Cancer develops in a complex mutational landscape. Cancer cells accumulate ‘driver mutations’ that are causally linked to disease, and ‘passenger mutations’ that, although present, have limited impact on disease. In recent years, factors encoded by cancer genes have become targets for successful anticancer drug development. Although cancer genome sequence data provide an unparalleled depth of information about the mutations present in different cancer genomes, identification of genetic alterations contributing to tumorigenesis and metastasis calls for the use of simple genetic model systems.

We have engineered Drosophila strains that activate different cancer-driver mutations. These flies allow, with a single genetic cross, the introduction of new mutations to identify genes that, when combined with driver mutations, lead to tumor formation and metastasis.

 Specific aims

(1) understand how different mutations cooperate during the process of cellular transformation

(2) study the oncogenic potential of epithelial tetraploid cells that result from cytokinesis failure

(3) better understand how the metabolic changes taking place in cancer cells contribute to cellular transformation and metastasis

(4) determine the role that miRNAs play in growth control during normal development and cancer

• Genetic models of oncogene cooperation
  
  
• microRNAs in growth control, development, and cancer
  
  
• Cytokinesis failure and cancer
  
  
• Cancer metabolism

Analysis of gene functions in development and disease, using Drosophila

Héctor Herranz, PhD
Department of Cellular and Molecular Medicine (ICMM) University of Copenhagen, Denmark
[email protected]

Education

2002   PhD. University Autónoma of Madrid, Spain 1997   Degree in Biochemistry. University of Salamanca, Spain 1996   Degree in Biology. University of Salamanca, Spain

Research Appointments