Dr Sam Faulkner

Dr Sam Faulkner

Postdoctoral Research Fellow

School of Biomedical Sciences and Pharmacy

Career Summary

Biography

Sam Faulkner is a passionate biochemist specialised in Cancer Neurobiology. He obtained a Bachelor of Biomedical Science, graduating with First Class Honours, from the University of Newcastle in 2013 and obtained his PhD in Molecular Biochemistry from the same institution in 2018. Sam's PhD focused on the role of neurotrophic growth factors and their receptors in the innervation and progression of human cancers.

Sam is currently a Postdoctoral Research Fellow at the University of Newcastle and Hunter Medical Research Institute (HMRI). In 2018 he was employed under a Innovation Connections Facilitation Grant from the Department of Industry, Innovation and Science (Australian Government), in collaboration with industry biotechnology company Biosensis Pty Ltd (Adelaide, Australia). During this time he investigated the utility of neuroproteins as potential blood biomarkers for aggressive prostate cancer as well as worked towards further elucidating the mechanisms underpinning the nerve-cancer cell cross-talk within the tumour microenvironment (cancer neurobiology). 


Qualifications

  • Doctor of Philosophy, University of Newcastle
  • Bachelor of Biomedical Sciences, University of Newcastle
  • Bachelor of Biomedical Sciences (Hons), University of Newcastle

Keywords

  • Biomarkers
  • Cancer
  • Growth Factors
  • Nerves
  • Tumour Microenvironment

Languages

  • English (Mother)

Fields of Research

Code Description Percentage
111201 Cancer Cell Biology 70
110106 Medical Biochemistry: Proteins and Peptides (incl. Medical Proteomics) 30

Professional Experience

UON Appointment

Title Organisation / Department
Casual Lecturer University of Newcastle
School of Biomedical Sciences and Pharmacy
Australia
Postdoctoral Research Fellow University of Newcastle
School of Biomedical Sciences and Pharmacy
Australia

Awards

Award

Year Award
2016 Margaret Taylor Travel Award
Hunter Medical Research Institute (HMRI)
2016 The Kellerman Award
Faculty of Health and Medicine, University of Newcastle
Edit

Publications

For publications that are currently unpublished or in-press, details are shown in italics.

Highlighted Publications

Year Citation Altmetrics Link
2017 Boilly B, Faulkner S, Jobling P, Hondermarck H, 'Nerve Dependence: From Regeneration to Cancer', Cancer Cell, 31 342-354 (2017) [C1]

© 2017 Elsevier Inc. Nerve dependence has long been described in animal regeneration, where the outgrowth of axons is necessary to the reconstitution of lost body parts and tissue... [more]

© 2017 Elsevier Inc. Nerve dependence has long been described in animal regeneration, where the outgrowth of axons is necessary to the reconstitution of lost body parts and tissue remodeling in various species. Recent discoveries have demonstrated that denervation can suppress tumor growth and metastasis, pointing to nerve dependence in cancer. Regeneration and cancer share similarities in regard to the stimulatory role of nerves, and there are indications that the stem cell compartment is a preferred target of innervation. Thus, the neurobiology of cancer is an emerging discipline that opens new perspectives in oncology.

DOI 10.1016/j.ccell.2017.02.005
Citations Scopus - 71Web of Science - 64
Co-authors Phillip Jobling, Hubert Hondermarck

Journal article (21 outputs)

