Dr Andrea Mathe

Dr Andrea Mathe

Postdoctoral Fellow - Hunter Genomics Facility Coordinator

School of Biomedical Sciences and Pharmacy

Career Summary

Biography

Dr. Mathe graduated with a Bachelor of Science (Molecular Biotechnology) with first class Honours from University of Technology Dresden, Germany. She then moved to Newcastle to undertake her PhD in Medical Genetics, from which she graduated 2016. She undertook postdoctoral research training in the Reproductive Science group at the University of Newcastle before joining the Gastrointestinal Research Group as a postdoctoral researcher at the Hunter Medical Research Institute (HMRI). Dr. Mathe worked under the lead of Associate Professor Simon Keely. Her research focused on the development of colorectal cancer. The aim of the study was to understand the mechanisms that lead to the development of colorectal cancer.

In 2018 Dr. Mathe joint the HCRA team to set up a Genomics Facility at HMRI (Level 3 West). Internal and external researchers can use the services provides by the facility. These include sample preperation, illumina microarrays as well as sequencing. 


Qualifications

  • Doctor of Philosophy, University of Newcastle

Keywords

  • DNA methylation
  • breast cancer
  • colorectal cancer
  • gene expression
  • microRNA
  • tissue culture

Languages

  • German (Mother)
  • English (Fluent)

Fields of Research

Code Description Percentage
111201 Cancer Cell Biology 20
111203 Cancer Genetics 60
060405 Gene Expression (incl. Microarray and other genome-wide approaches) 20

Professional Experience

UON Appointment

Title Organisation / Department
Postdoctoral Fellow - Hunter Genomics Facility Coordinator University of Newcastle
School of Biomedical Sciences and Pharmacy
Australia

Academic appointment

Dates Title Organisation / Department
26/11/2016 -  Postdoctoral Researcher University of Newcastle - Faculty of Health and Medicine
School of Biomedical Sciences and Pharmacy
14/06/2016 - 25/11/2016 Postdoctoral researcher Faculty of Science and Information Technology, The University of Newcastle | Australia
Australia
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Publications

For publications that are currently unpublished or in-press, details are shown in italics.


Journal article (13 outputs)

Year Citation Altmetrics Link
2019 B Biomed GB, Carroll G, Mathe A, Horvat J, Foster P, Walker MM, et al., 'Evidence for Local and Systemic Immune Activation in Functional Dyspepsia and the Irritable Bowel Syndrome: A Systematic Review', The American journal of gastroenterology, 114 429-436 (2019)

BACKGROUND: Subtle histopathologic features such as eosinophilia and increased mast cells have been observed in functional gastrointestinal disorders (FGIDs), including functional... [more]

BACKGROUND: Subtle histopathologic features such as eosinophilia and increased mast cells have been observed in functional gastrointestinal disorders (FGIDs), including functional dyspepsia (FD) and the irritable bowel syndrome (IBS). The mechanisms that drive recruitment of these cells to the gastrointestinal tract remain unexplained, largely due to the heterogeneity in phenotypes among patients diagnosed with such conditions. We aimed to systematically review the literature and collate the evidence for immune activation in FD and IBS, and where possible, detail the nature of activation. METHODS: Seven literature databases were searched using the keywords: 'functional gastrointestinal disorder', FGID, 'functional dyspepsia', 'non-ulcer dyspepsia', 'idiopathic dyspepsia', 'irritable bowel syndrome', IBS and 'immun*'. RESULTS: Fifty-one papers reporting discordant immune features met the selection criteria for this review. Changes in lymphocyte populations, including B and T lymphocyte numbers and activation status were reported in IBS and FD, in conjunction with duodenal eosinophilia in FD and increased colonic mast cells in IBS. Increases in circulating a4ß7 gut-homing T cells appear to be linked to the pathophysiology of both FD and IBS. Studies in the area are complicated by poor phenotyping of patients into subgroups and the subtle nature of the immune activity involved in FD and IBS. CONCLUSIONS: Alterations in proportions of gut-homing T lymphocytes in both FD and IBS indicate that a loss of mucosal homeostasis may drive the symptoms of FD and IBS. There is indirect evidence that Th17 responses may play a role in FGIDs, however the evidence for a Th2 immune phenotype in FD and IBS is limited. Although immune involvement is evident, large, well-characterised patient cohorts are required to elucidate the immune mechanisms driving the development of FGIDs.

