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Dr Tracey Martin

Dr Tracey Martin

Lecturer

School of Medicine

Email:
martinta1@cardiff.ac.uk
Telephone:
+44 29 2068 7209
Location:
Henry Wellcome Building

I have an international reputation for research in the role of Tight Junctions in the process of cancer metastasis.

After a PhD in molecular Biology at Cardiff University, I began a Post-doctoral career at The University of Wales College of Medicine, investigating the role of Hepatocyte Growth Factor (HGF) on endothelia. This led to the opportunity to examine HGF and its antagonist NK4 in cancer.

Since 1998, I have been involved in researching the role of tight junctions in cancer (during metastasis) and in endothelia (during angiogenesis). My research interests include investigating how tight junctions can be modulated to control cancer cell dissociation and invasion, together with a continued interest in angiogenic factors and their role in metastasis.

I also have a special interest in the mechanisms whereby HGF can control tight junction assembly and function in both cancer and endothelia.

Other research interests include the interaction of cancer cells in cell-adhesion and cell-signalling and in how the cell adhesion molecule VE-cadherin is involved in angiogenesis.

Other roles:

Departmental Safety Officer for the Cardiff China Medical Research Collaborative

Biological Safety Officer

Human Tissue Research Governance Officer

Risk Assessment Coordinator

Induction & Training coordinator

Nuffield Foundation placement coordinator

Education and qualifications

2013: University Leadership and Management (ILM).

1996: PhD: The Use of 16S Ribosomal RNA to Investigate Microbial Diversity of River Epilithon at the Department of Pure & Applied Biology University of Wales College Cardiff.

1992: BSc (hons) Microbiology & Genetics, Department of Pure & Applied Biology University of Wales College Cardiff. Honours Research Project: The Effect of Toxic Metal & Other External Factors on the Growth of the Basidiomycete Fungi Hypholoma fasciculare.

Career overview

August 2003 to present – Lecturer: My research interests are investigating the role of Tight Junctions in the progression of cancer, and investigating how they can be modulated in both benign and pathological disease. I also have a continued interest in angiogenic factors and their role in metastasis. I supervise a large number of PhD, MD and visiting research fellows, attend national and international conferences (I have presented over 70 papers), write original research papers, reviews (many invited) and book chapters (invited). During the last 10 years, I was employed to work on 2 major projects as a research scientist: the first was sponsored by Abbot Pharmaceuticals (2003-2005) and involved investigating factors that could affect benign and malignant breast cancer cells in regards to cellular “leakiness”. This directly involved Tight Junctions as controllers. From 2006-2011 I was employed as the research scientist on a Cancer-Research Wales sponsored program grant. This involved the examination of Hepatocyte Growth Factor (HGF) and how this cytokine influences stem cells markers in breast and prostate cancer (funded by Cancer Research Wales). This work led to the award of the AACR-CTR-SABSC-Susan G, Komen for the Cure Scholarship for “Evaluation of the distribution of stem cell markers (PSCA, CD44, CD49b and CD133) in human breast cancer reveals correlation with clinical progression and metastatic disease in ductal carcinoma”.

March 2000 - July 2003 Research Fellow: Undertook a program of research to determine, using molecular, cellular and in vivo techniques, the mechanisms of cancer metastasis in particular the possible application of newly discovered antagonists to growth factors as an anti-metastasis tool (Susan G. Komen Breast Cancer Foundation for a study on 'NK4, a HGF/SF antagonist, as a new anti-metastatic-agent in breast cancer). This was followed by a project sponsored by CR-UK that involved the creation of an anti-metastasis/angiogenesis compound. I also began to research the role that Tight Junctions and their molecular constituents may have in breast cancer metastasis. This research was recognised at the 2002 San Antonio Breast Cancer Symposium, where I was honoured with a Astra-Zeneca Scholar Awards showing that tight junction molecules are lost in those patients with metastatic breast cancer.

June 1997- March 2000 Research Fellow: Establishing the role of fibroblasts in the process of tissue repair and cancer metastasis, identifying fibroblast derived factors responsible for the regulatory effect of fibroblasts, in the promotion of angiogenesis, at the Wound Healing Research Unit, University Department of Surgery at UWCM, Cardiff, UK for Prof. K.G. Harding (funded by Smith & Nephew/Advanced Tissue Science Joint Venture).

Honours and awards

BACR Travel Award to the 7th Chinese Conference on Oncology (CCO) and The 11th Cross-Strait Academic Conference on Oncology and the China-UK-Japan Gastro-intestinal Cancer Symposium, 2012.

AACR Scholar-in Training Award, funded by Susan G. Komen for the Cure at the CTRC-AACR San Antonio Breast Cancer Symposium, Texas, December 2009 for “Evaluation of the distribution of stem cell markers in human breast cancer reveals correlation with clinical progression and metastatic disease in ductal carcinoma".