Year Citation Altmetrics Link
2020 Ferdoushi A, Li X, Griffin N, Faulkner S, Jamaluddin MFB, Gao F, et al., 'Schwann Cell Stimulation of Pancreatic Cancer Cells: A Proteomic Analysis', Frontiers in Oncology, 10 (2020) [C1]
DOI 10.3389/fonc.2020.01601
Co-authors Chenchen Jiang, Muhammad Jamaluddin, Dirk Vanhelden, Hubert Hondermarck, Phillip Jobling, Pradeep Tanwar
2020 Gao F, Griffin N, Faulkner S, Li X, King SJ, Jobling P, et al., 'The Membrane Protein Sortilin Can Be Targeted to Inhibit Pancreatic Cancer Cell Invasion.', The American journal of pathology, 190 (2020) [C1]
DOI 10.1016/j.ajpath.2020.05.018
Co-authors Chenchen Jiang, Jim Denham, Phillip Jobling, Hubert Hondermarck
2020 Liu H, Li X, Dun MD, Faulkner S, Jiang CC, Hondermarck H, 'Cold Shock Domain Containing E1 (CSDE1) Protein is Overexpressed and Can be Targeted to Inhibit Invasiveness in Pancreatic Cancer Cells.', Proteomics, 20 e1900331 (2020)
DOI 10.1002/pmic.201900331
Citations Web of Science - 1
Co-authors Chenchen Jiang, Matt Dun, Hubert Hondermarck
2020 Griffin N, Rowe CW, Gao F, Jobling P, Wills V, Walker MM, et al., 'Clinicopathological Significance of Nerves in Esophageal Cancer.', Am J Pathol, 190 1921-1930 (2020)
DOI 10.1016/j.ajpath.2020.05.012
Co-authors Marjorie Walker, Phillip Jobling, Hubert Hondermarck, Christopher W Rowe
2020 Griffin N, Marsland M, Roselli S, Oldmeadow C, Attia J, Walker MM, et al., 'The receptor tyrosine kinase trka is increased and targetable in HER2-positive breast cancer', Biomolecules, 10 1-13 (2020) [C1]

© 2020 by the authors. Licensee MDPI, Basel, Switzerland. The tyrosine kinase receptor A (NTRK1/TrkA) is increasingly regarded as a therapeutic target in oncology. In breast cance... [more]

© 2020 by the authors. Licensee MDPI, Basel, Switzerland. The tyrosine kinase receptor A (NTRK1/TrkA) is increasingly regarded as a therapeutic target in oncology. In breast cancer, TrkA contributes to metastasis but the clinicopathological significance remains unclear. In this study, TrkA expression was assessed via immunohistochemistry of 158 invasive ductal carcinomas (IDC), 158 invasive lobular carcinomas (ILC) and 50 ductal carcinomas in situ (DCIS). TrkA was expressed in cancer epithelial and myoepithelial cells, with higher levels of TrkA positively associated with IDC (39% of cases) (p < 0.0001). Interestingly, TrkA was significantly increased in tumours expressing the human epidermal growth factor receptor-2 (HER2), with expression in 49% of HER2-positive compared to 25% of HER2-negative tumours (p = 0.0027). A panel of breast cancer cells were used to confirm TrkA protein expression, demonstrating higher levels of TrkA (total and phosphorylated) in HER2-positive cell lines. Functional investigations using four different HER2-positive breast cancer cell lines indicated that the Trk tyrosine kinase inhibitor GNF-5837 reduced cell viability, through decreased phospho-TrkA (Tyr490) and downstream AKT (Ser473) activation, but did not display synergy with Herceptin. Overall, these data highlight a relationship between the tyrosine kinase receptors TrkA and HER2 and suggest the potential of TrkA as a novel or adjunct target for HER2-positive breast tumours.