DOI 10.1038/s41395-018-0377-0
Citations Scopus - 1Web of Science - 1
Co-authors Paul Foster, Marjorie Walker, Simon Keely, Jay Horvat, Nicholas Talley
2019 Arthurs AL, Lumbers ER, Delforce SJ, Mathe A, Morris BJ, Pringle KG, 'The role of oxygen in regulating microRNAs in control of the placental renin-angiotensin system.', Mol Hum Reprod, 25 206-217 (2019)
DOI 10.1093/molehr/gaz004
Co-authors E Lumbers, Kirsty Pringle
2019 B Biomed GB, Carroll G, Mathe A, Horvat J, Foster P, Walker MM, et al., 'Evidence for Local and Systemic Immune Activation in Functional Dyspepsia and the Irritable Bowel Syndrome: A Systematic Review.', Am J Gastroenterol, 114 429-436 (2019)
DOI 10.1038/s41395-018-0377-0
Co-authors Simon Keely, Jay Horvat, Nicholas Talley, Paul Foster, Marjorie Walker
2019 Liu G, Mateer SW, Hsu A, Goggins BJ, Tay H, Mathe A, et al., 'Platelet activating factor receptor regulates colitis-induced pulmonary inflammation through the NLRP3 inflammasome', Mucosal Immunology, (2019)

© 2019, Society for Mucosal Immunology. Extra-intestinal manifestations (EIM) are common in inflammatory bowel disease (IBD). One such EIM is sub-clinical pulmonary inflammation, ... [more]

© 2019, Society for Mucosal Immunology. Extra-intestinal manifestations (EIM) are common in inflammatory bowel disease (IBD). One such EIM is sub-clinical pulmonary inflammation, which occurs in up to 50% of IBD patients. In animal models of colitis, pulmonary inflammation is driven by neutrophilic infiltrations, primarily in response to the systemic bacteraemia and increased bacterial load in the lungs. Platelet activating factor receptor (PAFR) plays a critical role in regulating pulmonary responses to infection in conditions, such as chronic obstructive pulmonary disease and asthma. We investigated the role of PAFR in pulmonary EIMs of IBD, using dextran sulfate sodium (DSS) and anti-CD40 murine models of colitis. Both models induced neutrophilic inflammation, with increased TNF and IL-1ß levels, bacterial load and PAFR protein expression in mouse lungs. Antagonism of PAFR decreased lung neutrophilia, TNF, and IL-1ß in an NLRP3 inflammasome-dependent manner. Lipopolysaccharide from phosphorylcholine (ChoP)-positive bacteria induced NLRP3 and caspase-1 proteins in human alveolar epithelial cells, however antagonism of PAFR prevented NLRP3 activation by ChoP. Amoxicillin reduced bacterial populations in the lungs and reduced NLRP3 inflammasome protein levels, but did not reduce PAFR. These data suggest a role for PAFR in microbial pattern recognition and NLRP3 inflammasome signaling in the lung.

DOI 10.1038/s41385-019-0163-3
Co-authors Simon Keely, Alan Hsu, Peter Wark, Gang Liu, Steven Maltby, Paul Foster, Philip Hansbro, Michael Fricker
2018 Wang Y, Lumbers ER, Arthurs AL, de Meaultsart CC, Mathe A, Avery-Kiejda KA, et al., 'Regulation of the human placental (pro)renin receptor-prorenin-angiotensin system by microRNAs.', Molecular human reproduction, 24 453-464 (2018) [C1]
DOI 10.1093/molehr/gay031
Citations Scopus - 2Web of Science - 2
Co-authors Kirsty Pringle, E Lumbers, Kelly Kiejda
2018 Nixon B, De Iuliis GN, Hart HM, Zhou W, Mathe A, Bernstein IR, et al., 'Proteomic profiling of mouse epididymosomes reveals their contributions to post-testicular sperm maturation', Molecular and Cellular Proteomics, 18 S91-S108 (2018) [C1]
DOI 10.1074/mcp.RA118.000946
Citations Scopus - 3Web of Science - 3
Co-authors Elizabeth Bromfield, Matt Dun, Geoffry DeiuliIs, Brett Nixon, Muhammad Jamaluddin
2018 Mateer SW, Mathe A, Bruce J, Liu G, Maltby S, Fricker M, et al., 'IL-6 Drives Neutrophil-Mediated Pulmonary Inflammation Associated with Bacteremia in Murine Models of Colitis', American Journal of Pathology, 188 1625-1639 (2018) [C1]

