Najah started at UTS in 2003 and her primary research interests are in the investigation of the genetic and molecular basis of human disease with the aim of developing diagnostic/prognostic biomarkers and future novel therapies. Her current research is focussed on understanding how dysregulation of gene expression leads to disease, with a particular focus on cancer and diabetes. Her current research topics include examining the role of gene/pseudogene interactions in gene expression regulation and the role(s) of tumour suppressor gene mutations in the regulation of cancer development and progression.
In addition to her research, Najah is committed to student learning and teaching and coordinates and teaches subjects from second year undergraduate level to Honours. She is also a supervisor/co-supervisor of a number of research students at the Honours, Masters and PhD level.
Can supervise: YES
Najah coordinates Biochemistry and Molecular Biology subjects offered by the Faculty of Science, namely Molecular Biology 2 (subject number 91335) in autumn semester and Analytical Biochemistry (subject number 91326) spring semester.
Najah is also currently the Honours Program director.
Germline alterations of the tumor suppressor PTEN have been extensively characterized in patients with PTEN hamartoma tumor syndromes, encompassing subsets of Cowden syndrome, Bannayan-Riley-Ruvalcaba syndrome, Proteus and Proteus-like syndromes, as well as autism spectrum disorder. Studies have shown an increase in the risk of developing specific cancer types in the presence of a germline PTEN mutation. Furthermore, outside of the familial setting, somatic variants of PTEN occur in numerous malignancies. Here we introduce and discuss the prospect of moving toward a systems pathology approach for PTEN diagnostics, incorporating clinical and molecular pathology data with the goal of improving the clinical management of patients with a PTEN mutation. Detection of a germline PTEN mutation can inform cancer surveillance and in the case of somatic mutation, have value in predicting disease course. Given that PTEN functions in the PI3K/AKT/mTOR pathway, identification of a PTEN mutation may highlight new therapeutic opportunities and/or inform therapeutic choices.
Gerace, D, Martiniello-Wilks, R, Habib, R, Ren, B, Nassif, NT, O'Brien, BA & Simpson, AM 2019, 'Ex Vivo Expansion of Murine MSC Impairs Transcription Factor-Induced Differentiation into Pancreatic β-Cells.', Stem Cells International, vol. 2019.View/Download from: Publisher's site
Combinatorial gene and cell therapy as a means of generating surrogate β-cells has been investigated for the treatment of type 1 diabetes (T1D) for a number of years with varying success. One of the limitations of current cell therapies for T1D is the inability to generate sufficient quantities of functional transplantable insulin-producing cells. Due to their impressive immunomodulatory properties, in addition to their ease of expansion and genetic modification ex vivo, mesenchymal stem cells (MSCs) are an attractive alternative source of adult stem cells for regenerative medicine. To overcome the aforementioned limitation of current therapies, we assessed the utility of ex vivo expanded bone marrow-derived murine MSCs for their persistence in immune-competent and immune-deficient animal models and their ability to differentiate into surrogate β-cells. CD45-/Ly6+ murine MSCs were isolated from the bone marrow of nonobese diabetic (NOD) mice and nucleofected to express the bioluminescent protein, Firefly luciferase (Luc2). The persistence of a subcutaneous (s.c.) transplant of Luc2-expressing MSCs was assessed in immune-competent (NOD) (n = 4) and immune-deficient (NOD/Scid) (n = 4) animal models of diabetes. Luc2-expressing MSCs persisted for 2 and 12 weeks, respectively, in NOD and NOD/Scid mice. Ex vivo expanded MSCs were transduced with the HMD lentiviral vector (MOI = 10) to express furin-cleavable human insulin (INS-FUR) and murine NeuroD1 and Pdx1. This was followed by the characterization of pancreatic transdifferentiation via reverse transcriptase polymerase chain reaction (RT-PCR) and static and glucose-stimulated insulin secretion (GSIS). INS-FUR-expressing MSCs were assessed for their ability to reverse diabetes after transplantation into streptozotocin- (STZ-) diabetic NOD/Scid mice (n = 5). Transduced MSCs did not undergo pancreatic transdifferentiation, as determined by RT-PCR analyses, lacked glucose responsiveness, and upon transplantation did no...
Bryant, C, Aleks Lau, KH, Vuckovic, S, Marsh-Wakefield, F, Kruzins, A, McGuire, H, Yang, S, Fazekas de St. Groth, B, Nassif, N, Byrne, SN, Gibson, J, Brown, C, Larsen, S, McCulloch, D, Boyle, R, Joshua, D & Ho, PJ 2019, 'Accumulation of CD69+ Terminal Effector CD8+ T cells occurs in the bone marrow of newly diagnosed Myeloma patients who lack protective clonal Vb expanded cytotoxic T cells', Clinical Lymphoma Myeloma and Leukemia, vol. 19, no. 10, pp. e29-e29.View/Download from: Publisher's site
Marsh-Wakefield, F, Kruzins, A, McGuire, HM, Yang, S, Bryant, C, Fazekas de St Groth, B, Nassif, N, Byrne, SN, Gibson, J, Brown, C, Larsen, S, McCulloch, D, Boyle, R, Clark, G, Joshua, D, Ho, PJ & Vuckovic, S 2019, 'Mass Cytometry Discovers Two Discrete Subsets of CD39-Treg Which Discriminate MGUS From Multiple Myeloma.', Frontiers in immunology, vol. 10.View/Download from: Publisher's site
Multiple Myeloma (MM) is preceded by the clinically stable condition monoclonal gammopathy of undetermined significance (MGUS). Critical immune events that discriminate MGUS from newly diagnosed MM (ND)MM patients remain unknown, but may involve changes in the regulatory T cell (Treg) compartment that favor myeloma growth. To address this possibility, we used mass cytometry and the unsupervised clustering algorithm Flow self-organizing map (FlowSOM) to interrogate the distribution of multiple subsets within CD25+CD127low/negTreg in matched bone marrow (BM) and peripheral blood (PB) of MGUS and NDMM patients. Both mass cytometry and flow cytometry confirmed a trend toward prevalence of CD39-Treg within the Treg compartment in BM and PB of NDMM patients compared to CD39-Treg in MGUS patients. FlowSOM clustering displayed a phenotypic organization of Treg into 25 metaclusters that confirmed Treg heterogeneity. It identified two subsets which emerged within CD39-Treg of NDMM patients that were negligible or absent in CD39-Treg of MGUS patients. One subset was found in both BM and PB which phenotypically resembled activated Treg based on CD45RO, CD49d, and CD62L expression; another subset resembled BM-resident Treg based on its tissue-resident CD69+CD62L-CD49d- phenotype and restricted location within the BM. Both subsets co-expressed PD-1 and TIGIT, but PD-1 was expressed at higher levels on BM-resident Treg than on activated Treg. Within BM, both subsets had limited Perforin and Granzyme B production, whilst activated Treg in PB acquired high Perforin and Granzyme B production. In conclusion, the use of mass cytometry and FlowSOM clustering discovered two discrete subsets of CD39-Treg which are discordant in MGUS and NDMM patients and may be permissive of myeloma growth which warrants further study. Understanding the regulatory properties of these subsets may also advance MGUS and MM diagnosis, prognosis, and therapeutic implications for MM patients.