DOI 10.3390/biom10091329
Co-authors Marjorie Walker, Hubert Hondermarck, Severine Roselli, Christopher Oldmeadow, John Attia
2020 Rowe CW, Dill T, Griffin N, Jobling P, Faulkner S, Paul JW, et al., 'Innervation of papillary thyroid cancer and its association with extra-thyroidal invasion', Scientific Reports, 10 (2020) [C1]
DOI 10.1038/s41598-020-58425-5
Citations Scopus - 2
Co-authors Phillip Jobling, Christopher W Rowe, Roger Smith, Jonathan Paul, Hubert Hondermarck
2020 Dun MD, Mannan A, Rigby CJ, Butler S, Toop HD, Beck D, et al., 'Shwachman Bodian Diamond syndrome (SBDS) protein is a direct inhibitor of protein phosphatase 2A (PP2A) activity and overexpressed in acute myeloid leukaemia', Leukemia, (2020)
DOI 10.1038/s41375-020-0814-0
Co-authors David Skerrett-Byrne, Matt Dun, Geoffry DeiuliIs, Nikki Verrills, Hubert Hondermarck, Anoop Enjeti, Ryan Duchatel, Brett Nixon, Heather Murray
2020 March B, Faulkner S, Jobling P, Steigler A, Blatt A, Denham J, Hondermarck H, 'Tumour innervation and neurosignalling in prostate cancer', Nature Reviews Urology, 17 119-130 (2020) [C1]

© 2020, Springer Nature Limited. Prostate cancer progression has been shown to be dependent on the development of autonomic nerves into the tumour microenvironment. Sympathetic ne... [more]

© 2020, Springer Nature Limited. Prostate cancer progression has been shown to be dependent on the development of autonomic nerves into the tumour microenvironment. Sympathetic nerves activate adrenergic neurosignalling that is necessary in early stages of tumour progression and for initiating an angiogenic switch, whereas parasympathetic nerves activate cholinergic neurosignalling resulting in tumour dissemination and metastasis. The innervation of prostate cancer seems to be initiated by neurotrophic growth factors, such as the precursor to nerve growth factor secreted by tumour cells, and the contribution of brain-derived neural progenitor cells has also been reported. Current experimental, epidemiological and clinical evidence shows the stimulatory effect of tumour innervation and neurosignalling in prostate cancer. Using nerves and neurosignalling could have value in the management of prostate cancer by predicting aggressive disease, treating localized disease through denervation and relieving cancer-associated pain in bone metastases.

DOI 10.1038/s41585-019-0274-3
Citations Scopus - 5Web of Science - 4
Co-authors Phillip Jobling, Jim Denham, Hubert Hondermarck, Allison Steigler
2019 Rowe CW, Faulkner S, Paul JW, Tolosa JM, Gedye C, Bendinelli C, et al., 'The precursor for nerve growth factor (proNGF) is not a serum or biopsy-rinse biomarker for thyroid cancer diagnosis.', BMC endocrine disorders, 19 128 (2019) [C1]
DOI 10.1186/s12902-019-0457-1
Co-authors Jonathan Paul, Craig Gedye, Hubert Hondermarck, Roger Smith, Cino Bendinelli, John Attia, Katie-Jane Wynne, Christopher W Rowe
2019 Rowe CW, Dill T, Faulkner S, Gedye C, Paul JW, Tolosa JM, et al., 'The precursor for nerve growth factor (ProNGF) in thyroid cancer lymph node metastases: Correlation with primary tumour and pathological variables', International Journal of Molecular Sciences, 20 1-13 (2019) [C1]
DOI 10.3390/ijms20235924
Co-authors Jonathan Paul, Craig Gedye, Hubert Hondermarck, Christopher W Rowe, Roger Smith, Mark Jones
2019 Faulkner S, Jobling P, March B, Jiang CC, Hondermarck H, 'Tumor neurobiology and the war of nerves in cancer', Cancer Discovery, 9 702-710 (2019) [C1]

© 2019 American Association for Cancer Research. Nerves are emerging regulators of cancer progression. Cancer cells induce the outgrowth of nerves in the tumor microenvironment th... [more]

© 2019 American Association for Cancer Research. Nerves are emerging regulators of cancer progression. Cancer cells induce the outgrowth of nerves in the tumor microenvironment through the release of neu-rotrophic factors, and in return nerves liberate neurotransmitters that activate cancer growth and dissemination. Although sympathetic nerves drive tumor angiogenesis via the liberation of noradrena-line, sensory and parasympathetic nerves stimulate cancer stem cells. Interestingly, recent evidence indicates that parasympathetic nerves can eventually inhibit tumor progression, suggesting a yin¿yang type of regulation of cancer by nerves. From a broader perspective, the question of a higher level of control of cancer development by the central nervous system should be raised. Significance: Nerves are emerging regulators of cancer initiation, progression, and metastasis. Here, we review the evidence to date and explore the basic and clinical ramifications of these findings.

