Cancer PhD Programme | The School of Medicine, Medical Sciences and Nutrition

Cancer PhD Programme

The University of Aberdeen runs a Cancer PhD Programme, directed by Professor Anne Donaldson to initiate bench to bedside projects that link our basic and clincial cancer research programmes.

Students benefit from a tailored series of introductory talks from Aberdeen cancer scientists and clinicians, familiarising them with the cancer research landscape and collaboration opportunities. They also enjoy a dedicated research seminar series, giving students opportunities to present their own research and to invite external speakers.

Our Students

Abigail Dodson: Student: Abigail Dodson

Project: Investigating the adipose-inflammatory paradox in pre- and post-menopausal breast cancer development

Lead supervisor: Professor Valerie Speirs

Project synopsis: Breast cancer is the most common cancer in women in the UK, with around 24% of new cases each year being diagnosed in women 75 and over. A paradox within breast cancer risk factors is the link between obesity and menopausal status, with excess body weight being associated with an increased risk of breast cancer development in post-menopausal women, while in pre-menopausal women, obesity has more of a protective role. This project aims to test the hypothesis that hormonal backgrounds congruent with pre- and post-menopausal settings, influence the adipose-inflammatory microenvironment resulting in repression or enhancement of tumorigenesis, respectively. This will be done through incorporating mature adipocytes, taken from pre- and post-menopausal breast cancer samples, into 3D multicellular in vitro models to study how adipocytes effect cell phenotypes within the early stages of breast cancer development.
Raquel Barro Ferroso: Student: Raquel Barro Ferroso

Project title: Synthesis and analysis of chimaeric prophagocytic molecules to treat cancer

Lead supervisor: Professor Mark Vickers

Project synopsis: The overall aim of this project is to reprogram tumour associated macrophages, abundant within the tumour microenvironment, to recognise, phagocytose and kill ovarian cancer cells by decorating these cancer cells with a new "eat-me" signal. This "eat-me" signal will be genetically engineered onto a peptide linker within a single chain variable fragment directed against a tumour associated antigen (TAA) and whose pro-phagoctyic properties will be evaluated using an in vitro 3D model of ovarian cancer using immortalised cell lines expressing our TAA of interest.
Emma Parker: Student: Emma Parker

Project: Identifying the determinants of tumour susceptibility to replication-inhibiting chemotherapy

Lead supervisor: Professor Anne Donaldson

Project synopsis: RIF1 is a multifunctional protein involved in DNA replication and repair and is important for protecting cells from replication-stress. Humans have two different forms of RIF1 ('splice-variants'). One of these variants is better at protecting cells from replication stress, potentially conferring resistance to chemotherapeutic drugs that inhibit DNA replication. My project explores the changes in RIF1 splice-variant expression during carcinogenesis, to investigate the role of RIF1 in chemotherapy resistance. To do this I use a combination of experiments on cancer cell lines and information from clinical patient datasets.
Neve Read: Student: Neve Read

Project title: Can PTP1B inhibition rewire macrophage function to improve anti-tumour immunity in breast cancer treatments?

Lead supervisor: Professor Heather Wilson

Project synopsis: In breast cancer, tumour associated macrophages (TAMs) account for 50% of the tumour mass. TAMs are programmed to be highly immunosuppressive, promoting tumour development, and a high infiltration of TAMs is associated with aggressive tumour and resistance to immune checkpoint inhibitors and chemotherapy. For this reason, TAMs are being considered as promising target for cancer treatment. PTP1B is critical for cancer cell proliferation and metastasis and PTP1B inhibitors have reached phase I clinical trials for the treatment of metastatic breast cancer. Previous studies have demonstrated that inhibiting PTP1B in macrophages causes a shift in macrophage function improving the outcome of inflammatory diseases. However, it is unclear how PTP1B inhibitors can influence macrophage function within the breast cancer microenvironment where they are predominantly skewed to TAMs. We aim to explore whether PTP1B inhibition can rewire TAMs towards an anti-tumour phenotype by: 1) Establishing the effects of TAMs on mammosphere growth on mammospheres formed from ER positive ER negative and triple negative cancer cells; 2) Determining the effects of PTP1B inhibitors on TAMs and how this influences mammosphere growth; 3) Assessing the phenotype of TAMs (by qPCR, flow cytometry and immunohistochemical analysis) with and without PTP1B inhibitor treatment following co-culture with breast cancer cells to understand their pro-/anti-tumour effects.
Jodi Stewart: Student: Jodi Stewart

Project title: Impact of the immune landscape on androgen ablation and progression to therapy resistant prostate cancer.

Lead supervisor: Professor Iain McEwan

Project synopsis: Prostate cancer is the most common cancer in men in the UK and remains a major contributor of cancer-related mortality. The androgen receptor (AR) is an important driver of prostate cancer progression. Knowledge on the role of the immune landscape in prostate cancer is currently limited, however, there is growing evidence for the role of androgens and the androgen receptor in tumour-associated macrophages. We aim to understand the role of macrophage AR signalling on prostate cancer progression by 1) Analysing how AR gene and protein expression is regulated in macrophages in response to androgens and other soluble factors in the tumour microenvironment; 2) Identifying possible gene signatures associated with macrophage phenotype/function in response to hormone and/or anti-androgen therapy; 3) Assessing the role of crosstalk between immune and cancer cells in prostate cancer responsiveness to new therapies.