Skip to main contentSkip to footer
A finger pointing at a scan
Brighton & Sussex Medical School

staff profiles

BSMS > About BSMS > Contact us > Staff > Dr Fabio Simoes

Dr Fabio Simoes

A head and shoulders photo of Dr Fabio Simoes in a purple t shirt next to the medical research building on campus at the BSMS

Dr Fabio Simoes (PhD)

Assistant Professor in Cancer Research
E: F.A.Simoes@bsms.ac.uk
T: 01273 877041
Location: Medical Research Building, Brighton and Sussex Medical School, University of Sussex, Brighton, BN1 9PS

Area of expertise: Molecular pathology and in vivo disease modelling

Research areas: Acute myeloid leukaemia and the bone marrow microenvironment

Twitter handle: @DrFabioSimoes

Personal website: www.simoes.science

Biography

Fabio’s core research interest lies in the use of disease models to unravel pathological mechanisms underpinning disease phenotypes, with the aim of uncovering and testing novel targets for therapeutic intervention. In 2017, he completed his PhD at Brighton and Sussex Medical School (BSMS), focusing on the role of molecular motors and the cytoskeleton in the selective vulnerability of motor neurons to degeneration in motor neuron diseases. During his first postdoctoral position at the University of Sussex, he developed a novel model to investigate whether reduced function of a key molecular motor could increase susceptibility to motor neuron disease. Returning to BSMS for a second postdoctoral position, he utilised a surgical model of osteoarthritis to test the effectiveness of a novel potential therapy.

Fabio now leverages over a decade of experience in using in vivo models and a broad molecular biology background to investigate the tumour microenvironment in haematological malignancies such as acute myeloid leukaemia (AML). His goal is to identify novel approaches to make tumour cells more vulnerable to therapies.

Research

Fabio’s research focuses on understanding and disrupting the interactions between blood cancers and their microenvironments, with an emphasis on acute myeloid leukaemia (AML). His work examines how AML cells remodel the bone marrow microenvironment (BMME) to promote disease progression, therapy resistance, and relapse. A key focus is on whether different AML subtypes remodel the BMME through shared mechanisms or distinct pathways, uncovering potential opportunities for targeted therapeutic interventions.

He employs in vitro co-culture systems, RNA sequencing, and targeted therapeutic strategies to identify key molecules and pathways for intervention. Fabio’s research also involves developing translational in vivo models to replicate the complexities of the tumour microenvironment, enabling preclinical evaluation of novel therapies. By integrating these approaches, he aims to advance understanding of the tumour microenvironment and translate findings into treatments that improve outcomes for patients with blood cancers.

BACKGROUND IMAGE FOR PANEL

Teaching

Fabio contributes to teaching and mentoring across undergraduate and postgraduate levels. He serves as an Academic Skills Tutor and delivers Molecular Cell Biology tutorials as part of the BM BS programme at BSMS. He has also designed and delivered advanced neuroscience technique workshops for MSc, MRes, and MSci students. Fabio supervises students at various stages of their education, providing guidance on research projects and training in laboratory techniques. He is an Associate Fellow of the Higher Education Academy.

Selected publications

Ladikou EE, Sharp K, Simoes FA, Jones JR, Burley T, Stott L, Vareli A, Kennedy E, Vause S, Chevassut T, et al. A Novel In Vitro Model of the Bone Marrow Microenvironment in Acute Myeloid Leukemia Identifies CD44 and Focal Adhesion Kinase as Therapeutic Targets to Reverse Cell Adhesion-Mediated Drug Resistance. Cancers. 2025; 17(1):135. https://doi.org/10.3390/cancers17010135

Simoes FA, Christoforidou E, Cassel R, Dupuis L, Hafezparast M. Severe dynein dysfunction in cholinergic neurons exacerbates ALS-like phenotypes in a new mouse model. Biochim Biophys Acta (BBA) - Mol Basis Dis. 2025;1871(1):167540. doi:10.1016/j.bbadis.2024.167540

Norris R, Jones J, Mancini E, Chevassut T, Simoes FA, Pepper C, et al. Patient-specific computational models predict prognosis in B cell lymphoma by quantifying pro-proliferative and anti-apoptotic signatures from genetic sequencing data. Blood Cancer J. 2024;14(1):105. doi:10.1038/s41408-024-01090-y

Christoforidou E, Moody L, Joilin G, Simoes FA, Gordon D, Talbot K, et al. An ALS-associated mutation dysregulates microglia-derived extracellular microRNAs in a sex-specific manner. Dis Model Mech 2024. 17(5):dmm050638. doi:10.1242/dmm.050638

Christoforidou E, Simoes FA, Gordon D, Talbot K, Hafezparast M. Aberrant dynein function promotes TDP-43 aggregation and upregulation of p62 in male mice harboring transgenic human TDP-43. Amyotroph Lateral Scler Front Degener. 2023;24(7-8):746-755. doi:10.1080/21678421.2023.2239276

Simoes FA, Joilin G, Peters O, Schneider LS, Priller J, Spruth EJ, et al. Potential of Non-Coding RNA as Biomarkers for Progressive Supranuclear Palsy. Int J Mol Sci. 2022;23(23):14554. doi:10.3390/ijms232314554

Diaper DC, Adachi Y, Lazarou L, Greenstein M, Simoes FA, Domenico AD, et al. Drosophila TDP-43 dysfunction in glia and muscle cells cause cytological and behavioural phenotypes that characterize ALS and FTLD. Hum Mol Genet. 2013;22(19):3883-3893. doi:10.1093/hmg/ddt243

Click here to ORCID profile >

Click here to Elements profile >