1301419
Type Of Funding Internal
Category INTE
UON Y

Transforming Women's Health via Translational Investigation, Florence Italy, 26-29 March 2014$1,500

Funding body: University of Newcastle - Faculty of Health and Medicine

Funding body University of Newcastle - Faculty of Health and Medicine
Project Team Doctor Pradeep Tanwar
Scheme Travel Grant
Role Lead
Funding Start 2014
Funding Finish 2014
GNo G1400204
Type Of Funding Internal
Category INTE
UON Y

20135 grants / $879,380

mTOR signalling in serous ovarian cancer$784,784

Funding body: ARC (Australian Research Council)

Funding body ARC (Australian Research Council)
Project Team Doctor Pradeep Tanwar
Scheme Future Fellowships
Role Lead
Funding Start 2013
Funding Finish 2017
GNo G1300140
Type Of Funding Aust Competitive - Commonwealth
Category 1CS
UON Y

High Resolution Triple Fluorescence Stereomicroscope$30,000

Funding body: NHMRC (National Health & Medical Research Council)

Funding body NHMRC (National Health & Medical Research Council)
Project Team Doctor Pradeep Tanwar
Scheme Equipment Grant
Role Lead
Funding Start 2013
Funding Finish 2014
GNo G1301311
Type Of Funding Other Public Sector - Commonwealth
Category 2OPC
UON Y

Role of Wnt-P13K-mTOR signalling reproductive functions and gynecology/genitourinary cancers$5,000

Funding body: University of Newcastle

Funding body University of Newcastle
Project Team Doctor Pradeep Tanwar
Scheme New Staff Grant
Role Lead
Funding Start 2013
Funding Finish 2013
GNo G1300983
Type Of Funding Internal
Category INTE
UON Y
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Research Supervision

Number of supervisions

Completed2
Current12

Total current UON EFTSL

Masters0.9
PhD9.5

Current Supervision

Commenced Level of Study Research Title Program Supervisor Type
2016 PhD The Role of Tumour Microenvironment in Ovarian Cancer PhD (Pharmacy), Faculty of Health and Medicine, The University of Newcastle Principal Supervisor
2015 PhD The Role of mTOR Hyperactivation in the Pathogenesis of PCOS PhD (Medical Biochemistry), Faculty of Health and Medicine, The University of Newcastle Principal Supervisor
2015 Masters Role of microenvironment and extracellular matrix stiffness in Ovarian Cancer Progression M Philosophy (Medical Biochem), Faculty of Health and Medicine, The University of Newcastle Principal Supervisor
2015 PhD Early serous ovarian carcinogenesis : Understanding the genetic and lifestyle factors PhD (Medical Biochemistry), Faculty of Health and Medicine, The University of Newcastle Principal Supervisor
2015 PhD Genesis of ovarian cancer: understanding the mechanisms of oviductal epithelial cell homoeostasis PhD (Medical Biochemistry), Faculty of Health and Medicine, The University of Newcastle Principal Supervisor
2015 PhD Levels of Steroids and Endometrial Proteins as an Infertility Indicators Markers in Women with Reproductive Pathologies of Immune Origin. PhD (Medical Biochemistry), Faculty of Health and Medicine, The University of Newcastle Principal Supervisor
2014 PhD Role of mTOR signalling in Ovarian Cancer PhD (Medical Biochemistry), Faculty of Health and Medicine, The University of Newcastle Principal Supervisor
2014 PhD Role of microenvironment in endometrial cancer progression, metastasis and drug resistance PhD (Medical Biochemistry), Faculty of Health and Medicine, The University of Newcastle Principal Supervisor
2014 PhD To Study the Female Lower Reproductive Tract Cell Dynamics, Homeostasis and Cancer PhD (Medical Biochemistry), Faculty of Health and Medicine, The University of Newcastle Principal Supervisor
2013 PhD Role of Wnt Signalling in Testicular Morphogenesis and Carcinogenesis PhD (Medical Biochemistry), Faculty of Health and Medicine, The University of Newcastle Principal Supervisor
2013 PhD Role of Wnt Signalling in Endometrial Homeostasis and Cancer PhD (Medical Biochemistry), Faculty of Health and Medicine, The University of Newcastle Principal Supervisor
2013 PhD Endometrial Stem/Progenitor Cells in Endometrial Regeneration, Carcinogenesis and Aging PhD (Medical Biochemistry), Faculty of Health and Medicine, The University of Newcastle Principal Supervisor

Past Supervision

Year Level of Study Research Title Program Supervisor Type
2015 Honours The Role of mTOR Hyperactivation in the Pathogenesis of PCOS Biochemistry & Cell Biology, The University of Newcastle Principal Supervisor
2015 Honours Interrogating nuclear organisation and the transcription factory model using cytotrophoblast to syncytiotrophoblast differentiation Biological Sciences, Faculty of Engineering and Built Environment - The University of Newcastle (Australia) Co-Supervisor
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News

Ovarian Cancer Breakthrough

September 6, 2016

A team of Newcastle researchers, led by UON’s Dr Pradeep Tanwar, has identified a game-changing link between the use of the contraceptive pill and the risk of developing ovarian cancer.

UON researchers scoop reproductive biology awards

September 1, 2016

UON reproductive science researchers have been highly recognised with a host of awards at the Society For Reproductive Biology (SRB) Conference.

Dr Pradeep Tanwar

New approach to chemo-resistant ovarian cancer

March 12, 2015

Dr Pradeep Tanwar is working on a protein that has the potential to treat chemotherapy-resistant ovarian cancer.

Dr Mark Lock

$8.8M ARC funding

November 8, 2013

The Australian Research Council (ARC) has today awarded $8.8 million in Discovery Project research funding to the University of Newcastle. The funding will extend across 19 projects, an increase of 6 projects and $4.2 million since last year.

Dr Pradeep Tanwar

Position

ARC Future Fellow
School of Biomedical Sciences and Pharmacy
Faculty of Health and Medicine

Focus area

Medical Biochemistry

Contact Details

Email pradeep.tanwar@newcastle.edu.au
Phone (02) 4921 5148

Office

Room LS2-36
Building Life Sciences Building: 236
Location Callaghan
University Drive
Callaghan, NSW 2308
Australia
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