Ren, B, La, QT, O'Brien, BA, Nassif, NT, Tan, Y, Gerace, D, Martiniello-Wilks, R, Torpy, F, Dane, AP, Alexander, IE & Simpson, AM 2018, 'Partial pancreatic transdifferentiation of primary human hepatocytes in the livers of a humanised mouse model.', The journal of gene medicine, vol. 20, no. 5.View/Download from: Publisher's site
Gene therapy is one treatment that may ultimately cure type 1 diabetes. We have previously shown that the introduction of furin-cleavable human insulin (INS-FUR) to the livers in several animal models of diabetes resulted in the reversal of diabetes and partial pancreatic transdifferentiation of liver cells. The present study investigated whether streptozotocin-diabetes could be reversed in FRG mice in which chimeric mouse-human livers can readily be established and, in addition, whether pancreatic transdifferentiation occurred in the engrafted human hepatocytes.Engraftment of human hepatocytes was confirmed by measuring human albumin levels. Following delivery of the empty vector or the INS-FUR vector to diabetic FRG mice, mice were monitored for weight and blood glucose levels. Intraperitoneal glucose tolerance tests (IPGTTs) were performed. Expression levels of pancreatic hormones and transcription factors were determined by a reverse transcriptase-polymerase chain reaction (RT-PCR) and immunohistochemistry.Diabetes was reversed for a period of 60 days (experimental endpoint) after transduction with INS-FUR. IPGTTs of the insulin-transduced animals were not significantly different from nondiabetic animals. Immunofluorescence microscopy revealed the expression of human albumin and insulin in transduced liver samples. Quantitative RT-PCR showed expression of human and mouse endocrine hormones and β-cell transcription factors, indicating partial pancreatic transdifferentiation of mouse and human hepatocytes. Nonfasting human C-peptide levels were significantly higher than mouse levels, suggesting that transdifferentiated human hepatocytes made a significant contribution to the reversal of diabetes.These data show that human hepatocytes can be induced to undergo partial pancreatic transdifferentiation in vivo, indicating that the technology holds promise for the treatment of type 1 diabetes.
Lees, T, Fatima-Shad, K, Simpson, A, Nassif, N, Lin, Y & Lal, S 2018, 'Heart Rate Variability as a Biomarker for Predicting Stroke, Post-stroke Complications and Functionality', Biomarker Insights, vol. 13, pp. 1-13.View/Download from: Publisher's site
Background: Heart rate variability (HRV) is a non-invasive measure of the function of the autonomic nervous system, and its dynamic nature may provide a means through which stroke and its associated complications may be predicted, monitored, and managed.
Objective: The objective of this review is to identify and provide a critique on the most recent uses of HRV in stroke diagnosis/management and highlight areas that warrant further research.
Methods: The MEDLINE, CINAHL, and OVID MEDLINE databases were canvassed using a systematic search strategy, for articles investigating the use of HRV in stroke diagnosis and management. Initial paper selections were based on title alone, and final paper inclusion was informed by a full-text critical appraisal.
Results: The systematic search returned 98 records, of which 51 were unique. Following screening, 22 records were included in the final systematic review. The included papers provided some information regarding predicting incident stroke, which largely seems to be best predicted by time- and frequency-domain HRV parameters. Furthermore, post-stroke complications and functionality are similarly predicted by time- and frequency-domain parameters, as well as non-linear parameters in some instances.
Conclusions: Current research provides good evidence that HRV parameters may have utility as a biomarker for stroke and for post-stroke complications and/or functionality. Future research would benefit from the integration of non-linear, and novel parameters, the hybridisation of HRV parameters, and the expansion of the utilisation of predictive regression and hazard modelling.
Chen, H, McGowan, E, Ren, N, Nassif, N, Lal, S, Qu, X & Lin, Y 2018, 'Nattokinase: A Promising Alternative in Prevention andTreatment of Cardiovascular Diseases', Biomarker Insights, vol. 13.View/Download from: Publisher's site
Cardiovascular disease (CVD) is the leading cause of death in the world, however our approach to the control and management of CVD mortality is limited. Nattokinase (NK), the most active ingredient of natto, possesses a variety of favourable cardiovascular effects and the consumption of natto has been linked to a reduction in CVD mortality. Recent research has demonstrated that NK has potent fibrinolytic activity, antihypertensive, anti-atherosclerotic, lipid lowering, anti-platelet and neuroprotective effects. This review covers the major pharmacological effects of NK with a focus on its clinical relevance to CVD. It outlines the advantages of NK and the outstanding issues pertaining to NK pharmacokinetics. Available evidence suggests that NK is a unique natural compound that possesses several key cardiovascular beneficial effects for CVD patients and is therefore an ideal drug candidate for the prevention and treatment of CVD. NK is therefore a promising alternative in the management of CVD.
Haddadi, N, Lin, Y, Travis, G, Simpson, AM, Nassif, NT & McGowan, EM 2018, 'PTEN/PTENP1: 'Regulating the regulator of RTK-dependent PI3K/Akt signalling', new targets for cancer therapy.', Molecular cancer, vol. 17, no. 1.View/Download from: Publisher's site
Regulation of the PI-3 kinase (PI3K)/Akt signalling pathway is essential for maintaining the integrity of fundamental cellular processes, cell growth, survival, death and metabolism, and dysregulation of this pathway is implicated in the development and progression of cancers. Receptor tyrosine kinases (RTKs) are major upstream regulators of PI3K/Akt signalling. The phosphatase and tensin homologue (PTEN), a well characterised tumour suppressor, is a prime antagonist of PI3K and therefore a negative regulator of this pathway. Loss or inactivation of PTEN, which occurs in many tumour types, leads to overactivation of RTK/PI3K/Akt signalling driving tumourigenesis. Cellular PTEN levels are tightly regulated by a number of transcriptional, post-transcriptional and post-translational regulatory mechanisms. Of particular interest, transcription of the PTEN pseudogene, PTENP1, produces sense and antisense transcripts that exhibit post-transcriptional and transcriptional modulation of PTEN expression respectively. These additional levels of regulatory complexity governing PTEN expression add to the overall intricacies of the regulation of RTK/PI-3 K/Akt signalling. This review will discuss the regulation of oncogenic PI3K signalling by PTEN (the regulator) with a focus on the modulatory effects of the sense and antisense transcripts of PTENP1 on PTEN expression, and will further explore the potential for new therapeutic opportunities in cancer treatment.
Gerace, D, Martiniello-Wilks, R, Nassif, NT, Lal, S, Steptoe, R & Simpson, AM 2017, 'CRISPR-targeted genome editing of mesenchymal stem cell-derived therapies for type 1 diabetes: a path to clinical success?', STEM CELL RESEARCH & THERAPY, vol. 8.View/Download from: Publisher's site
Lees, T, Nassif, N, Simpson, A, Shad-Kaneez, F, Martiniello-Wilks, R, Lin, Y, Jones, A, Qu, X & Lal, S 2017, 'Recent advances in molecular biomarkers for diabetes mellitus: a systematic review.', Biomarkers, vol. 22, no. 7, pp. 604-613.View/Download from: Publisher's site
CONTEXT: Diabetes is a growing global metabolic epidemic. Current research is focussing on exploring how the biological processes and clinical outcomes of diabetes are related and developing novel biomarkers to measure these relationships, as this can subsequently improve diagnostic, therapeutic and management capacity. OBJECTIVE: The objective of this study is to identify the most recent advances in molecular biomarkers of diabetes and directions that warrant further research. METHODS: Using a systematic search strategy, the MEDLINE, CINAHL and OVID MEDLINE databases were canvassed for articles that investigated molecular biomarkers for diabetes. Initial selections were made based on article title, whilst final inclusion was informed by a critical appraisal of the full text of each article. RESULTS: The systematic search returned 246 records, of which 113 were unique. Following screening, 29 records were included in the final review. Three main research strategies (the development of novel technologies, broad biomarker panels, and targeted approaches) identified a number of potential biomarkers for diabetes including miR-126, C-reactive protein, 2-aminoadipic acid and betatrophin. CONCLUSION: The most promising research avenue identified is the detection and quantification of micro RNA. Further, the utilisation of functionalised electrodes as a means to detect biomarker compounds also warrants attention.