© 2018 American Society for Investigative Pathology Inflammatory bowel disease (IBD) is associated with several immune-mediated extraintestinal manifestations. More than half of a... [more]

© 2018 American Society for Investigative Pathology Inflammatory bowel disease (IBD) is associated with several immune-mediated extraintestinal manifestations. More than half of all IBD patients have some form of respiratory pathology, most commonly neutrophil-mediated diseases, such as bronchiectasis and chronic bronchitis. Using murine models of colitis, we aimed to identify the immune mechanisms driving pulmonary manifestations of IBD. We found increased neutrophil numbers in lung tissue associated with the pulmonary vasculature in both trinitrobenzenesulfonic acid¿ and dextran sulfate sodium¿induced models of colitis. Analysis of systemic inflammation identified that neutrophilia was associated with bacteremia and pyrexia in animal models of colitis. We further identified IL-6 as a systemic mediator of neutrophil recruitment from the bone marrow of dextran sulfate sodium animals. Functional inhibition of IL-6 led to reduced systemic and pulmonary neutrophilia, but it did not attenuate established colitis pathology. These data suggest that systemic bacteremia and pyrexia drive IL-6 secretion, which is a critical driver for pulmonary manifestation of IBD. Targeting IL-6 may reduce neutrophil-associated extraintestinal manifestations in IBD patients.

DOI 10.1016/j.ajpath.2018.03.016
Citations Scopus - 2Web of Science - 1
Co-authors Robert Callister, Marjorie Walker, Philip Hansbro, Simon Keely, Gang Liu, Hock Tay, Jay Horvat, Paul Foster, Steven Maltby, Michael Fricker
2017 Avery-Kiejda KA, Mathe A, Scott RJ, 'Genome-wide miRNA, gene and methylation analysis of triple negative breast cancer to identify changes associated with lymph node metastases', GENOMICS DATA, 14 1-4 (2017)
DOI 10.1016/j.gdata.2017.07.004
Citations Scopus - 1Web of Science - 1
Co-authors Kelly Kiejda, Rodney Scott
2016 Mathe A, Wong-Brown M, Locke WJ, Stirzaker C, Braye SG, Forbes JF, et al., 'DNA methylation profile of triple negative breast cancer-specific genes comparing lymph node positive patients to lymph node negative patients', SCIENTIFIC REPORTS, 6 (2016) [C1]
DOI 10.1038/srep33435
Citations Scopus - 9Web of Science - 9
Co-authors Kelly Kiejda, Michelle Wong-Brown, Rodney Scott
2015 Mathe A, Scott RJ, Avery-Kiejda KA, 'MiRNAs and other epigenetic changes as biomarkers in triple negative breast cancer', International Journal of Molecular Sciences, 16 28347-28376 (2015) [C1]

© 2015 by the authors; licensee MDPI, Basel, Switzerland. Triple negative breast cancer (TNBC) is characterised by the lack of receptors for estrogen (ER), progesterone (PR), and ... [more]

© 2015 by the authors; licensee MDPI, Basel, Switzerland. Triple negative breast cancer (TNBC) is characterised by the lack of receptors for estrogen (ER), progesterone (PR), and human epidermal growth factor 2 (HER2). Since it cannot be treated by current endocrine therapies which target these receptors and due to its aggressive nature, it has one of the worst prognoses of all breast cancer subtypes. The only treatments remain chemo- and/or radio-therapy and surgery and because of this, novel biomarkers or treatment targets are urgently required to improve disease outcomes. MicroRNAs represent an attractive candidate for targeted therapies against TNBC, due to their natural ability to act as antisense interactors and regulators of entire gene sets involved in malignancy and their superiority over mRNA profiling to accurately classify disease. Here we review the current knowledge regarding miRNAs as biomarkers in TNBC and their potential use as therapeutic targets in this disease. Further, we review other epigenetic changes and interactions of these changes with microRNAs in this breast cancer subtype, which may lead to the discovery of new treatment targets for TNBC.

