We study the most common skin cancer (Basal Cell Carcinoma) and the most malignant skin cancer (Melanoma) to uncover the mechanisms that drive their initiation, progression and therapy response.
Basal Cell Carcinoma is the most common human cancer, it is a skin cancer that arises upon constitutive activation of the Hedgehog signalling pathway in skin keratinocytes.
In the lab we are interested in uncovering the cancer cell intrinsic and extrinsic factors that drive Basal Cell Carcinoma formation.
We have recently identified Survivin/Birc5 as a novel key driver of Basal Cell Carcinoma formation. Survivin is required in the skin stem cells to evolve into a Basal Cell Carcinoma upon oncogenic activation. Specifically, we showed that Survivin mediates competence to Basal Cell Carcinoma formation by promoting proliferation while preventing cell differentiation and apoptosis (Canato et al, Cancer Discovery, 2025)
We identified the mechanical forces as a new key driver of Basal Cell Carcinoma initiation (Sahu et al, Nature Communications, 2025).
MECHANISMS MEDIATING ADULT AND PAEDIATRIC MELANOMA FORMATION, PROGRESSION AND THERAPY RESPONSE
Melanoma is the deadliest form of skin cancer across children, adolescents, and adults. However, paediatric and adult melanoma differ significantly in their underlying biology, and the mechanisms driving these differences remain poorly understood. A central goal of our research is to directly compare paediatric and adult melanoma to identify key divergences in tumour initiation, progression, and therapeutic response. In our lab, we generate novel models of paediatric melanoma by combining genetic mouse models, grafting approaches, and in vitro systems. These models enable us to uncover the unique biology of paediatric disease in comparison to adult melanoma and to develop more effective, tailored therapies for patients affected by this aggressive cancer.
We have recently contributed to the discovery of a new mechanisms of cellular plasticity the drives aggressivness and invasivness in melanoma (Chocarro-Calvo et al, Genes & Development 2025)
Neuroblastoma and medulloblastoma share a common developmental origin, arising from embryonic progenitor cells of the nervous system, highlighting how disruptions in early neural lineage specification can give rise to distinct but related paediatric malignancies.
MECHANISMS MEDIATING MEDULLOBLASTOMA INITIATION, PROGRESSION AND THERAPY RESISTANCE
Medulloblastomas are one of the most common paediatric brain tumours. In our lab, we focus on generating novel models of medulloblastoma and also use the already developed models to uncover the cellular and molecular drivers of medulloblastoma progression and therapy resistance.
MECHANISMS DRIVING NEUROBLASTOMA HETEROGENEITY AND PROGRESSION
Neuroblastomas (NBs) are among the most common solid tumours and a leading cause of paediatric death. They are composed of different tumour and tumour microenvironment cell populations, and present cellular heterogeneity. Cellular heterogeneity has been proposed to be responsible for tumour progression and therapy resistance.
We are interested to identify the cell populations that mediate tumour progression in those tumours. In addition, we aim at uncovering how these cell populations dynamically evolve during therapy and infer which populations resist the therapy, potentially leading to tumour relapse. To this end, we combine state-of-the art genetic mouse models, grafting experiments and in vitro cultures.