Haddadi, N, Lin, Y, Simpson, AM, Nassif, NT & McGowan, EM 2017, '“Dicing and Splicing” Sphingosine Kinase and Relevance to Cancer', International Journal of Molecular Sciences, vol. 18, no. 9, pp. 1-25.View/Download from: Publisher's site
Sphingosine kinase (SphK) is a lipid enzyme that maintains cellular lipid homeostasis. Two SphK isozymes, SphK1 and SphK2, are expressed from different chromosomes and several variant isoforms are expressed from each of the isozymes, allowing for the multi-faceted biological diversity of SphK activity. Historically, SphK1 is mainly associated with oncogenicity, however in reality, both SphK1 and SphK2 isozymes possess oncogenic properties and are recognized therapeutic targets. The absence of mutations of SphK in various cancer types has led to the theory that cancer cells develop a dependency on SphK signaling (hyper-SphK signaling) or “non-oncogenic addiction”. Here we discuss additional theories of SphK cellular mislocation and aberrant “dicing and splicing” as contributors to cancer cell biology and as key determinants of the success or failure of SphK/S1P (sphingosine 1 phosphate) based therapeutics.
Hatoum, D, Haddadi, N, Lin, Y, Nassif, NT & McGowan, EM 2017, 'Mammalian sphingosine kinase (SphK) isoenzymes and isoform expression: challenges for SphK as an oncotarget.', Oncotarget, vol. 8, no. 22, pp. 36898-36929.View/Download from: Publisher's site
The various sphingosine kinase (SphK) isoenzymes (isozymes) and isoforms, key players in normal cellular physiology, are strongly implicated in cancer and other diseases. Mutations in SphKs, that may justify abnormal physiological function, have not been recorded. Nonetheless, there is a large and growing body of evidence demonstrating the contribution of gain or loss of function and the imbalance in the SphK/S1P rheostat to a plethora of pathological conditions including cancer, diabetes and inflammatory diseases. SphK is expressed as two isozymes SphK1 and SphK2, transcribed from genes located on different chromosomes and both isozymes catalyze the phosphorylation of sphingosine to S1P. Expression of each SphK isozyme produces alternately spliced isoforms. In recent years the importance of the contribution of SpK1 expression to treatment resistance in cancer has been highlighted and, additionally, differences in treatment outcome appear to also be dependent upon SphK isoform expression. This review focuses on an exciting emerging area of research involving SphKs functions, expression and subcellular localization, highlighting the complexity of targeting SphK in cancer and also comorbid diseases. This review also covers the SphK isoenzymes and isoforms from a historical perspective, from their first discovery in murine species and then in humans, their role(s) in normal cellular function and in disease processes, to advancement of SphK as an oncotarget.
Hatoum, D, Yagoub, D, Ahadi, A, Nassif, NT & McGowan, EM 2017, 'Annexin/S100A protein family regulation through p14ARF-p53 activation: A role in cell survival and predicting treatment outcomes in breast cancer', PLoS ONE, vol. 12, no. 1.View/Download from: Publisher's site
© 2017 Hatoum et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. The annexin family and S100A associated proteins are important regulators of diverse calcium- dependent cellular processes including cell division, growth regulation and apoptosis. Dysfunction of individual annexin and S100A proteins is associated with cancer progression, metastasis and cancer drug resistance. This manuscript describes the novel finding of differential regulation of the annexin and S100A family of proteins by activation of p53 in breast cancer cells. Additionally, the observed differential regulation is found to be beneficial to the survival of breast cancer cells and to influence treatment efficacy. We have used unbiased, quantitative proteomics to determine the proteomic changes occurring post p14ARF-p53 activation in estrogen receptor (ER) breast cancer cells. In this report we identified differential regulation of the annexin/S100A family, through unique peptide recognition at the N-terminal regions, demonstrating p14ARF-p53 is a central orchestrator of the annexin/S100A family of calcium regulators in favor of pro-survival functions in the breast cancer cell. This regulation was found to be cell-type specific. Retrospective human breast cancer studies have demonstrated that tumors with functional wild type p53 (p53wt) respond poorly to some chemotherapy agents compared to tumors with a non-functional p53. Given that modulation of calcium signaling has been demonstrated to change sensitivity of chemotherapeutic agents to apoptotic signals, in principle, we explored the paradigm of how p53 modulation of calcium regulators in ER+ breast cancer patients impacts and influences therapeutic outcomes.
Winata, P, Williams, M, McGowan, E, Nassif, N, Van Zandwijk, N & Reid, G 2017, 'The analysis of novel microRNA mimic sequences in cancer cells reveals lack of specificity in stem-loop RT-qPCR-based microRNA detection', BMC Research Notes, vol. 10, no. 1, pp. 1-7.View/Download from: Publisher's site
© 2017 The Author(s). Objective: MicroRNAs are frequently downregulated in cancer, and restoring expression has tumour suppressive activity in tumour cells. Our recent phase I clinical trial investigated microRNA-based therapy in patients with malignant pleural mesothelioma. Treatment with TargomiRs, microRNA mimics with novel sequence packaged in EGFR antibody-targeted bacterial minicells, revealed clear signs of clinical activity. In order to detect delivery of microRNA mimics to tumour cells in future clinical trials, we tested hydrolysis probe-based assays specific for the sequence of the novel mimics in transfected mesothelioma cell lines using RT-qPCR. Results: The custom assays efficiently and specifically amplified the consensus mimics. However, we found that these assays gave a signal when total RNA from untransfected and control mimic-transfected cells were used as templates. Further investigation revealed that the reverse transcription step using stem-loop primers appeared to introduce substantial non-specific amplification with either total RNA or synthetic RNA templates. This suggests that reverse transcription using stem-loop primers suffers from an intrinsic lack of specificity for the detection of highly similar microRNAs in the same family, especially when analysing total RNA. These results suggest that RT-qPCR is unlikely to be an effective means to detect delivery of microRNA mimic-based drugs to tumour cells in patients.
