Dr Manish Kumar Jhamb
School of Biomedical Sciences and Pharmacy
- Phone:(02) 4921 6934
Commitment, dedication, hard work and collaboration are the pillars of my research career in the area of reproductive sciences. My work mainly focuses on reproductive tract cancers. We aim to understand the normal reproductive tract development and abnormalities resulting in reproductive malignancies.
I submitted my PhD thesis very recently on February 08, 2017. I was fortunate to be supervised by two internationally known scientists in the field of oncology, Dr Pradeep Tanwar (principal supervisor) and Dr Hubert Hondermarck (co-supervisor). My PhD program of research is achieved by four first author and three co-author publications. I manage to publish all the papers before submission of my thesis and accorded with six national research recognitions. These publications and awards subsequently laid the foundations for me to start working as Associate Lecturer in the School of Biomedical Sciences & Pharmacy at the University of Newcastle which is priority research centre for research in reproductive sciences.
My research program focused on understanding the mechanisms involved in development, progression and metastasis of gynaecological malignancies. We are also keen to understand the genetic mutations that cause unlimited growth, survival and proliferation of cancer cells. I am very fortunate to have Dr Pradeep Tanwar, as my mentor who is a leader in the area of gynaecology oncology, and has a vast national and international (5-year post-doctoral Fellowship in gynaecology oncology at the Harvard Medical School, USA) experience in the field of cancer biology. Our lab has extensive national and international collaborations with the leading scientists in the field of reproductive system cancers which provides access to state of art facilities, latest technologies and relevant patient samples. This is advantageous for me to nurture and progress in the field of gynaecology oncology and attract peer-reviewed competitive funding for continuing my research in the field of gynaecology oncology. This will aid in expanding my research program to international level, establish collaborations and take it to translational grade.
- Doctor of Philosophy in Medical Biochemistry, University of Newcastle
- Developmental Biology
- Gynaecology Oncology
- Medical Biochemistry
|Title||Organisation / Department|
Mammalian Growth and Development
The University of Newcastle
This course will provide students with an overview of the biomolecular, cellular, genetic, physiological and anatomical aspects of reproductive growth and development, from the creation of the germ cells in the developing embryo to reproductive senescence in the ageing adult. The course will examine how sperm and eggs (gametes) are made; fertilisation achieved; and successful pregnancy initiated, maintained and stopped at birth. Developmental principles will be studied. The course will focus only on mammals with an emphasis on humans. Current research findings and techniques will be a key focus of this course.
|Tutor||27/2/2017 - 24/5/2017|
For publications that are currently unpublished or in-press, details are shown in italics.
Journal article (17 outputs)
Syed SM, Kumar M, Ghosh A, Tomasetig F, Ali A, Whan RM, et al., 'Endometrial Axin2 Cells Drive Epithelial Homeostasis, Regeneration, and Cancer following Oncogenic Transformation', Cell Stem Cell, 26 64-80.e13 (2020) [C1]
Ghosh A, Syed SM, Kumar M, Carpenter TJ, Teixeira JM, Houairia N, et al., 'In Vivo Cell Fate Tracing Provides No Evidence for Mesenchymal to Epithelial Transition in Adult Fallopian Tube and Uterus', CELL REPORTS, 31 (2020) [C1]
Al-Juboori AAA, Ghosh A, Bin Jamaluddin MF, Kumar M, Sahoo SS, Syed SM, et al., 'Proteomic Analysis of Stromal and Epithelial Cell Communications in Human Endometrial Cancer Using a Unique 3D Co-Culture Model', PROTEOMICS, 19 (2019) [C1]
Goad J, Ko Y-A, Kumar M, Jamaluddin MFB, Tanwar PS, 'Oestrogen fuels the growth of endometrial hyperplastic lesions initiated by overactive Wnt/ß-catenin signalling.', Carcinogenesis, 39 1105-1116 (2018) [C1]
Jamaluddin MFB, Ko YA, Kumar M, Brown Y, Bajwa P, Nagendra PB, et al., 'Proteomic profiling of human uterine fibroids reveals upregulation of the extracellular matrix protein periostin', Endocrinology, 159 1106-1118 (2018) [C1]
Copyright © 2018 Endocrine Society The central characteristic of uterine fibroids is excessive deposition of extracellular matrix (ECM), which contributes to fibroid growth and bu... [more]
Copyright © 2018 Endocrine Society The central characteristic of uterine fibroids is excessive deposition of extracellular matrix (ECM), which contributes to fibroid growth and bulk-type symptoms. Despite this, very little is known about patterns of ECM protein expression in fibroids and whether these are influenced by the most common genetic anomalies, which relate to MED12. We performed extensive genetic and proteomic analyses of clinically annotated fibroids and adjacent normal myometrium to identify the composition and expression patterns of ECM proteins in MED12 mutation-positive and mutation-negative uterine fibroids. Genetic sequencing of tissue samples revealed MED12 alterations in 39 of 65 fibroids (60%) from 14 patients. Using isobaric tagged-based quantitative mass spectrometry on three selected patients (n = 9 fibroids), we observed a common set of upregulated (.1.5-fold) and downregulated (,0.66-fold) proteins in small, medium, and large fibroid samples of annotated MED12 status. These two sets of upregulated and downregulated proteins were the same in all patients, regardless of variations in fibroid size and MED12 status. We then focused on one of the significant upregulated ECM proteins and confirmed the differential expression of periostin using western blotting and immunohistochemical analysis. Our study defined the proteome of uterine fibroids and identified that increased ECM protein expression, in particular periostin, is a hallmark of uterine fibroids regardless of MED12 mutation status. This study sets the foundation for further investigations to analyze the mechanisms regulating ECM overexpression and the functional role of upregulated ECM proteins in leiomyogenesis.
Kumar M, Tanwar PS, 'Canonical Wnt/ß-catenin signaling regulates postnatal mouse epididymal development but does not affect epithelial cell differentiation.', Endocrinology, 158 4286-4299 (2017) [C1]
Goad J, Ko YA, Kumar M, Syed SM, Tanwar PS, 'Differential Wnt signaling activity limits epithelial gland development to the anti-mesometrial side of the mouse uterus', Developmental Biology, 423 138-151 (2017) [C1]
Kumar M, Tanwar P, 'Organ Culture and Whole Mount Immunofluorescence Staining of Mouse Wolffian Ducts', JOVE-JOURNAL OF VISUALIZED EXPERIMENTS, (2017) [C1]
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.
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.
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]
|Show 14 more journal articles|
Conference (1 outputs)
Kumar M, Sahoo SS, Tanwar P, 'MTOR: A NOVEL TARGET FOR TESTICULAR CANCER', ASIA-PACIFIC JOURNAL OF CLINICAL ONCOLOGY, Newcastle, NSW (2014) [E3]
Dr Manish Kumar Jhamb
School of Biomedical Sciences and Pharmacy
College of Health, Medicine and Wellbeing
|Phone||(02) 4921 6934|
|Building||Life Sciences Building|
Callaghan, NSW 2308