DOI 10.1158/2159-8290.CD-18-1398
Citations Scopus - 28Web of Science - 26
Co-authors Chenchen Jiang, Phillip Jobling, Hubert Hondermarck
2018 Gao F, Griffin N, Faulkner S, Rowe CW, Williams L, Roselli S, et al., 'The neurotrophic tyrosine kinase receptor TrkA and its ligand NGF are increased in squamous cell carcinomas of the lung', SCIENTIFIC REPORTS, 8 (2018) [C1]
DOI 10.1038/s41598-018-26408-2
Citations Scopus - 8Web of Science - 6
Co-authors Marjorie Walker, Hubert Hondermarck, Rick Thorne, Phillip Jobling, Christopher W Rowe, Severine Roselli
2018 Griffin N, Faulkner S, Jobling P, Hondermarck H, 'Targeting neurotrophin signaling in cancer: The renaissance', Pharmacological Research, 135 12-17 (2018) [C1]

© 2018 Nerve outgrowth in the tumor microenvironment (tumor neurogenesis) has recently been shown to be essential for cancer progression and the concept of nerve dependence is eme... [more]

© 2018 Nerve outgrowth in the tumor microenvironment (tumor neurogenesis) has recently been shown to be essential for cancer progression and the concept of nerve dependence is emerging in oncology. Neurotrophins such as nerve growth factor (NGF) have long been identified as drivers of neurogenesis during development and regeneration, but intriguingly they were also known to be expressed in human tumors where they can stimulate cancer cell growth. Recent findings have unraveled that NGF released by cancer cells is also a driver of tumor neurogenesis, via the stimulation of NGF receptors on nerve endings. In return, nerves infiltrated in the tumor microenvironment secrete neurotransmitters, which can stimulate both the growth of tumor cells and angiogenesis. This neurotrophic role of NGF in cancer is likely to be relevant to a large variety of human malignancies, as well as other neurotrophins, and may have ramifications in cancer pain. Therefore, pharmacological interventions against neurotrophin signaling have the potential not only to target cancer cells directly, but also to inhibit neurogenesis and its stimulatory impact on cancer progression and pain.

DOI 10.1016/j.phrs.2018.07.019
Citations Scopus - 17Web of Science - 18
Co-authors Hubert Hondermarck, Phillip Jobling
2018 Li X, Dun MD, Faulkner S, Hondermarck H, 'Neuroproteins in Cancer: Assumed Bystanders Become Culprits', PROTEOMICS, 18 (2018) [C1]
DOI 10.1002/pmic.201800049
Citations Scopus - 4Web of Science - 4
Co-authors Matt Dun, Hubert Hondermarck
2018 Faulkner S, Jobling P, Rowe CW, Rodrigues Oliveira SM, Roselli S, Thorne RF, et al., 'Neurotrophin Receptors TrkA, p75

© 2018 American Society for Investigative Pathology Neurotrophin receptors are emerging targets in oncology, but their clinicopathologic significance in thyroid cancer is unclear.... [more]