Ren, B, Tao, C, Swan, MA, Joachim, N, Martiniello-Wilks, R, Nassif, NT, O'Brien, BA & Simpson, AM 2016, 'Pancreatic Transdifferentiation and Glucose-Regulated Production of Human Insulin in the H4IIE Rat Liver Cell Line', INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES, vol. 17, no. 4.View/Download from: Publisher's site
Suen, H, Brown, R, Yang, S, Weatherburn, C, Ho, PJ, Woodland, N, Nassif, N, Barbaro, P, Bryant, C, Hart, D, Gibson, J & Joshua, D 2016, 'Multiple myeloma causes clonal T-cell immunosenescence: identification of potential novel targets for promoting tumour immunity and implications for checkpoint blockade', LEUKEMIA, vol. 30, no. 8, pp. 1716-1724.View/Download from: Publisher's site
Archer, NS, Nassif, NT & O'Brien, BA 2015, 'Genetic variants of SLC11A1 are associated with both autoimmune and infectious diseases: systematic review and meta-analysis', GENES AND IMMUNITY, vol. 16, no. 4, pp. 275-283.View/Download from: Publisher's site
McAuliffe, S, Brown, R, Catalano, A, Ho, PJ, Nassif, N, Woodland, N, Hart, D, Weatherburn, C, Yang, S, Suen, H, Paul, C, Joshua, D & Gibson, J 2015, 'Using digital polymerase chain reaction to detect minimal residual disease in myeloma by identifying FGFR3 up-regulation', LEUKEMIA & LYMPHOMA, vol. 56, no. 9, pp. 2714-2716.View/Download from: Publisher's site
Lawandi, J, Tao, C, Ren, B, Williams, P, Ling, D, Swan, MA, Nassif, NT, Torpy, FR, O'Brien, BA & Simpson, AM 2015, 'Reversal of diabetes following transplantation of an insulin-secreting human liver cell line: Melligen cells', MOLECULAR THERAPY-METHODS & CLINICAL DEVELOPMENT, vol. 2.View/Download from: Publisher's site
Haass, NK, Nassif, N & McGowan, EM 2015, 'Switching the Sphingolipid Rheostat in the Treatment of Diabetes and Cancer Comorbidity from a Problem to an Advantage', BIOMED RESEARCH INTERNATIONAL.View/Download from: Publisher's site
Nield, BS, Guzowski, R, Nassif, N, Simpson, AM & Martiniello-Wilks, R 2014, 'First use of Re: View: A tool to combine assessment tasks, marking criteria and graduate attributes for biochemistry students', International Journal of Innovation in Science and Mathematics Education, vol. 22, no. 7, pp. 49-64.
In order to improve clarity of the link between assessment tasks and graduate attributes to students, Re:View was introduced across three undergraduate biochemistry subjects. Re:View is an online assessment tool which provides a direct visual link between graduate attributes and marking criteria. It also provides students with an easy access portal to retrieve their grade and assessor feedback on assessment tasks. Our aim was to improve the second and third year biochemistry student laboratory-based learning experience by developing and clarifying the link between assessment tasks, marking criteria and graduate attributes, using Re:View as the assessment tool. Student opinion showed Re:View was of benefit to align marking criteria with graduate attributes, and provided easy access to feedback which could be used to improve future work. This first use of Re:View, with development of criterion-referenced marking criteria and rubrics, has revolutionised assessment in the three biochemistry subjects under study. With the use of Re:View we have clarified the link between assessment tasks and marking criteria, and enhanced student engagement with laboratory-based assessment tasks, which has improved their written assessment performance.
Favaloro, J, Liyadipitiya, T, Brown, R, Yang, S, Suen, H, Woodland, N, Nassif, N, Hart, D, Fromm, P, Weatherburn, C, Gibson, J, Ho, PJ & Joshua, D 2014, 'Myeloid derived suppressor cells are numerically, functionally and phenotypically different in patients with multiple myeloma', LEUKEMIA & LYMPHOMA, vol. 55, no. 12, pp. 2893-2900.View/Download from: Publisher's site
Gerace, D, Ren, B, Hawthorne, W, Byrne, M, Phillips, P, O'Brien, B, Nassif, N, Alexander, I & Simpson, AM 2013, 'Pancreatic transdifferentiation in porcine liver following lentiviral delivery of human furin-cleavable insulin', Transplantation Proceedings, vol. 45, no. 5, pp. 1869-1874.View/Download from: Publisher's site
Type I diabetes mellitus (TID) results from the autoimmune destruction of the insulin-producing pancreatic ß-cells. Gene therapy is one strategy being actively explored to cure TID by affording non-ß-cells the ability to secrete insulin in response to physiologic stimuli. In previous studies, we used a novel surgical technique to express furin-cleavable human insulin (INS-FUR) in the livers of streptozotocin (STZ)-diabetic Wistar rats and nonobese diabetic (NOD) mice with the use of the HMD lentiviral vector. Normoglycemia was observed for 500 and 150 days, respectively (experimental end points). Additionally, some endocrine transdifferentiation of the liver, with storage of insulin in granules, and expression of some ß-cell transcription factors (eg, Pdx1, Neurod1, Neurog3, Nkx2-2, Pax4) and pancreatic hormones in both studies. The aim of this study was to determine if this novel approach could induce liver to pancreatic transdifferentiation to reverse diabetes in pancreatectomized Westran pigs. Nine pigs were used in the study, however only one pig maintained normal fasting blood glucose levels for the period from 10 to 44 days (experimental end point). This animal was given 2.8 × 10(9) transducing units/kg of the lentiviral vector expressing INS-FUR. A normal intravenous glucose tolerance test was achieved at 30 days. Reverse-transcription polymerase chain reaction analysis of the liver tissue revealed expression of several ß-cell transcription factors, including the key factors, Pdx-1 and Neurod1, pancreatic hormones, glucagon, and somatostatin; however, endogenous pig insulin was not expressed.
Ren, B, O'Brien, B, Byrne, M, Ch'ng, E, Gatt, PN, Swan, MA, Nassif, N, Wei, M, Gijsbers, R, Debyser, Z & Simpson, AM 2013, 'Long-term reversal of diabetes in non-obese diabetic mice by liver-directed gene therapy.', The Journal of gene Medicine, vol. 15, no. 1, pp. 28-41.View/Download from: Publisher's site
Background Type 1 diabetes (T1D) results from an autoimmune attack against the insulin-producing ß-cells of the pancreas. The present study aimed to reverse T1D by gene therapy. Methods We used a novel surgical technique, which involves isolating the liver from the circulation before the delivery of a lentiviral vector carrying furin-cleavable human insulin (INS-FUR) or empty vector to the livers of diabetic non-obese diabetic mice (NOD). This was compared with the direct injection of the vector into the portal circulation. Mice were monitored for body weight and blood glucose. Intravenous glucose tolerance tests were performed. Expression of insulin and pancreatic transcription factors was determined by the reverse transcriptase-polymerase chain reaction and immunohistochemistry and immunoelectron microscopy was used to localise insulin. Results Using the novel surgical technique, we achieved long-term transduction (42% efficiency) of hepatocytes, restored normoglycaemia for 150 days (experimental endpoint) and re-established normal glucose tolerance. We showed the expression of ß-cell transcription factors, murine insulin, glucagon and somatostatin, and hepatic storage of insulin in granules. The expression of hepatic markers, C/EBP-ß, G6PC, AAT and GLUI was down-regulated in INS-FUR-treated livers. Liver function tests remained normal, with no evidence of intrahepatic inflammation or autoimmune destruction of the insulin-secreting liver tissue. By comparison, direct injection of INS-FUR reduced blood glucose levels, and no pancreatic transdifferentiation or normal glucose tolerance was observed.
