2025- present: Senior Lecturer, University of Sheffield (UK)

2016- 2024: Lecturer, University of Sheffield (UK)

2015–2016: Research Fellow, University of Sheffield (UK)

2009–2015: Post-doctoral researcher, the Beatson Institute for Cancer Research, Glasgow (UK)

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My group is interested in understanding the role of extracellular matrix internalisation in cell migration and invasion. The extracellular matrix (ECM) is a complex network of secreted proteins that, beyond providing physical support to organs and tissues, regulates many cell functions, including proliferation, polarity, migration and oncogenic transformation. Our aims are to understand the basic molecular events regulating ECM endocytosis, as well as how ECM uptake impinges on cell migration and invasion in complex 3D environments

2020- present: Post-doctoral Research Associate in Cancer Biology, School of Biosciences, University of Sheffield (UK)

2017- 2021: PhD student, Department of Biomedical Science, University of Sheffield (UK).

2016: Master, Stem cell and Regenerative Medicine, University of Sheffield (UK).

2014: Bachelor, Biology, Baha’i Institute for Higher Education (BIHE), Tehran (Iran).

Contact: mnazemi1@sheffield.ac.uk 

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Tumour development is defined as a process in which cells constantly accumulate genetic mutations and epigenetic alterations. However, there is growing evidence that the tumour microenvironment could also facilitates tumour growth and survival. Tumour microenvironment consists of stromal cells and extracellular matrix (ECM), which is highly dynamic and provides structural and mechanical support to the tissues while interacting with cells through different receptors. The focus of my PhD project is on the interaction of breast cancer cells with extracellular matrix (ECM) from a novel angle; I am interested to investigate how ECM internalization affect cell growth and metabolism in invasive breast cancer cells compare to the normal mammary epithelial cells. So far, I have tried to elucidate the effect of ECMs on growth and survival of breast cancer cells under specific nutrient depletion conditions. Now, I am exploring the role of ECM on cancer cells’ metabolic changes and adaptations under those conditions.     

2020-present: Research technician/ part-time PhD student, School of Biosciences, University of Sheffield, UK

2018-2020: Lab technician, Ballestrem Lab, University of Manchester, UK

2016-2018: MSc Molecular Medicine/ Cancer pathway, University of Sheffield, UK

2016: Lab technician, SGS limited, Bradford, UK.

2014-2015: MSc Analytical Sciences, Bradford University, UK.

2007-2012: BSc Pharmacy and Pharmaceutical technology, Damascus University, Syria.

Contact: b.yanes@sheffield.ac.uk

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Like many people, I have lost family members who were diagnosed with cancer. This driven me to pursue a job that allows me to play a role in finding a cure for cancer and helping other people to avoid its impact.

Breast cancer is one of the most common types of cancer in women worldwide with 30% diagnostic rate. Cancer cells can change their metabolism according to their progression and their needs which can be provided by the interaction with the surrounding microenvironment. The extracellular matrix (ECM) forms most of the tumour microenvironment and the expression of its proteins is high in some types of cancer including breast cancer.

In my project, the role of the extracellular matrix in breast cancer metabolism with be investigated. I will test how ECM helps cancer cells to proliferate under starvation conditions and what is the role of ECM in mitochondria dynamics.

Contact: smalhadid1@sheffield.ac.uk

2025-Present: Research Associate in Cancer Biology, University of Sheffield

2021-2025: PhD, School of Biosciences, University of Sheffield

2017-2021: MSc, Biomedical Science, University of Sheffield

Contact: rbacchetti1@sheffield.ac.uk

I have found cancer biology highly interesting since the beginning of my Undergraduate degree, as it affects millions of people worldwide. I am particularly interested in cancer cell migration and invasion as there is still a lack of understanding on how cancer cells migrate from primary tumours and invade surrounding tissues. My research focuses on investigating the relation among different regulators of cell motility, such as integrins, ADAMTS and Rab25, in ovarian cancer. The project aims to elucidate the mechanism through which ovarian cancer cells increase their motility and invade, possibly establishing ADAMTS5 as a potential therapeutic target.

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Contact: zbao10@sheffield.ac.uk

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Cancer cells are exposed to a hypoxic and nutrient-depleted tumour microenvironment due to the increased tumour cell nutrient consumption and tumour vascular malformations. Therefore, cancer cells utilise alternative methods to obtain essential nutrients to maintain their metabolism. 

Macropinocytosis, a form of endocytosis that non-selectively uptakes large amounts of extracellular matrix (ECM) and extracellular fluid, is a crucial supply route for cancer cells. The breakdown of these macropinocytic cargoes contributes to maintaining intracellular amino acids and lipids pools to support cancer cell growth and proliferation. However, the regulation of macropinocytosis remains unclear in tumours. Therefore, my PhD project aims to discover novel regulators of macropinocytosis and study their role in controlling ECM internalisation and regulating the growth and metabolism of cancer cells.

