Overview
Cancer metastasis is deeply influenced by the host’s biology. Cancer interacts dynamically with the host’s immune system, metabolism, and microenvironment, including surrounding tissues, blood vessels, and extracellular components. Host factors such as age, sex, diet, genetics and comorbidities shape tumour progression, response to therapy, and metastatic patterns. We aim to understand how host-specific factors and site-specific cues drive melanoma progression and therapeutic outcomes. Our aim is to develop personalised melanoma rationales that consider the entire organism, not just the tumour itself.
Our group aims to understand the melanoma metastatic process to solid organs, and how melanoma adapts to new environments and how new sites impact the response to therapy. Our aim is to find vulnerabilities during the metastatic process that we can target and change patient outcomes, reducing relapses.
We are studying the transcriptional and metabolic programmes that affect the melanoma metastatic process, from the primary site (skin) to solid organs. We integrate next generation sequencing, mass cytometry, metabolic profiling and imaging of cancer cells and the tumour microenvironment to profile how metastases develop in different hosts and organs.
We use mouse and human tissue to study spatial localisation to study the physical association between stroma and cancer cells. We aim to elucidate the programmes in primary tumours that promote metastasis, the similarities between primary and metastatic sites, as well as the site-specific differences that are linked to progression and therapy resistance.
Finally, we are developing biomarkers to predicts metastasis from primary sites.
Featured Publications

Ultraviolet light-induced collagen degradation inhibits melanoma invasion
12th May 2021
Authors studied how UVR modifies dermal fibroblast function, the extracellular matrix (ECM) and melanoma invasion. They highlight the prognostic power of collagen in aged primary melanoma tumours.

Female Immunity Protects from Cutaneous Squamous Cell Carcinoma
1st June 2021
Sex bias affects cancer incidence, mortality, and therapy response; and the molecular landscape of cancer differs by sex. This work reveals men are more susceptible to cutaneous aggressive squamous cell carcinoma, in contrast to women who activate stronger immune responses when challenged with the same carcinogens.

Molecular subtype, biological sex and age shape melanoma tumour evolution
1st February 2021
The authors use mathematical modelling of somatic mutations in 396 melanomas from The Cancer Genome Atlas to evaluate how sex and age collectively influence TMB, subtype and mutational signatures and confirmed that clock‐like mutations accumulate with age.

Molecular characterization of fast-growing melanomas
1st February 2022
Fast-growing melanomas are aggressive and linked to early death. Rapid growth is more frequent in patients with less accumulated sun exposure and is associated with thicker, ulcerated tumors with fibroblast growth factor receptor 2 mutations. Ulceration, thickness, and fibroblast growth factor receptor 2 mutations are biomarkers for aggressive disease and could stratify patients for adjuvant therapy.
Meet the group
It is a pleasure to introduce my team who work to deliver our research goals. We work in a friendly and collaborative environment, supporting each other’s projects.

Institute Fellow
FAQs
Yes, I continue to see NHS patients in my weekly general dermatology and high-risk skin cancer clinic at Salford Royal NHS. It is a very important part of our work, as it is always patient concerns that guide our next scientific experiments.
We are keen to expand our research network and work collaboratively within the University of Manchester, in the UK and internationally. Get in touch with us using the contact form below, we’re always open to new ideas and collaborations.
All Institute Publications
https://doi.org/10.1186/s12943-024-02157-x
The PI3K-AKT-mTOR axis persists as a therapeutic dependency in KRASG12D-driven non-small cell lung cancer
12 November 2024
Institute Authors (1)
Amaya Viros
Labs & Facilities
Genome Editing and Mouse Models
Research Group
Skin Cancer & Ageing
12 November 2024
https://doi.org/10.1186/s13045-024-01610-0
The small inhibitor WM-1119 effectively targets KAT6A-rearranged AML, but not KMT2A-rearranged AML, despite shared KAT6 genetic dependency
8 October 2024
Institute Authors (6)
Georges Lacaud, Mathew Sheridan, Michael Lie-a-ling, Liam Clayfield, Jessica Whittle, Jingru Xu
Research Group
Stem Cell Biology
8 October 2024
/wp-content/uploads/2024/11/Annual-Report-2023.pdf
2023 Annual Report
13 September 2024
13 September 2024
https://doi.org/10.1126/science.adh7954
Vitamin D regulates microbiome-dependent cancer immunity
25 April 2024
Institute Authors (1)
Evangelos Giampazolias
Research Group
Cancer Immunosurveillance
25 April 2024
https://doi.org/10.1038/s41684-024-01363-w
Streamlining mouse genome editing by integrating AAV repair template delivery and CRISPR-Cas electroporation
10 April 2024
Institute Authors (1)
Natalia Moncaut
Labs & Facilities
Genome Editing and Mouse Models
10 April 2024
https://www.biorxiv.org/content/10.1101/2023.12.13.568969v1
A novel human model to deconvolve cell-intrinsic phenotypes of genetically dysregulated pathways in lung squamous cell carcinoma
14 December 2023
Institute Authors (3)
Carlos Lopez-Garcia, Caroline Dive, Anthony Oojageer
Research Group
Translational Lung Cancer Biology
14 December 2023
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A note from the Group Leader – Amaya Viros
My research is focused on studying why some melanomas are more metastatic. I am particularly keen to understand how cancer cells travel from the primary site to metastatic organs, and why some organs are more likely to be seeded by metastatic cells than others. We are focusing on the lungs, liver and brain as primary sites of metastasis. After decades of clinical experience and research, we still don’t fully understand why some patients have a more aggressive course of disease. We investigate local factors in the skin that promote metastasis, as well systemic and organ factors that allow melanoma cells to spread and thrive in a new environment. Understanding why cancer spreads will allow us to develop new agents to stop melanoma deaths.