© 2018 American Society for Investigative Pathology Neurotrophin receptors are emerging targets in oncology, but their clinicopathologic significance in thyroid cancer is unclear. In this study, the neurotrophin tyrosine receptor kinase TrkA (also called NTRK1), the common neurotrophin receptor p75NTR, and the proneurotrophin receptor sortilin were analyzed with immunohistochemistry in a cohort of thyroid cancers (n = 128) and compared with adenomas and normal thyroid tissues (n = 62). TrkA was detected in 20% of thyroid cancers, compared with none of the benign samples (P = 0.0007). TrkA expression was independent of histologic subtypes but associated with lymph node metastasis (P = 0.0148), suggesting the involvement of TrkA in tumor invasiveness. Nerves in the tumor microenvironment were positive for TrkA. p75NTR was overexpressed in anaplastic thyroid cancers compared with papillary and follicular subtypes (P < 0.0001). Sortilin was overexpressed in thyroid cancers compared with benign thyroid tissues (P < 0.0001). Neurotrophin receptor expression was confirmed in a panel of thyroid cancer cell lines at the mRNA and protein levels. Functional investigations using the anaplastic thyroid cancer cell line CAL-62 found that siRNA against TrkA, p75NTR, and sortilin decreased cell survival and cell migration through decreased SRC and ERK activation. Together, these data reveal TrkA, p75NTR, and sortilin as potential therapeutic targets in thyroid cancer.

DOI 10.1016/j.ajpath.2017.09.008
Citations Scopus - 15Web of Science - 12
Co-authors Christopher W Rowe, Christopher Oldmeadow, Severine Roselli, Phillip Jobling, Rick Thorne, Hubert Hondermarck, Xu Zhang, Chenchen Jiang, John Attia, Marjorie Walker
2017 Boilly B, Faulkner S, Jobling P, Hondermarck H, 'Nerve Dependence: From Regeneration to Cancer', Cancer Cell, 31 342-354 (2017) [C1]

© 2017 Elsevier Inc. Nerve dependence has long been described in animal regeneration, where the outgrowth of axons is necessary to the reconstitution of lost body parts and tissue... [more]

© 2017 Elsevier Inc. Nerve dependence has long been described in animal regeneration, where the outgrowth of axons is necessary to the reconstitution of lost body parts and tissue remodeling in various species. Recent discoveries have demonstrated that denervation can suppress tumor growth and metastasis, pointing to nerve dependence in cancer. Regeneration and cancer share similarities in regard to the stimulatory role of nerves, and there are indications that the stem cell compartment is a preferred target of innervation. Thus, the neurobiology of cancer is an emerging discipline that opens new perspectives in oncology.

DOI 10.1016/j.ccell.2017.02.005
Citations Scopus - 71Web of Science - 64
Co-authors Phillip Jobling, Hubert Hondermarck
2016 Faulkner S, Roselli S, Demont Y, Pundavela J, Choquet G, Leissner P, et al., 'ProNGF is a potential diagnostic biomarker for thyroid cancer', Oncotarget, 7 28488-28497 (2016) [C1]

The precursor for nerve growth factor (proNGF) is expressed in some cancers but its clinicopathological significance is unclear. The present study aimed to define the clinicopatho... [more]

The precursor for nerve growth factor (proNGF) is expressed in some cancers but its clinicopathological significance is unclear. The present study aimed to define the clinicopathological significance of proNGF in thyroid cancer. ProNGF expression was analysed by immunohistochemistry in two cohorts of cancer versus benign tumors (adenoma) and normal thyroid tissues. In the first cohort (40 thyroid cancers, 40 thyroid adenomas and 80 normal thyroid tissues), proNGF was found overexpressed in cancers compared to adenomas and normal samples (p<0.0001). The area under the receiver-operating characteristic (ROC) curve was 0.84 (95% CI 0.75-0.93, p<0.0001) for cancers versus adenomas, and 0.99 (95% CI 0.98-1.00, p<0.0001) for cancers versus normal tissues. ProNGF overexpression was confirmed in a second cohort (127 cancers of various histological types and 55 normal thyroid tissues) and using a different antibody (p<0.0001). ProNGF staining intensity was highest in papillary carcinomas compared to other histological types (p<0.0001) and there was no significant association with age, gender, tumor size, stage and lymph node status. In conclusion, proNGF is increased in thyroid cancer and should be considered as a new potential diagnostic biomarker.