Simpson, AM, Ren, B, O'Brien, BA & Nassif, NT 2013, 'Response to the letter to the editor by M. Elsner et al: "Comment on Binhai Ren et al (2013;15:28-41). Long term reversal of diabetes in non-obese diabetic mice by liver-directed gene therapy"', JOURNAL OF GENE MEDICINE, vol. 15, no. 8-9, pp. 309-310.View/Download from: Publisher's site
Bryant, C, Suen, H, Brown, R, Yang, S, Favaloro, J, Aklilu, E, Gibson, J, Ho, PJ, Iland, H, Fromm, P, Woodland, N, Nassif, N, Hart, D & Joshua, DE 2013, 'Long-term survival in multiple myeloma is associated with a distinct immunological profile, which includes proliferative cytotoxic T-cell clones and a favourable Treg/Th17 balance', Blood Cancer Journal, vol. 3, pp. 1-7.View/Download from: Publisher's site
Despite improved outcomes in multiple myeloma (MM), a cure remains elusive. However, even before the current therapeutic era, 5% of patients survived
for >10 years and we propose that immune factors contribute to this longer survival. We identified patients attending our clinic, who had survived
for >10 years (n=20) and analysed their blood for the presence of T-cell clones, T-regulatory cells (Tregs) and T helper 17 (Th17) cells. These results were compared with MM patients with shorter follow-up and age-matched healthy control donors. The frequency of cytotoxic T-cell clonal expansions in patients with <10 years follow-up (MM patients) was 54% (n=144), whereas it was 100% (n=19/19) in the long-survivors (LTS-MM). T-cell clones from MM patients proliferated poorly in vitro, whereas those from LTS-MM patients proliferated readily (median proliferations 6.1% and 61.5%, respectively (P<0.0001)). In addition, we found significantly higher Th17 cells and lower Tregs in the LTS-MM group when compared with the MM group. These results indicate that long-term survival in MM is associated with a distinct immunological profile, which is consistent with decreased immune suppression.
Brown, R, Kabani, K, Favaloro, J, Yang, S, Ho, PJ, Gibson, J, Fromm, P, Suen, H, Woodland, NB, Nassif, N, Hart, D & Joshua, D 2012, 'CD86+ or HLA-G+ can be transferred via trogocytosis from myeloma cells to T cells and are associated with poor prognosis', Blood, vol. 120, pp. 2055-2063.View/Download from: Publisher's site
The transfer of membrane proteins between cells during contact, known as trogocytosis, can create novel cells with a unique phenotype and altered function. We demonstrate that trogocytosis is more common in multiple myeloma (MM) than chronic lymphocytic leukemia and Waldenstrom macroglobulinaemia; that T cells are more probable to be recipients than B or natural killer cells; that trogocytosis occurs independently of either the T-cell receptor or HLA compatibility; and that after trogocytosis, T cells with acquired antigens can become novel regulators of T-cell proliferation. We screened 168 patients with MM and found that CD86 and human leukocyte antigen G (HLA-G) were antigens commonly acquired by T cells from malignant plasma cells. CD3+ CD86acq+ and CD3+ HLA-Gacq+ cells were more prevalent in bone marrow than peripheral blood samples. The presence of either CD86 or HLA-G on malignant plasma cells was associated with a poor prognosis. CD38++ side population cells expressed HLA-G, suggesting that these putative myeloma stem cells could generate immune tolerance. HLA-G+ T cells had a regulatory potency similar to natural Tregs, thus providing another novel mechanism for MM to avoid effective immune surveillance
Daniel, R, Sanchez, JJ, Nassif, N, Hernandez, A & Walsh, SJ 2009, 'Partial forensic validation of a 16plex SNP assay for the inference of biogeographical ancestry', Forensic Science International: Genetics Supplement Series, vol. 2, pp. 477-478.View/Download from: Publisher's site
A partial forensic validation study demonstrated the suitability of an ancestry informative 16 locus SNP assay to forensic casework.
Lobo, G, Waite, KA, Planchon, P, Todd, R, Nassif, N & Eng, C 2009, 'Germline and somatic cancer-associated mutations in the ATP-binding motifs of PTEN influence its subcellular localization and tumor suppressive function', Human Molecular Genetics, vol. 18, no. 15, pp. 2851-2862.View/Download from: Publisher's site
Germline and somatic PTEN mutations are found in Cowden syndrome (CS) and multiple sporadic malignancies, respectively. PTEN function appears to be modulated by subcellular compartmentalization, and mislocalization may affect function. We have shown that cellular ATP levels affect nuclear PTEN levels. Here, we examined the ATP-binding capabilities of PTEN and functional consequences, relevant to cancer-associated mutations. PTEN mutation analysis of CS patients and sporadic colorectal carcinomas and comparative aminoacid analysis were utilized to identify mutations in ATP-binding motifs. The ability of wild-type (WT) or mutant PTEN to bind ATP was assessed by ATP-agarose-binding assays. Subcellular fractionation, western blotting, confocal microscopy and growth assays were used to determine relative nuclear-cytoplasmic localization and function. Somatic colorectal carcinoma-derived PTEN missense mutations were associated with nuclear mislocalization. These mutations altered cellular proliferation, apoptosis and anchorage-dependent growth. Examination of PTEN's amino acid sequence revealed these mutations resided in previously undescribed ATP-binding motifs (c.60-73; c.122-136). In contrast to WT PTEN, both cancer-associated somatic and germline-derived PTEN missense mutations, which lie within the ATP-binding motifs, result in mutant PTEN that does not bind ATP efficiently. We also show that CS patients with germline ATP-binding motif-mutations had nuclear PTEN mislocalization. Of four unrelated patients with functional germline ATP-binding domain mutations, all three female patients had breast cancers. Germline and somatic mutations within PTEN's ATP-binding domain play important pathogenic roles in both heritable and sporadic carcinogenesis by PTEN nuclear mislocalization resulting in altered signaling and growth. Manipulation of ATP may represent novel therapies in tumors with such PTEN alterations.
O'Brien, B, Archer, NS, Simpson, AM, Torpy, FR & Nassif, N 2008, 'Association of SLC11A1 promoter polymorphisms with the incidence of autoimmune and inflammatory diseases: A meta-analysis', Journal Of Autoimmunity, vol. 31, no. 1, pp. 42-51.View/Download from: Publisher's site
Solute carrier family 11 member a1 (SLC11A1) exerts pleiotropic effects on macrophage function. Expression of SLC11A1 is regulated by a (GT)(n) microsatellite promoter repeat polymorphism of which nine alleles have been described. Enhanced activation of
Ren, B, O'Brien, B, Swan, MA, Koina, ME, Nassif, N, Wei, MQ & Simpson, AM 2007, 'Long-term Correction Of Diabetes In Rats After Lentiviral Hepatic Insulin Gene Therapy', Diabetologia, vol. 50, no. 9, pp. 1910-1920.View/Download from: Publisher's site
Aims/hypothesis Type 1 diabetes results from the autoimmune destruction of pancreatic beta cells. Exogenous insulin therapy cannot achieve precise physiological control of blood glucose concentrations, and debilitating complications develop. Lentiviral v
Nassif, N, Lobo, GP, Wu, X, Henderson, CJ, Morrison, CD, Eng, C, Jalaludin, B & Segelov, E 2004, 'PTEN mutations are common in sporadic microsatellite stable colorectal cancer', Oncogene, vol. 23, no. 1, pp. 617-628.View/Download from: Publisher's site
The tumour suppressor gene PTEN, located at chromosome sub-band 10q23.3, encodes a dual-specificity phosphatase that negatively regulates the phosphatidylinositol 3'-kinase (PI3 K)/Akt-dependent cellular survival pathway. PTEN is frequently inactivated in many tumour types including glioblastoma, prostate and endometrial cancers. While initial studies reported that PTEN gene mutations were rare in colorectal cancer, more recent reports have shown an approximate 18% incidence of somatic PTEN mutations in colorectal tumours exhibiting microsatellite instability (MSI+). To verify the role of this gene in colorectal tumorigenesis, we analysed paired normal and tumour DNA from 41 unselected primary sporadic colorectal cancers for PTEN inactivation by mutation and/or allelic loss. We now report PTEN gene mutations in 19.5% (8/41) of tumours and allele loss, including all or part of the PTEN gene, in a further 17% (7/41) of the cases.
