Dr Sam Faulkner

Technical Officer

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, with a particular interest in tumours of both the thyroid and breast.

Sam worked as a post-doctoral researcher at the University of Newcastle and Hunter Medical Research Institute (HMRI) throughout 2018, where 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

Professional appointment

Dates Title Organisation / Department
1/03/2018 -  Postdoctoral Fellow The University of Newcastle - School of Biomedical Sciences and Pharmacy
Cancer Neurobiology Group
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
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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For publications that are currently unpublished or in-press, details are shown in italics.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 - 22Web of Science - 17
Co-authors Phillip Jobling, Hubert Hondermarck

Journal article (10 outputs)

Year Citation Altmetrics Link
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 - 2Web of Science - 1
Co-authors Christopher W Rowe, Phillip Jobling, Rick Thorne, Hubert Hondermarck, Marjorie Walker
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 - 1Web of Science - 1
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 - 1Web of Science - 1
Co-authors Hubert Hondermarck, Matt Dun
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 - 5Web of Science - 4
Co-authors Christopher W Rowe, Christopher Oldmeadow, Phillip Jobling, Marjorie Walker, Rick Thorne, Chenchen Jiang, Xu Zhang, Hubert Hondermarck, John Attia
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 - 22Web of Science - 17
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 - 7Web of Science - 6
Co-authors John Attia, Marjorie Walker, Christopher Oldmeadow, Hubert Hondermarck
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 - 19Web of Science - 19
Co-authors Hubert Hondermarck, Murray Cairns, Matt Dun, Rodney Scott, Kelly Kiejda
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 - 12Web of Science - 11
Co-authors Hubert Hondermarck, Xu Zhang, Chenchen Jiang, Marjorie Walker, John Attia
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 - 20Web of Science - 21
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 - 12Web of Science - 10
Co-authors John Forbes, Marjorie Walker, John Attia, Hubert Hondermarck, Rodney Scott, Rick Thorne, Phillip Jobling
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Grants and Funding

Summary

Number of grants 4
Total funding $52,500

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


20183 grants / $50,000

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

HMRI Project Grant - Prostate Cancer$20,000

Funding body: Hunter Medical Research Institute (HMRI)

Funding body Hunter Medical Research Institute (HMRI)
Scheme Project Grant
Role Lead
Funding Start 2018
Funding Finish 2020
GNo
Type Of Funding C3120 - Aust Philanthropy
Category 3120
UON N

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
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Dr Sam Faulkner

Positions

Technical Officer
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

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

Casual Research Assistant
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 7953
Mobile N/A
Fax N/A

Office

Room LS3.05
Building Life Sciences Building
Location Callaghan Campus
University Drive
Callaghan, NSW 2308
Australia
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