DOI 10.3390/ijms161226090
Citations Scopus - 26Web of Science - 26
Co-authors Rodney Scott, Kelly Kiejda
2015 Mathe A, Wong-Brown M, Morten B, Forbes JF, Braye SG, Avery-Kiejda KA, Scott RJ, 'Novel genes associated with lymph node metastasis in triple negative breast cancer', Scientific Reports, 5 (2015) [C1]

Triple negative breast cancer (TNBC) is the most aggressive breast cancer subtype with the worst prognosis and no targeted treatments. TNBC patients are more likely to develop met... [more]

Triple negative breast cancer (TNBC) is the most aggressive breast cancer subtype with the worst prognosis and no targeted treatments. TNBC patients are more likely to develop metastases and relapse than patients with other breast cancer subtypes. We aimed to identify TNBC-specific genes and genes associated with lymph node metastasis, one of the first signs of metastatic spread. A total of 33 TNBCs were used; 17 of which had matched normal adjacent tissues available, and 15 with matched lymph node metastases. Gene expression microarray analysis was used to reveal genes that were differentially expressed between these groups. We identified and validated 66 genes that are significantly altered when comparing tumours to normal adjacent samples. Further, we identified 83 genes that are associated with lymph node metastasis and correlated these with miRNA-expression. Pathway analysis revealed their involvement in DNA repair, recombination and cell death, chromosomal instability and other known cancer-related pathways. Finally, four genes were identified that were specific for TNBC, of which one was associated with overall survival. This study has identified novel genes involved in LN metastases in TNBC and genes that are TNBC specific that may be used as treatment targets or prognostic indicators in the future.

DOI 10.1038/srep15832
Citations Scopus - 12Web of Science - 13
Co-authors Kelly Kiejda, Michelle Wong-Brown, Rodney Scott
2014 Avery-Kiejda KA, Braye SG, Mathe A, Forbes JF, Scott RJ, 'Decreased expression of key tumour suppressor microRNAs is associated with lymph node metastases in triple negative breast cancer', BMC Cancer, 14 (2014) [C1]

Background: Breast cancer is the most common malignancy that develops in women, responsible for the highest cancer-associated death rates. Triple negative breast cancers represent... [more]

Background: Breast cancer is the most common malignancy that develops in women, responsible for the highest cancer-associated death rates. Triple negative breast cancers represent an important subtype that have an aggressive clinical phenotype, are associated with a higher likelihood of metastasis and are not responsive to current targeted therapies. miRNAs have emerged as an attractive candidate for molecular biomarkers and treatment targets in breast cancer, but their role in the progression of triple negative breast cancer remains largely unexplored.Methods: This study has investigated miRNA expression profiles in 31 primary triple negative breast cancer cases and in 13 matched lymph node metastases compared with 23 matched normal breast tissues to determine miRNAs associated with the initiation of this disease subtype and those associated with its metastasis.Results: 71 miRNAs were differentially expressed in triple negative breast cancer, the majority of which have previously been associated with breast cancer, including members of the miR-200 family and the miR-17-92 oncogenic cluster, suggesting that the majority of miRNAs involved in the initiation of triple negative breast cancer are not subtype specific. However, the repertoire of miRNAs expressed in lymph node negative and lymph node positive triple negative breast cancers were largely distinct from one another. In particular, miRNA profiles associated with lymph node negative disease tended to be up-regulated, while those associated with lymph node positive disease were down-regulated and largely overlapped with the profiles of their matched lymph node metastases. From this, 27 miRNAs were identified that are associated with metastatic capability in the triple negative breast cancer subtype.Conclusions: These results provide novel insight into the repertoire of miRNAs that contribute to the initiation of and progression to lymph node metastasis in triple negative breast cancer and have important implications for the treatment of this breast cancer subtype. © 2014 Avery-Kiejda et al.; licensee BioMed Central Ltd.

DOI 10.1186/1471-2407-14-51
Citations Scopus - 48Web of Science - 46
Co-authors Kelly Kiejda, Rodney Scott
2014 Avery-Kiejda KA, Morten B, Wong-Brown MW, Mathe A, Scott RJ, 'The relative mRNA expression of p53 isoforms in breast cancer is associated with clinical features and outcome.', Carcinogenesis, 35 586-596 (2014) [C1]
DOI 10.1093/carcin/bgt411
Citations Scopus - 32Web of Science - 31
Co-authors Michelle Wong-Brown, Kelly Kiejda, Rodney Scott
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Conference (13 outputs)