Indsto, J, Nassif, N, Kefford, RF & Mann, GJ 2003, 'Frequent loss of heterozygosity targeting the inactive X chromosome in melanoma', Clinical Cancer Research, vol. 9, pp. 6476-6482.
Kahnoski, K, Khoo, SK, Nassif, N, Chen, J, Lobo, GP, Segelov, E & Teh, BT 2003, 'Alterations of the Birt-Hogg-Dube gene (BHD) in sporadic colorectal tumours', Journal of Medical Genetics, vol. 40, no. 7, pp. 511-515.
Colorectal cancer (CRC) is the third most common cancer diagnosed in both men and women, and the second most common cause of cancer deaths in the United States. There were approximately 150 000 new cases resulting in 57 000 deaths in 2002.1 CRC is one of the most studied cancer types and its underlying aetiology best, elucidated. Colorectal tumorigenesis involves a multistep process including genetic and epigenetic alterations of numerous CRC related genes that may act as either oncogenes or tumour suppressor genes.2-5 The majority of sporadic CRCs are characterised by deletions of large chromosomal segments, which are thought to represent the loss of wild type tumour suppressor genes.6 7 About 15% of sporadic CRCs, on the other hand, show microsatellite instability (MSI), characterised by the insertion and/or deletion of simple repeat sequences and indicative of the involvement of defective mismatch repair.
Zhou, X, Waite, KA, Pilarski, R, Hampel, H, Fernandez, MJ, Bos, C, Dasouki, M, Feldman, GL, Greenberg, LA, Ivanovich, J, Matloff, E, Patterson, A, Pierpont, ME, Russo, D, Nassif, N & Eng, C 2003, 'Germline PTEN promoter mutations and deletions in Cowden/Bannayan-Riley-Ruvalcaba syndrome result in aberrant PTEN protein and dysregulation of the phosphoinositol-3-kinase/Akt pathway', American Journal of Human Genetics, vol. 73, no. 2, pp. 404-411.View/Download from: Publisher's site
Germline intragenic mutations in PTEN are associated with 80% of patients with Cowden syndrome (CS) and 60% of patients with Bannayan-Riley-Ruvalcaba syndrome (BRRS). The underlying genetic causes remain to be determined in a considerable proportion of classic CS and BRRS without a polymerase chain reaction (PCR)detectable PTEN mutation. We hypothesized that gross gene deletions and mutations in the PTEN promoter might alternatively account for a subset of apparently mutation-negative patients with CS and BRRS. Using real time and multiplex PCR techniques, we identified three germline hemizygous PTEN deletions in 122 apparently mutationnegative patients with classic CS (N=95) or BRRS (N=27). Fine mapping suggested that one deletion encompassed the whole gene and the other two included exon 1 and encompassed exons 1-5 of PTEN, respectively. Two patients with the deletion were diagnosed with BRRS, and one patient with the deletion was diagnosed with BRRS/CS overlap (features of both).
Kennerson, ML, Nassif, N & Nicholson, GA 2000, 'The cmt1a-rep binary repeat: from disease causing genomic rearrangements to a role in gene evolution', Current Genomics, vol. 1, no. 1, pp. 81-90.
Delatycki, M, Paris, D, Gardner, RJ, Nicholson, GA, Nassif, N, Storey, E, MacMillan, JC, Collins, V, Williamson, R & Forrest, SM 1999, 'Clinical and genetic study of Friedreich ataxia in an Australian population', American Journal of Medical Genetics, vol. 87, no. 2, pp. 168-174.View/Download from: 3.0.CO;2-2">Publisher's site
Delatycki, MB, Paris, DBBP, Gardner, RJMK, Nicholson, GA, Nassif, N, Storey, E, Macmillan, JC, Collins, V, Williamson, R & Forrest, SM 1999, 'Clinical and genetic study of friedreich ataxia in an Australian population', American Journal of Medical Genetics, vol. 87, no. 2, pp. 168-174.View/Download from: 3.0.CO;2-2">Publisher's site
Friedreich ataxia is an autosomal recessive disorder caused by mutations in the FRDA gene that encodes a 210-amino acid protein called frataxin. An expansion of a GAA trinucleotide repeat in intron 1 of the gene is present in more than 95% of mutant alleles. Of the 83 people we studied who have mutations in FRDA, 78 are homozygous for an expanded GAA repeat; the other five patients have an expansion in one allele and a point mutation in the other. Here we present a detailed clinical and genetic study of a subset of 51 patients homozygous for an expansion of the GAA repeat. We found a correlation between the size of the smaller of the two expanded alleles and age at onset, age into wheelchair, scoliosis, impaired vibration sense, and the presence of foot deformity. There was no significant correlation between the size of the smaller allele and cardiomyopathy, diabetes mellitus, loss of proprioception, or bladder symptoms. The larger allele size correlated with bladder symptoms and the presence of foot deformity. The duration of disease is correlated with wheelchair use and the presence of diabetes, scoliosis, bladder symptoms and impaired proprioception, and vibration sense but no other complications studied.
Jarrard, DF, Sarkar, S, Shi, Y, Yeager, TR, Magrane, G, Kinoshita, H, Nassif, N, Meisner, L, Newton, MA, Waldman, FM & Reznikoff, CA 1999, 'p16/pRb pathway alterations are required for bypassing senescence in human prostate epithelial cells', CANCER RESEARCH, vol. 59, no. 12, pp. 2957-2964.
Nassif, NT, Kok, C, Lobo, GP & Nicholson, GA 1999, 'Prostate cancer risk and repeat (CAG and GGN) polymorphism of the androgen receptor gene in an Australian population.', AMERICAN JOURNAL OF HUMAN GENETICS, vol. 65, no. 4, pp. A312-A312.
Delatycki, MB, Paris, D, Gardner, RJM, Forshaw, K, Nicholson, GA, Nassif, N, Williamson, R & Forrest, SM 1998, 'Sperm DNA analysis in a Friedreich ataxia premutation carrier suggests both meiotic and mitotic expansion in the FRDA gene', JOURNAL OF MEDICAL GENETICS, vol. 35, no. 9, pp. 713-716.View/Download from: Publisher's site
Forrest, SM, Knight, M, Delatycki, M, Paris, D, Williamson, R, King, J, Yeung, L, Nassif, N & Nicholson, GA 1998, 'The correlation of clinical phenotype in Friedreich ataxia with the site of point mutations in the FRDA gene', Neurogenetics, vol. 1, no. 4, pp. 253-257.View/Download from: Publisher's site
Kennerson, ML, Nassif, N & Nicholson, GA 1998, 'Genomic structure and physical mapping of C17orf1: a gene associated with the proximal element of the CMT1A-REP binary repeat.', Genomics, vol. 53, no. 1, pp. 110-112.View/Download from: Publisher's site
Kennerson, ML, Nassif, N, Dawkins, JL, DeKroon, RM, Yang, JG & Nicholson, GA 1997, 'The Charcot-Marie-Tooth binary repeat contains a gene transcribed from the opposite strand of a partially duplicated region of the COX10 gene.', Genomics, vol. 46, no. 1, pp. 61-69.View/Download from: Publisher's site
Trent, RJ, Sheffield, LJ, Deng, Z, Kim, W, Nassif, N, Ryce, C, Woods, CG, Michaelis, RC, Tarleton, J & Smith, A 1997, 'The elusive Angelman syndrome critical region.', Journal of Medical Genetics, vol. 34, no. 9, pp. 714-718.View/Download from: Publisher's site
Kim, W, Deng, Z, Nassif, N, Smith, A & Trent, RJ 1996, 'Establishment of sequence-tagged sites on 15q11-q13 by Alu-vector PCR cloning of YAC-generated fragments', Disease Markers, vol. 12, no. 4, pp. 241-246.