Welsh Urologists March 2006 Asware N., Martin T.A., Matthews P.N., Jiang W.G. Welsh Urologists March 2003 Brown G.M., Martin T.A., Matthews P.N., Jiang W.G. “The expression of tight junction molecules in human bladder cancer”

San Antonio Breast Cancer Symposium, December 2004 Lane J, Martin TA, Watkins G, Mansel RE, Jiang WG. “ROCK1 and the aggressive nature of breast cancer cells”.

Welsh Urologists March 2003 Brown G.M., Martin T.A., Matthews P.N., Jiang W.G. “The expression of tight junction molecules in human bladder cancer”

Astra-Zeneca Scholar at the San Antonio Breast Cancer Symposium, December 2002 for “Expression and distribution of tight junction molecules in breast cancer and their association with clinical outcomes” and invited give an oral presentation.

AACR Scholarship April 2002 Davies G, Martin TA, Parr C, Grimshaw D, Mason MD, Jiang WG. “NK4 reduced the growth of prostate cancer in vivo”.

Certificate of Merit at the American Society of Tissue Regeneration Conference, April 2001 for Martin TA, Jiang WG, and Harding KG. Effect of human fibroblast derived dermis on human tissue expansion. American Society of Tissue Regeneration Conference.

Professional memberships

  • American Association of Cancer Research (AACR)
  • Women in Cancer Research (WICR)
  • British Association of Cancer Research
  • European Association of Cancer Research

Academic positions

2014-present –Group Leader, Cardiff-China Medical Research Collaborative

2003 to 2014 – Lecturer, Metastasis and Angiogenesis Research Group, Cardiff University

2000-2003 Research Fellow, Metastasis and Angiogenesis Research Group, Cardiff University

1997- 2000 Research Fellow, Wound Healing Research Unit, University Department of Surgery at University of Wales College of Medicine

1996 Research Assistant,  University of Wales Cardiff

Committees and reviewing

2004-present HTRGC

2015-present ICAGE Health and Safety Team

2017 DCG EDHR Committee

2019

2018

2017

2016

2015

2014

2013

2012

2011

2010

2009

2008

2007

2006

2005

2003

2001

1999

Post-graduate research supervision: PhD and MD

Current students - Emily Telford, Zubair Khanzadar

Undergraduate research supervision:

SSC component of year 1, 2, 3 and 4 C21 MB BCh

CUROP research project placements

CUReS pleacements

Undergraduate teaching:

SSC Literature project year 1 C21 MB BCh

Group teaching year 1 C21 MB BCh

Postgraduate teaching:

MSc Cancer and Therapeutics

Cell junctions as mediators or barriers to cell dissemination and the regulators thereof

  • The Tight Junction (TJ) is a region where the plasma membrane of adjacent cells forms a series of contacts that appear to completely occlude the extracellular space thus creating an intercellular barrier and intramembrane diffusion fence.
  • In epithelial cells the TJ functions in an adhesive manner and can prevent cell dissociation whereas TJs in endothelial cells function as a barrier through which molecules and inflammatory cells can pass.
  • A considerable body of now work exists on TJ and their role in a number of diseases.
  • TJs have become recognised as key players in cancer metastasis. Early studies suggested a link between the reduction of TJ proteins and tumour differentiation and increasing experimental evidence has emerged to place TJs in the frontline as the structure that cancer cells must overcome in order to metastasize.
  • Interaction and penetration of the vascular endothelium by dissociated cancer cells is an important step in the formation of cancer metastases.
  • Changes in both tumour and endothelial cells are necessary for successful growth and spread of cancer cells and that these changes are somewhat similar.
  • A change in cancer cells by up-regulation or down-regulation of relevant TJ proteins results in loss of cell–cell association, cell contact inhibition, leading to uncontrolled growth, loss of adhesion to and degradation of the basement.
  • These must be a concurrent loss of cell–cell association in the endothelium and modulation of TJ proteins involved in facilitating the passage of the cancer cells through this barrier.
  • We have shown there is a differential expression of a number of transmembrane TJ proteins, notably Occludin, Claudin-5 and the Nectin and that they are correlated with the disruption of TJs in tumours.
  • Modulation of expression of these proteins results in key changes in barrier function leading to the progression of cancer and progression of metastasis.

Areas of research

Blood brain barrier (BBB):

  1. Modulators of BBB dynamics
  2. Comparison of different BBB endothelial cells and the role of HGF in brain metastasis.

HAVcR-1:

  1. Function of HAVcR-1 in breast cancer and its control of barrier function.
  2. HAVcR-1 as a significant modulator of HGF signalling in prostate cancer metastasis via the control of TJs.

Occludin:

Control of TJ function by Occludin and its different isoforms in breast cancer metastasis to bone.

Signalling and control of TJs:

  1. How SIPA-1 is integrated into the HGF signalling pathway of TJ function in breast cancer.
  2. Exploration of N-Wasp in TJ function
  3. BDNf and the metastatic cascade

Current Funding:

Life Sciences Rsearch Network Wales Platform Grant: Cancer Metastasis Platform

Cancer Research Wales PhD Studentship 2014-2017