Year Citation Altmetrics Link
2018 Mathe A, Wong-Brown M, Morten BC, Braye SG, Locke WJ, Stirzaker C, et al., 'Defining the Key Mediators of Breast Cancer Progression and Treatment Resistance in the triple Negative Subtype', ASIA-PACIFIC JOURNAL OF CLINICAL ONCOLOGY (2018)
Co-authors Kelly Kiejda, Rodney Scott, Michelle Wong-Brown
2017 Mathe A, Zierau O, Keely S, 'Can Hormonal Changes Influence DNA Integrity to Protect us from Colorectal Cancer?', ASIA-PACIFIC JOURNAL OF CLINICAL ONCOLOGY (2017)
Co-authors Simon Keely
2016 Mathe A, Wong-Brown M, Locke W, Stirzaker C, Braye S, Forbes J, et al., 'DNA METHYLATION PROFILE OF TRIPLE NEGATIVE BREAST CANCER-SPECIFIC GENES COMPARING LYMPH NODE POSITIVE PATIENTS TO LYMPH NODE NEGATIVE PATIENTS', ASIA-PACIFIC JOURNAL OF CLINICAL ONCOLOGY (2016)
Co-authors Rodney Scott, Michelle Wong-Brown
2014 Morten B, Campbell HG, Brown MW, Mathe A, Braithwaite AW, Scott RJ, Kiejda KA, '¿40p53 regulation of estrogen responsiveness in breast cancer.', 16th International p53 Workshop Proceedings, Stockholm, Sweden (2014) [E3]
Co-authors Kelly Kiejda, Michelle Wong-Brown, Rodney Scott
2014 Mathe A, Avery-Kiejda KA, Wong-Brown M, Forbes JF, Braye SG, Scott RJ, 'Can microRNAs impact cell migration in triple negative breast cancer?', The Australian Society for Medical Research (ASMR) Satellite Scientific Meeting Programme, Newcastle, NSW, Australia (2014) [E3]
Co-authors Rodney Scott, Kelly Kiejda
2014 Avery-Kiejda KA, Morten B, Wong-Brown MW, Mathe A, Scott RJ, 'The relationship between p53 isoforms and prognosis in breast cancer.', The Australian Society for Medical Research (ASMR) Satellite Scientific Meeting Programme, Newcastle, NSW, Australia (2014) [E3]
Co-authors Rodney Scott, Michelle Wong-Brown, Kelly Kiejda
2014 Mathe A, Avery-Kiejda KA, Wong-Brown M, Morten B, Forbes JF, Braye SG, Scott RJ, 'IDENTIFICATION OF NOVEL TRANSCRIPTS SPECIFIC TO TRIPLE NEGATIVE BREAST CANCER THAT ARE ASSOCIATED WITH LYMPH NODE METASTASIS', ASIA-PACIFIC JOURNAL OF CLINICAL ONCOLOGY (2014) [E3]
DOI 10.1111/ajco.12335
Co-authors Michelle Wong-Brown, Rodney Scott, Kelly Kiejda
2014 Mathe A, Avery-Kiejda KA, Wong-Brown M, Forbes JF, Braye SG, Scott RJ, 'Eight microRNAs as biomarkers for metastatic spread in triple negative breast cancer', EUROPEAN JOURNAL OF CANCER (2014) [E3]
DOI 10.1016/S0959-8049(14)50110-4
Co-authors Michelle Wong-Brown, Rodney Scott, Kelly Kiejda
2013 Morten B, Mathe A, Scott RJ, Avery-Kiejda KA, 'mRNA expression analysis of p53 isoforms in breast cancer.', 25th Lorne Cancer Conference Proceedings, Lorne, VIC, Australia (2013) [E3]
Co-authors Rodney Scott, Kelly Kiejda
2013 Avery-Kiejda KA, Mathe A, Braye SG, Forbes JF, Scott RJ, 'The expression of Dicer and Drosha in lymph node metastases of triple negative breast cancer.', 25th Lorne Cancer Conference Proceedings, Lorne, VIC, Australia (2013) [E3]
Co-authors Kelly Kiejda, Rodney Scott
2013 Mathe A, Avery-Kiejda KA, Wong-Brown MW, Forbes JF, Braye SG, Scott RJ, 'Target gene identification of microRNAs associated with lymph node metastases in triple negative breast cancer.', 25th Lorne Cancer Conference Proceedings, Lorne, VIC, Australia (2013) [E3]
Co-authors Michelle Wong-Brown, Kelly Kiejda, Rodney Scott
2013 Mathe A, Avery-Kiejda KA, Wong-Brown M, Forbes JF, Braye SG, Scott RJ, 'Integration of microRNA and gene expression profiling in triple negative breast cancer to identify possible biomarkers for metastases.', Breakthrough Breast Cancer TNBC Conference Proceedings, London, UK (2013) [E3]
Co-authors Kelly Kiejda, Rodney Scott, Michelle Wong-Brown
2013 Mathe A, Wong-Brown M, Forbes JF, Braye SG, Scott RJ, Avery-Kiejda KA, 'Identification of biomarkers for metastatic spread in triple negative breast cancer.', Translational Cancer Research Conference Abstract booklet, Newcastle, Australia (2013) [E3]
Co-authors Rodney Scott, Kelly Kiejda, Michelle Wong-Brown
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Grants and Funding