DOI 10.18632/oncotarget.8652
Citations Scopus - 15Web of Science - 13
Co-authors Hubert Hondermarck, Christopher Oldmeadow, Severine Roselli, Marjorie Walker, John Attia
2015 Dun MD, Chalkley RJ, Faulkner S, Keene S, Avery-Kiejda KA, Scott RJ, et al., 'Proteotranscriptomic profiling of 231-BR breast cancer cells: Identification of potential biomarkers and therapeutic targets for brain metastasis', Molecular and Cellular Proteomics, 14 2316-2330 (2015) [C1]

© 2015 by The American Society for Biochemistry and Molecular Biology, Inc. Brain metastases are a devastating consequence of cancer and currently there are no specific biomarkers... [more]

© 2015 by The American Society for Biochemistry and Molecular Biology, Inc. Brain metastases are a devastating consequence of cancer and currently there are no specific biomarkers or therapeutic targets for risk prediction, diagnosis, and treatment. Here the proteome of the brain metastatic breast cancer cell line 231-BR has been compared with that of the parental cell line MDA-MB-231, which is also metastatic but has no organ selectivity. Using SILAC and nanoLC-MS/MS, 1957 proteins were identified in reciprocal labeling experiments and 1584 were quantified in the two cell lines. A total of 152 proteins were confidently determined to be up- or down-regulated by more than twofold in 231-BR. Of note, 112/152 proteins were decreased as compared with only 40/152 that were increased, suggesting that down-regulation of specific proteins is an important part of the mechanism underlying the ability of breast cancer cells to metastasize to the brain. When matched against transcriptomic data, 43% of individual protein changes were associated with corresponding changes in mRNA, indicating that the transcript level is a limited predictor of protein level. In addition, differential miRNA analyses showed that most miRNA changes in 231-BR were up- (36/45) as compared with down-regulations (9/45). Pathway analysis revealed that proteome changes were mostly related to cell signaling and cell cycle, metabolism and extracellular matrix remodeling. The major protein changes in 231-BR were confirmed by parallel reaction monitoring mass spectrometry and consisted in increases (by more than fivefold) in the matrix metalloproteinase-1, ephrin-B1, stomatin, myc target-1, and decreases (by more than 10-fold) in transglutaminase-2, the S100 calcium-binding protein A4, and L-plastin. The clinicopathological significance of these major proteomic changes to predict the occurrence of brain metastases, and their potential value as therapeutic targets, warrants further investigation.

DOI 10.1074/mcp.M114.046110
Citations Scopus - 32Web of Science - 29
Co-authors Rodney Scott, Hubert Hondermarck, Matt Dun, Kelly Kiejda, Murray Cairns
2015 Roselli S, Pundavela J, Demont Y, Faulkner S, Keene S, Attia J, et al., 'Sortilin is associated with breast cancer aggressiveness and contributes to tumor cell adhesion and invasion', Oncotarget, 6 10473-10486 (2015) [C1]

The neuronal membrane protein sortilin has been reported in a few cancer cell lines, but its expression and impact in human tumors is unclear. In this study, sortilin was analyzed... [more]

The neuronal membrane protein sortilin has been reported in a few cancer cell lines, but its expression and impact in human tumors is unclear. In this study, sortilin was analyzed by immunohistochemistry in a series of 318 clinically annotated breast cancers and 53 normal breast tissues. Sortilin was detected in epithelial cells, with increased levels in cancers, as compared to normal tissues (p = 0.0088). It was found in 79% of invasive ductal carcinomas and 54% of invasive lobular carcinomas (p < 0.0001). There was an association between sortilin expression and lymph node involvement (p = 0.0093), suggesting a relationship with metastatic potential. In cell culture, sortilin levels were higher in cancer cell lines compared to non-tumorigenic breast epithelial cells and siRNA knockdown of sortilin inhibited cancer cell adhesion, while proliferation and apoptosis were not affected. Breast cancer cell migration and invasion were also inhibited by sortilin knockdown, with a decrease in focal adhesion kinase and SRC phosphorylation. In conclusion, sortilin participates in breast tumor aggressiveness and may constitute a new therapeutic target against tumor cell invasion.

