About Dr Carlos Lopez-Garcia

Lung Cancer is a cancer type characterised by multiple histological subtypes (such as small cell and non-small cell lung cancer), which can also be subdivided into molecular subtypes with different prognosis, driver genes and dysregulated pathways. This heterogeneity is especially prominent in lung squamous cell carcinoma (LUSC), the second most frequent type of non-small lung cancer after lung adenocarcinoma, and one of the most aggressive forms of lung cancer. Multiple driver genes and pathways have been involved in LUSC progression, including inactivation of TP53 and CDKN2A tumour suppressors and somatic alterations in components of multiple oncogenic pathways. These alterations, which arise in a defined order during LUSC evolution, occur in subsets of patients with no clear correlation with molecular subtypes or trends towards co-occurrence or mutual exclusivity. The poor understanding of this inter-patient heterogeneity hinders the development of therapeutic approaches to treat LUSC, which is currently without targeted therapies. Additionally, this lack of therapies to treat LUSC patients emphasises the importance of early detection and the identification of methods to detect preinvasive LUSC stages to prevent deaths by LUSC.

In our laboratory, we intend to disentangle the biological meaning of this heterogeneity, using a multiangle approach to explore the individual and cooperative role of major LUSC drivers in the transformation of the homeostatic bronchial epithelium into preinvasive stages and ultimately invasive. In addition, we are investigating the therapeutic potential of targeting genes located in focal chromosomal amplifications and deletions that have been frequently observed in subsets of LUSC patients. Understanding the biological meaning of this LUSC evolution and inter-patient heterogeneity is necessary to design new personalised therapeutic strategies and to gain a better knowledge about the mechanisms that drive LUSC progression.