Summary

Number of grants 4
Total funding $148,750

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


20183 grants / $138,750

Mary Sawyer Postgraduate Scholarship in Cancer Research$85,500

Funding body: Hunter Medical Research Institute

Funding body Hunter Medical Research Institute
Project Team Dr Georgia Carroll, Associate Professor Simon Keely, Doctor Peter Pockney, Professor Marjorie Walker, Doctor Steve Smith, Doctor Andrea Mathe
Scheme Postgraduate Research Scholarship
Role Investigator
Funding Start 2018
Funding Finish 2020
GNo G1800612
Type Of Funding C3120 - Aust Philanthropy
Category 3120
UON Y

Non- immunosuppressive strategies for the treatment of IBD$33,250

Funding body: Hunter Medical Research Institute

Funding body Hunter Medical Research Institute
Project Team Associate Professor Simon Keely, Doctor Andrea Mathe, Doctor Gang Liu
Scheme Project Grant
Role Investigator
Funding Start 2018
Funding Finish 2018
GNo G1800196
Type Of Funding C3120 - Aust Philanthropy
Category 3120
UON Y

Analysis of luminal bacteria at the site of colorectal anastomoses and their association with anastomotic leaks$20,000

Funding body: Hunter Medical Research Institute

Funding body Hunter Medical Research Institute
Project Team Associate Professor Simon Keely, Doctor Peter Pockney, Doctor Steve Smith, Associate Professor Ian Grainge, Doctor Andrea Mathe
Scheme Project Grant
Role Investigator
Funding Start 2018
Funding Finish 2018
GNo G1701630
Type Of Funding C3120 - Aust Philanthropy
Category 3120
UON Y

1 grants / $10,000

miRNA regulation of growth, invasion and treatment response in triple negative breast cancer$10,000

Funding body: Hunter Medical Research Institute

Funding body Hunter Medical Research Institute
Project Team Doctor Kelly Kiejda, Doctor Andrea Mathe
Scheme Project Grant
Role Investigator
Funding Start
Funding Finish
GNo G1300728
Type Of Funding Grant - Aust Non Government
Category 3AFG
UON Y
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Research Supervision

Number of supervisions

Completed0
Current3

Current Supervision

Commenced Level of Study Research Title Program Supervisor Type
2018 PhD The Role of Microbial Oxygen Sensing in the Development of Anastomotic Leaks PhD (Human Physiology), Faculty of Health and Medicine, The University of Newcastle Co-Supervisor
2018 PhD Epithelial Metabolism as a Mediator of Host-Microbiome Interactions in Inflammatory Bowel Disease PhD (Immunology & Microbiol), Faculty of Health and Medicine, The University of Newcastle Co-Supervisor
2017 PhD The Impact of Surgery, Inflammation and Sepsis on Neutrophil Extracellular Trap (NET) Formation and Subsequent Metastatic Disease in Colorectal Cancer PhD (Surgical Science), Faculty of Health and Medicine, The University of Newcastle Co-Supervisor
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Dr Andrea Mathe

Position

Postdoctoral Fellow - Hunter Genomics Facility Coordinator
HCRA
School of Biomedical Sciences and Pharmacy
Faculty of Health and Medicine

Contact Details

Email andrea.mathe@newcastle.edu.au
Phone (02) 4042 0311
Mobile 0487316554

Office

Room HMRI L3W
Building HMRI
Location HMRI

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