Nassif, N & Mackinlay, AG 1996, 'Detection and characterization of two novel hypervariable microsatellite repeat regions within intron 2 of the alpha-globin gene of the bivalve mollusc Anadara Trapezia', Gene, vol. 183, no. 1-2, pp. 225-230.View/Download from: Publisher's site
Nassif, N, Glenn, WK & Mackinlay, AG 1994, 'The organization of the beta-globin gene of the bivalve mollusc Anadara Trapezia and its evolutionary relationship to other invertebrate and vertebrate globin genes', Journal of Molecular Evolution, vol. 39, no. 1, pp. 47-55.
Nassif, N, Mackinlay, AG & Thompson, EO 1993, 'PCR amplification of partial mRNA sequences encoding the alpha- and bet-globin chains of the bivalve mollusc Anadara Trapezia: correction of the C-terminal amino acid sequence of the alpha-chain', Comparative Biochemistry and Physiology Part B: Biochemistry and Molecular Biology, vol. 105, no. 2, pp. 283-287.
Titchen, DA, Glenn, WK, Nassif, N, Thompson, AR & Thompson, EO 1991, 'A minor globin gene of the bivalve mollusc Anadara trapezia', Biochimica et Biophysica Acta, vol. 1089, no. 1, pp. 61-67.
LA, QT, REN, B, LOGAN, GJ, CUNNINGHAM, SC, KHANDEKAR, N, NASSIF, NT, O'BRIEN, BA, ALEXANDER, IE & SIMPSON, AM 2019, '1778-P: Delivery of the Insulin Gene Using an Integrating Adeno-Associated Viral Vector (AAV) to Diabetic NOD Mice', Diabetes, American Diabetes Association, pp. 1778-P.View/Download from: Publisher's site
Ren, B, La, QT, O'Brien, BA, Nassif, NT, Tan, Y, Gerace, D, Martiniello-Wilks, R, Torpy, F, Dane, AP, Alexander, IE & Simpson, AM 2017, 'EXPRESSION OF HUMAN PANCREATIC TRANSCRIPTION FACTORS IN THE LIVERS OF FRG MICE', JOURNAL OF GENE MEDICINE, Joint 10th Annual Scientific Meeting of the Australian-Gene-and-Cell-Therapy-Society (AGCTS) and Australasian-Society-for-Stem-Cell-Research (ASSCR), WILEY, Univ Technol Sydney, Sydney, AUSTRALIA.
Eslami, A, Zaslawski, C, Nassif, N & Lal, S 2018, 'CARDIOVASCULAR CHANGES DURING WORKING MEMORY AND ATTENTION TASKS: AN ASSESSMENT OF BLUE- AND WHITE-COLLAR WORKERS', PSYCHOPHYSIOLOGY, 58th Annual Meeting of the Society-for-Psychophysiological-Research, WILEY, Quebec City, CANADA, pp. S136-S136.
Lees, T, Maharaj, S, Kalatzis, G, Nassif, N, Newton, P & Lal, S 2018, 'THE NEUROCOGNITIVE RELATIONSHIP BETWEEN STRESS AND ANXIETY, AND MEMORY AND DECISION MAKING PERFORMANCE OF AUSTRALIAN NURSES', PSYCHOPHYSIOLOGY, 58th Annual Meeting of the Society-for-Psychophysiological-Research, WILEY, Quebec City, CANADA, pp. S48-S48.
Stress and anxiety have been consistently linked with impaired memory and decision making ability which can reduce workplace performance. While such impairments pose a risk to nurse performance, hence quality of patient care, research examining the cognitive impact of stress and anxiety in nurses is limited. The present study analysed data from 61 nurses and 51 non‐health professionals. The Depression, Anxiety, Stress Scale (DASS) measured state stress and anxiety levels. Global and domain specific cognitive performance was assessed using the Mini‐mental state exam and Cognistat, respectively. Additionally, a 32 lead electroencephalogram (EEG) montage was also captured as a physiological measure of cognitive performance. Stress was found to be associated with facilitated decision‐making in non‐health professionals (r = 0.37, p = 0.01), and impaired memory performance in nurses (r = ‐0.28, p < 0.05). Anxiety was associated with impaired memory in nurses (r = ‐0.39, p < 0.01) but no such association was observed in non‐health professionals. Analysis of EEG data revealed associations between stress and anxiety, and delta, beta and gamma activity variations, mostly localised to frontotemporal and frontoparietal brain regions. Overall, stress and anxiety are experienced by both non‐health professionals and nurses alike, and may influence cognitive performance in a unique manner for each group. Findings suggest that development and implementation of countermeasure strategies may help preserve nurse performance, and potentially reduce adverse medical events.
Gerace, D, Martiniello-Wilks, R, Nassif, NT, Ren, B & Simpson, AM 2017, 'Ex Vivo Expanded Murine Mesenchymal Stem Cells as Targets for the Generation of a Cell Replacement Therapy for Type 1 Diabetes', DIABETES, 77th Scientific Sessions of the American-Diabetes-Association, AMER DIABETES ASSOC, San Diego, CA, pp. A83-A83.
Kalatzis, G, Lees, T, Nassif, N, Zaslawski, C & Lal, S 2017, 'Exploring cognitive function in diabetes and non-diabetes samples using electroencephalography (EEG) and psychometric assessment: a comparative study', 37th Annual Scientific Meeting of the Australasian Neuroscience Society.
Haddadi, N, McGowan, E & Nassif, N 2017, 'Cancer-associated PTEN mutations alter PTEN cellular function.', Australasian Genomic Technologies Association (AGTA) Annual Conference 2017, Hobart, Tasmania.
Kalatzis, G, Lees, T, Nassif, N, Zaslawski, C & Lal, S 2016, 'Investigating cognitive function in diabetes and healthy samples using electroencephalography (EEG) and psychometric assessment: a comparative study.', Inter-University Neuroscience & Mental Health Conference.
Ren, B, O'Brien, BA, Alexander, IE, Nassif, NT, Tan, Y, Martiniello-Wilks, R & Simpson, AM 2015, 'Pancreatic Transdiffereniation of Human Hepatocytes in the Livers of a Humanized Mouse Model', MOLECULAR THERAPY, 18th Annual Meeting of the American-Society-of-Gene-and-Cell-Therapy (ASGCT), NATURE PUBLISHING GROUP, New Orleans, LA, pp. S110-S110.View/Download from: Publisher's site
Simpson, A, Ren, B, O'Brien, BA, Alexander, IE, Nassif, NT, Tan, Y & Martiniello-Wilks, R 2015, 'GENE THERAPY FOR DIABETES: REVERSAL OF DIABETES IN THE HUMANISED FRG MOUSE MODEL.', TRANSPLANTATION, Joint Congress of the International-Pancreas-and-Islet-Transplantation-Association, International-Xenotransplantation-Association and Cell-Transplant-Society, LIPPINCOTT WILLIAMS & WILKINS, Melbourne, AUSTRALIA, pp. S67-S67.
