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Origins of metastasis – are unfaithful enhancers to blame?

22 febr. 18

Speaker: Sakari Vanharanta, Ph.D.  MRC Cancer Unit, University of Cambridge, Cambridge, UK

Imatge

Presentation

Organizers: IRB Barcelona

Date: Thursday, February 22th, 12:00h

Place: Aula Fèlix Serratosa, Parc Científic de Barcelona

Host: Dr. Roger Gomis (IRB Barcelona)

Abstract

The mechanisms through which cancers acquire metastatic transcriptional traits remain poorly understood. Genetic analysis of human patient samples and model systems have failed to identify specific metastasis mutations. Yet, stable cancer clones with enhanced metastatic potential have been isolated from several different tumour types, and the expression of defined gene expression signatures correlate with poor patient outcome in clinical data sets. This raises the possibility that non-mutational heritable alterations support the emergence and maintenance of metastatic transcriptional programmes. Using experimental metastasis models combined with functional genomics we have investigated the mechanisms of metastasis gene activation in VHL mutant renal cell carcinoma. Our results support a model whereby cross-lineage co-option of physiological enhancer states promotes the activation of metastasis genes. Thus, epigenetic modulation of the oncogenic signals that drive tumour initiation and early progression may underlie metastatic cancer progression.

Oncology Programme Seminar