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Prof Pablo Rodriguez-Viciana
Prof Pablo Rodriguez-Viciana profile picture
  • Professor of Cell Signalling
  • Research Department of Cancer Bio
  • Cancer Institute
  • Faculty of Medical Sciences

Following a BSc by the Universidad Autonoma of Madrid, Spain, PR-V completed his PhD thesis in Julian Downward's laboratory at the ICRF in London, where his work resulted in the identification of PI3K as a direct target of RAS and showed that RAS can use multiple effectors to signal downstream. He then carried out post-doctoral studies in Frank McCormick's lab at the University of California, San Francisco, where his work  led to the identification of the SHOC2 phosphatase complex as a unique regulatory node required for efficient RAS-ERK pathway activation with properties of an attractive therapeutic target. In 2008 he returned to London as a group leader at the UCL Cancer Institute where a major focus of his group is to study the function of the SHOC2 phosphatase complex in the context of diseases such as cancer and RASopathies.

Research Groups
Research Summary
Cell proliferation is normally tightly regulated by signals received from the extracellular environment that are relayed from the cell surface through signalling cascades that ultimately lead to cell division. Malfunction in components of these signalling cascades can cause uncontrolled cell proliferation and cancer.
RAS proteins are central components of the signalling cascades regulating cell proliferation. They function as ON/OFF switches that when active relay the signal downstream by activating a variety of other proteins, including the RAF-MEK-ERK kinase cascade.
Around a third of human cancers have mutations in RAS genes that produce a protein that is always ON, the cells proliferate and create tumours. It is estimated that RAS is responsible for over one million deaths from cancer worldwide every year. Up-regulation of the RAS-ERK pathway is also responsible for a family of developmental disorders referred to as RASopathies.
Unfortunately, it has proven very difficult to target RAS directly therapeutically. Intense efforts have also focused on other points in the RAS signalling pathway, particularly the RAF-MEK-ERK kinase cascade. However, it has not yet been possible to develop effective ways to block RAS function without unacceptable toxicity for normal cells. The lab focuses on studying RAS signalling and identifying mechanisms to inhibit RAS function in cancer cells that will spare normal cells.
Although much drug development has focused on kinases (such as RAF and MEK), the phosphatases that remove phosphate groups also play a key role in the regulation of signalling pathways. We are particularly interested in a multi-subunit phosphatase formed by SHOC2, MRAS and PP1 (the SHOC2 phosphatase complex) that removes a specific phosphate group on RAF kinases that is key for their activation. Crucially, cancer cells with hyperactive RAS preferentially rely on the activity of the SHOC2 complex compared to normal cells, which thus provides a therapeutic opportunity.
The lab focuses on understanding the function of the SHOC2 phosphatase complex in normal and cancer cells and using this knowledge to help develop new therapies to selectively target the many cancers with hyper-active RAS function.

Teaching Summary

PR-V is lead for the Cancer Biology and Therapeutics module.  He also lectures on Cell Signalling in Health and Disease and MSc Cancer courses.

Academic Background
1997   Doctor of Philosophy University College London
1992   Bachelor of Science Universidad Autonoma de Madrid
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