Simpson, A, Ren, B, O'Brien, BA, Alexander, IE, Nassif, NT, Tan, Y & Martiniello-Wilks, R 2015, 'Gene therapy for diabetes: reversal of diabetes in the humanised FRG mouse model', XENOTRANSPLANTATION, IPITA/IXA/CTS Joint Congress, WILEY-BLACKWELL, Melbourne, AUSTRALIA, pp. S41-S42.
McAuliffe, S, Joshua, D, Brown, R, Catalano, A, Ho, PJ, Nassif, N, Woodland, N, Hart, D, Weatherburn, C, Yang, S, Suen, H, Paul, C & Gibson, J 2015, 'Digital PCR for MRD detection of myeloma', Clinical Lymphoma, Myeloma & Leukemia, 15th International Myeloma Workshop, Elsevier, Rome, Italy, pp. E95-E95.View/Download from: Publisher's site
A pilot study was performed to investigate the use of digital PCR (dPCR) to detect minimal residual disease (MRD) in patients with multiple myeloma. dPCR allows greater quantitative specificity in PCR reactions by performing multiple, minute PCR reactions on individual DNA templates.
Lawandi, J, Tao, C, Ren, B, Williams, P, Ling, D, Swan, MA, Nassif, NT, Torpy, FR, O'Brien, BA & Simpson, AM 2015, 'MELLIGEN CELSS: AN INSULIN-SECRETING HUMAN LIVER CELL LINE WHICH IS RESISTANT TO CYTOKINE-INDUCED IMMUNE ATTACK', JOURNAL OF GENE MEDICINE, 9th Biennial Meeting of the Australasian-Gene-and-Cell-Therapy-Society (AGCTS), WILEY-BLACKWELL, Univ Melbourne, Univ Coll, Parkville, AUSTRALIA, pp. 189-189.
Hatoum, D, Bok, CF, Touw, A, Nassif, N & McGowan, E 2015, 'Sphingosine Kinase 1 (SK1-43kDa) isoform expression may contribute to cancer aggressiveness', New Horizons 2015, University of Technology Sydney.
Hatoum, D, Yagoub, D, Nassif, N & McGowan, E 2015, 'P14ARF-p53-p21: P14ARF-p53-p21: reprogramming metabolic regulation and function in breast cancer', New Horizons 2015, University of Technology Sydney (UTS).
Johnson, T, Cheng, YY, Williams, M, Nassif, N, McGowan, E & Reid, G 2015, 'YB1: a potential therapeutic target in malignant pleural mesothelioma', New Horizons 2015, University of Technology Sydney (UTS).
McGowan, EM & hatoum, D 2015, 'P14ARF-p53-p21 alters the metabolic pathway in breast cancer – a novel proteomic global approach', Annals of Oncology 26, IMPAKT Breast cancer conference, Brussels May 6th-9th, Brussels.
Moulder, D, Mitchell, H, Hatoum, D, Bajan, S, Hutvagner, G, Johnson, M, Mills, K, Brennan, S, Nassif, N & McGowan, E 2015, 'P14ARF-p53 plays a major role in mitochondria dynamics in breast cancer cells', New Horizons 2015, University of Technolgy Sydney (UTS).
Elliott, J, Lees, T, Nassif, N & Lal, S 2014, 'Cardiovascular measures and sleep health associations with shift work in police officers: A physiological assessment', 31st Combined Health Science Conference; New Horizons, Sydney, Australia.
Gerace, D, Ren, B, Hawthorne, WJ, Byrne, MR, Phillips, P, O'Brien, BA, Nassif, N, Alexander, IE & Simpson, AM 2013, 'REVERSAL OF DIABETES IN A PORCINE MODEL FOLLOWING LIVER-DIRECTED GENE THERAPY', JOURNAL OF GENE MEDICINE, 8th Meeting of the Australasian-Gene-Therapy-Society, WILEY-BLACKWELL, Univ Technol, Sydney, AUSTRALIA, pp. 326-326.
Nield, BS, Martiniello-Wilks, R, Guzowski, R, Simpson, A & Nassif, N 2013, 'First use of Re:view – a tool to combine assessment tasks, marking criteria and graduate attributes', Australian Conference on Science and Mathematics Education, Canberra, ACT.
Hatoum, D, Martiniello-Wilks, R, Nassif, N, Yagoub, D & McGowan, EM 2013, 'THE MISNOMER OF ACTIVATING P14ARF-P53 FOR BREAST CANCER THERAPY', JOURNAL OF GENE MEDICINE, 8th Meeting of the Australasian-Gene-Therapy-Society, WILEY, Univ Technol, Sydney, AUSTRALIA, pp. 333-334.
Bryant, CE, Brown, R, Yang, S, Suen, H, Aklilu, E, Favaloro, J, Hart, D, Fromm, P, Woodland, NB, Nassif, N, Iland, H, Gibson, J, Ho, PJ & Joshua, D 2011, 'Ten Year Survivors of Multiple Myeloma Demonstrate a Differential Expression of Immunological Biomarkers Including a High Incidence of Cytotoxic T-Cell Clones Which Have Not Acquired Myeloma-Associated Anergy', 53rd Annual Meeting and Exposition of the American Society of Hematology (ASH), 53rd Annual Meeting and Exposition of the American Society of Hematology (ASH)., The American Society of Hematology, San Diego, California, pp. 1678-1678.
Daniel, R, Sanchez, JJ, Nassif, N, Hernandez, A & Walsh, SJ 2008, 'SNPs associated with physical traits: A valuable tool for the inference of biogeographical ancestry', Forensics Science International Supplemt Series - Proceedings of the 22nd International ISFG Congress, International Society for Forensic Genetics Congress, Elsevier, Copenhagen, Denmark, pp. 538-540.View/Download from: Publisher's site
Sixteen autosomal SNPs were selected to differentiate major populations in Australia. A SNP multiplex assay was developed for the inference of biogeographical ancestry.
Ren, B, O'Brien, B, Swan, MA, Koina, ME, Nassif, N & Wei, MQ 2007, 'Delivery of furin-cleavable insulin to diabetic rat livers resulted in long-term correction of diabetes and partial pancreatic transdifferentiation of the liver', Journal of Gene Medicine, Wiley, Canberra, pp. 532-532.
Bacher, JW, Helms, C, Donis-Keller, H, Hennes, L, Nassif, N & Schumm, JW 1999, 'Chromosome localization of CODIS loci and new pentanucleotide repeat loci', PROGRESS IN FORENSIC GENETICS 8, 18th Congress of the International-Society-for-Forensic-Haemogenetics (ISFH), ELSEVIER SCIENCE BV, SAN FRANCISCO, CA, pp. 33-36.
TRENT, RJ, NASSIF, N, DENG, ZM, KIM, S, PRASAD, M, SMITH, A & ROSS, DA 1995, 'A PHYSICAL MAP OF THE ANGELMAN SYNDROME CRITICAL REGION AT LOCUS D15S113 (LS6-1)', AMERICAN JOURNAL OF HUMAN GENETICS, UNIV CHICAGO PRESS, pp. 1580-1580.
DENG, ZM, KIM, WS, NASSIF, NT, WOODAGE, T, SMITH, A & TRENT, RJ 1994, 'CONSTRUCTION AND CHARACTERIZATION OF LAMBDA-PHAGE CONTIGS OF YACS MAPPING TO 15Q11-]Q13', CYTOGENETICS AND CELL GENETICS, KARGER, pp. 20-20.
1. Asbestos Diseases Research Institute (ADRI), Concord NSW.
2. EnGeneIC Pty Ltd (Lane Cove, NSW).
3. Kolling Instutue of Medical Research, St Leonards, NSW.