DOI 10.18632/oncotarget.3401
Citations Scopus - 25Web of Science - 21
Co-authors Hubert Hondermarck, Xu Zhang, Chenchen Jiang, Marjorie Walker, John Attia, Severine Roselli
2015 Faulkner S, Dun MD, Hondermarck H, 'Proteogenomics: Emergence and promise', Cellular and Molecular Life Sciences, 72 953-957 (2015) [C1]

© Springer Basel 2015. Proteogenomics, or the integration of proteomics with genomics and transcriptomics, is emerging as the next step towards a unified understanding of cellular... [more]

© Springer Basel 2015. Proteogenomics, or the integration of proteomics with genomics and transcriptomics, is emerging as the next step towards a unified understanding of cellular functions. Looking globally and simultaneously at gene structure, RNA expression, protein synthesis and posttranslational modifications have become technically feasible and offer a new perspective to molecular processes. Recent publications have highlighted the value of proteogenomics in oncology for defining the molecular signature of human tumors, and translation to other areas of biomedicine and life sciences is anticipated. This minireview will discuss recent developments, challenges and perspectives in proteogenomics.

DOI 10.1007/s00018-015-1837-y
Citations Scopus - 25Web of Science - 26
Co-authors Matt Dun, Hubert Hondermarck
2015 Pundavela J, Roselli S, Faulkner S, Attia J, Scott RJ, Thorne RF, et al., 'Nerve fibers infiltrate the tumor microenvironment and are associated with nerve growth factor production and lymph node invasion in breast cancer', Molecular Oncology, 9 1626-1635 (2015) [C1]
DOI 10.1016/j.molonc.2015.05.001
Citations Scopus - 31Web of Science - 29
Co-authors Phillip Jobling, Severine Roselli, Marjorie Walker, John Attia, Hubert Hondermarck, Rodney Scott, Rick Thorne
Show 18 more journal articles

Conference (3 outputs)

Year Citation Altmetrics Link
2019 Ferdoushi A, Li X, Faulkner S, Jobling P, Hondermarck H, 'The Schwann Cell Secretome: A Novel Reservoir of Biomarkers and Potential Therapeutic Targets for Pancreatic Cancer', ASIA-PACIFIC JOURNAL OF CLINICAL ONCOLOGY (2019)
Citations Web of Science - 1
Co-authors Hubert Hondermarck, Phillip Jobling
2019 Eden E, Faulkner S, Gao F, Li X, Hondermarck H, Jiang CC, 'Endoplasmic Reticulum Stress Drives Tumour Axonogenesis in Pancreatic Cancer', ASIA-PACIFIC JOURNAL OF CLINICAL ONCOLOGY (2019)
Co-authors Chenchen Jiang, Hubert Hondermarck
2018 Rowe CW, Dill T, Faulkner S, Griffin N, Jobling P, King S, et al., 'Increased nerve density around papillary thyroid cancers and primary thyroid cancers with nodal metastases.', Adelaide (2018)
Co-authors Roger Smith, Jonathan Paul, Craig Gedye, Christopher W Rowe, Phillip Jobling, Hubert Hondermarck
Edit

Grants and Funding

Summary

Number of grants 8
Total funding $636,507

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


20201 grants / $377,829

The perineural niche to predict the development of bone metastases in prostate cancer$377,829

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

Funding body NHMRC (National Health & Medical Research Council)
Project Team Professor Hubert Hondermarck, Conjoint Professor Jim Denham, Doctor Sam Faulkner, Associate Professor Phil Jobling
Scheme Ideas Grants
Role Investigator
Funding Start 2020
Funding Finish 2021
GNo G1900413
Type Of Funding Aust Competitive - Commonwealth
Category 1CS
UON Y

