Claire Wells

Claire Wells


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Personal profile

Research interests

The laboratory is interested in how cancer cells are able to dissociate from the primary tumour, invade the surrounding tissue and subsequently metastasise to distal sites. Tissue invasion and migration require cancer cells to reorganise their actin cytoskeleton as well as adhere to and degrade the surrounding extracellular matrix. It is well established that cytoskeletal rearrangement, cell adhesion formation and turnover is regulated by Rho GTPases, Rho, Rac and Cdc42. PAKs are serine/threonine kinases that operate downstream of Rho GTPases to control cytoskeletal organisation and substratum adhesion. The PAK family can be sub-divided into two groups; Group 1 PAKs (1-3) and Group 2 PAKs (4-6) based on sequence homology and members of both groups are activated by growth factor signalling pathways. We use live cell imaging, biochemical and molecular approaches to investigate the role of PAK family kinases in cancer cell migration, adhesion and invasion.

Work in the Wells lab is supported by Pancreatic Cancer Resrach Fund

Please go to to find out more about the Wells Lab 

Research interests (short)

Cancer cell invasion:live cell imaging, biochemical and molecular approaches

Research interests

Wells Lab belongs to 

Prostate Cancer Programme

Breast Cancer Programme

Cancer Biology Programme

GI cancer Programme (pancreatic cancer)

Expertise related to UN Sustainable Development Goals

In 2015, UN member states agreed to 17 global Sustainable Development Goals (SDGs) to end poverty, protect the planet and ensure prosperity for all. This person’s work contributes towards the following SDG(s):

  • SDG 3 - Good Health and Well-being

Education/Academic qualification

Doctor of Philosophy, King's College London

Award Date: 1 Jan 1998

Bachelor of Science, UCL University College London

Award Date: 1 Jan 1993

External positions

Chair RMS Life Sciences Section

1 Jul 20161 Jul 2019


  • QH301 Biology
  • cancer
  • migration
  • P-21 activated kinases
  • invasion
  • actin cytoskeleton


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