2023 - Present - PhD student, School of Bioscience, University of Sheffield, UK

2017 - 2018 - M.Sc Biomedical Science, University of Sheffield, UK

Contact: ifoyelade1@sheffield.ac.uk

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One of the most impactful breakthroughs in cancer research would be a relapse-free cancer treatment. I am interested in understanding the roles of the Extracellular Matrix of the Tumour Microenvironment in chemoresistance, metastases and cancer relapse.

I am currently studying the mechanisms that regulate survival of cancer cells in a nutrient-deprived condition. Furthermore, I am studying the mechanisms involved in formation and regulation of dormant tumour cells. Tumour dormancy is a reversible process in which cancer cells pause their cell cycle progression and revert to the G₀ phase. Here, these cancer cells remain viable but in a dormant, nonproliferative state, making them insensitive to chemotherapeutic agents (because they target rapidly growing cells), and they can survive in their dormant state as long as they remain unperturbed.

Specifically, my focus is on understanding the roles of various Extracellular Matrix proteins in survival of cancer cells in a nutrient-deprived state as well as the role of extracellular matrix proteins in the formation and reactivation of dormant tumour cells.

2024-present: Postdoctoral Research Fellow, University of Sheffield.
2022-2023: Clinical Innovation Facilitator, University of Nottingham.
2017-2023: Postdoctoral Research Fellow, University of Nottingham.
Contact: e.vancauwenberghe@sheffield.co.uk

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While considerable progress has been made in breast cancer diagnosis and early treatment, there is still room for improvement as this malignant cancer still kills over half a million women yearly over the world. These deaths generally happen following the metastasis of breast cancer cells that have acquired a range of adaptative capabilities allowing them to
survive in harsh environments: fibrotic and stiffer tissue and/or acidic environments combined with a low supply of nutrients and oxygen. By their plasticity, breast tumour cells can evade immunity, resist treatments and use their microenvironment, including the extracellular matrix (ECM), to their own advantage. This allows them to invade and to grow
in distant organs, ultimately impairing critical organ functions. Treating the cancer at this stage becomes incredibly challenging. That is why it is our mission as scientists to find and to develop new prevention and treatment strategies against these cells with high metastatic potential, significantly enhancing personalised advanced cancer therapy.
In this context, our team has established that breast cancer cells are able to internalise ECM key components, such as Collagen I, followed by lysosomal degradation to support their own
growth under amino acid starvation conditions. This nutrient scavenging process is mediated by a2b1 integrin binding to ECM components, inducing their internalisation via macropinocytosis, a form of endocytosis. Using complex in vitro and in vivo models, my project aim is to deepen our understanding how nutrient scavenging is controlled via a2b1 integrin and regulators of its lysosomal delivery. This will reveal their impact on breast
cancer cell growth, invasion and ultimately metastasis.

2025-present: PhD, Department of Biomedical Science, University of Sheffield.​

2019-2021: MSc Molecular Medicine/ Cancer pathway, University of Sheffield, UK​

2015-2019: Master Phytotherapy, Institute of health sciences, Yeditepe University, Turkey.​

2012-2016: BSc Pharmacy, Yeditepe University, Turkey.

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Contact: fgyoldas1@sheffield.ac.uk

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I have wanted to study cancer research since my first year of pharmacy, but I was not sure which type of cancer to focus on. My master’s project was related to overcoming chemoresistance in multiple myeloma, and I was looking for a project involving cancer and chemotherapy. Meanwhile, I learned of the death of my lecturer, Prof. Dr. Erdem Yeşilada, due to pancreatic cancer. I then learned that pancreatic cancer is often diagnosed at a late stage and has a low survival rate. This strongly encouraged me to focus my research on pancreatic cancer.

My current project focuses on characterizing extracellular matrix–cell interactions in therapy response in pancreatic cancer.

2025-present: PhD student, Department of Biosciences, University of Sheffield, UK

2022-2023: Master student, cancer molecular pathology and therapeutics, University of Leicester, UK

2016-2021: Bachelor, medical laboratory sciences, University of Tehran, Iran

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Contact: fpirhayaty1@sheffield.ac.uk

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Tumour progression is increasingly recognised as a process shaped not only by genetic alterations but also by the tumour microenvironment, particularly the extracellular matrix (ECM). The ECM is a dynamic structure that actively regulates cancer cell growth, survival, and invasion, especially under nutrient-limited conditions.

My research focuses on understanding how cancer cells exploit the ECM as a nutrient source, with an emphasis on the role of extracellular proteases, particularly cathepsins. Using invasive breast cancer models, I am interested to investigate how cathepsin-mediated ECM remodelling and internalisation support cancer cell survival during metabolic stress.

By combining pharmacological approaches with quantitative imaging and 2D and 3D cell culture models, my work aims to define the mechanisms by which cathepsins regulate ECM utilisation and cancer cell adaptation, with the goal of identifying potential therapeutic vulnerabilities in fibrotic and therapy-resistant tumours.