20194 grants / $226,178

Targeting the neuro-cancer cell crosstalk in glioblastoma$146,428

Funding body: Hunter Medical Research Institute

Funding body Hunter Medical Research Institute
Project Team Professor Hubert Hondermarck, Doctor Chen Chen Jiang, Doctor Sam Faulkner, Associate Professor Phil Jobling
Scheme Project Grant
Role Investigator
Funding Start 2019
Funding Finish 2020
GNo G1900631
Type Of Funding C3112 - Aust Not for profit
Category 3112
UON Y

PRC CaRIT ‘Career Advancement Fellowship in Cancer Research'$50,000

Funding body: Hunter Cancer Research Alliance (HCRA)

Funding body Hunter Cancer Research Alliance (HCRA)
Project Team

Dr Sam Faulkner

Scheme Fellowship grant
Role Lead
Funding Start 2019
Funding Finish 2019
GNo
Type Of Funding C3120 - Aust Philanthropy
Category 3120
UON N

A new diagnostic test for prostate cancer$15,000

Funding body: Hunter Medical Research Institute

Funding body Hunter Medical Research Institute
Project Team Mr Brayden March, Doctor Sam Faulkner, Doctor Jude Weidenhofer, Doctor Peter Pockney
Scheme Research Grant
Role Investigator
Funding Start 2019
Funding Finish 2020
GNo G1901603
Type Of Funding C3120 - Aust Philanthropy
Category 3120
UON Y

RADAR prostate cancer trial: Pathology substudy$14,750

Funding body: Hunter Medical Research Institute

Funding body Hunter Medical Research Institute
Project Team Conjoint Professor Jim Denham, Professor Hubert Hondermarck, Doctor Sam Faulkner, Mrs Allison Steigler
Scheme Project Grant
Role Investigator
Funding Start 2019
Funding Finish 2020
GNo G1901177
Type Of Funding C3120 - Aust Philanthropy
Category 3120
UON Y

20182 grants / $30,000

A Novel Neuronal Biomarker for Aggressive Prostate Cancer$20,000

Funding body: Hunter Medical Research Institute

Funding body Hunter Medical Research Institute
Project Team Doctor Sam Faulkner, Professor Hubert Hondermarck, Doctor Sam Faulkner
Scheme Project Grant
Role Lead
Funding Start 2018
Funding Finish 2018
GNo G1801389
Type Of Funding C3120 - Aust Philanthropy
Category 3120
UON Y

Strategic Pilot Grant (Research and Teaching)$10,000

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

Funding body Faculty of Health and Medicine, University of Newcastle
Scheme Strategic Pilot Grant
Role Lead
Funding Start 2018
Funding Finish 2018
GNo
Type Of Funding Internal
Category INTE
UON N

20161 grants / $2,500

Margaret Taylor Research Travel Award$2,500

Funding body: Hunter Medical Research Institute

Funding body Hunter Medical Research Institute
Project Team Doctor Sam Faulkner
Scheme Margaret Taylor Research Travel Award
Role Lead
Funding Start 2016
Funding Finish 2016
GNo G1600786
Type Of Funding C3120 - Aust Philanthropy
Category 3120
UON Y
Edit

Dr Sam Faulkner

Positions

Postdoctoral Research Fellow
Hondermarck - Cancer Neurobiology
School of Biomedical Sciences and Pharmacy
Faculty of Health and Medicine

Casual Lecturer
Hondermarck - Cancer Neurobiology
School of Biomedical Sciences and Pharmacy
Faculty of Health and Medicine

Senior Technical Officer
Hondermarck - Cancer Neurobiology
School of Biomedical Sciences and Pharmacy
Faculty of Health and Medicine

Contact Details

Email sam.faulkner@newcastle.edu.au
Phone (02) 4921 7233
Mobile N/A
Fax N/A

Office

Room LS3.35
Building Life Sciences Building
Location Callaghan Campus
University Drive
Callaghan, NSW 2308
Australia
Edit