Translational Molecular Pathology

Our group aims to unravel the molecular mechanisms of cancer progression and metastasis to identify new diagnostic, prognostic and therapeutic targets in cancer. By combining the knowledge and availability of human tumors in the Pathology department with the expertise of the basic molecular cell biology research group, we focus on:

Understanding: the molecular mechanisms underlying clonal cooperation and intercellular communication in heterogeneous tumors.
The role of MNK kinases in cellular stress resistance.
The role of ITGB3 in intercellular communication via extracellular vesicles in cancer metastasis (Santiago Ramon y Cajal).
The role of direct cell-cell communication via gap junctions and intercellular protrusions in cancer (Trond Aasen)
The malignant transition of Plexiform Neurofibromas (Cleofe Romagosa).

Research lines

Etiology, diagnosis and prognosis of congenital heart disease

IP: Silvia Arévalo Martínez

Etiology, diagnosis and prognosis of recurrent miscarriage

IP: Silvia Arévalo Martínez

Exercise capacity, peripheral muscle dysfunction and genotype in adults with cystic fibrosis.

To study the degree and types of skeletal muscle involvement in CF patients who present exercise intolerance and its relationship with the genotype.

To determine the relationship between the type and/or degree of skeletal muscle involvement by histologic and mitochondrial respiratory chain function study, and the CF genotype.

Correlation study between exercise capacity, pulmonary function and genotype.

IP: -

Expression analysis and functional elucidation of connexins and pannexins in relation to human cancer progression and malignancy.

Connexins and pannexins are structural units of gap junctions permitting direct intercellular communication. Deregulation of gap junctions is a frequent feature of carcinogenesis. We are characterizing the expression level of a variety of connexins and pannexins in primary and metastatic human tumours. In vitro we are studying how these proteins affect features related to the degree of malignancy such as migration, invasion and resistance to hypoxia. In connexin-deficient cell lines we are over-expressing specific wild-type or truncated forms of connexins and pannexins using retroviral constructs recently generated. In cell lines expressing high levels of specific connexins, we knockdown the expression levels using established lentiviral shRNA strategies. We aim to correlate connexin expression and cell communication with malignancy using a variety of well characterized assays with particular focus on colony formation, migration, invasion, epithelial-to-mesenchymal transition, changes in tumour stem cell populations, and hypoxia and drug resistance. The aim of the study is to: 1) Identify any significant correlation between the expression of various gap junction proteins and the malignancy, prognosis, chemo-resistance and overall survival in a variety of cancers 2) Gain mechanistic insight and identify direct functional roles of connexins and pannexins during tumour progression.

IP: Trond Aasen