Cancer kinomics: Kinome-wide analysis of drug-resistance mechanisms in human cancers
Lead Research Organisation:
University of Liverpool
Department Name: Institute of Integrative Biology
Abstract
Abstracts are not currently available in GtR for all funded research. This is normally because the abstract was not required at the time of proposal submission, but may be because it included sensitive information such as personal details.
Publications




Venkat A
(2023)
Mechanistic and evolutionary insights into isoform-specific 'supercharging' in DCLK family kinases.
in eLife

Harris JA
(2022)
Analysis of human Tribbles 2 (TRIB2) pseudokinase.
in Methods in enzymology
Studentship Projects
Project Reference | Relationship | Related To | Start | End | Student Name |
---|---|---|---|---|---|
MR/R502339/1 | 30/09/2017 | 30/08/2022 | |||
1961582 | Studentship | MR/R502339/1 | 30/09/2017 | 30/03/2021 | Emma Fairweather |
Description | UGA Franklin college |
Organisation | University of Georgia |
Country | United States |
Sector | Academic/University |
PI Contribution | Previous work between the Eyers (UoL) and Kannan (UoG) labs has led to the publication of eight research papers, which have fundamentally advanced our understanding of how kinases are regulated. I wish to examine how, and why, drug resistance occurs in tyrosine kinases. This will be achieved by using multidisciplinary approaches that combine skills and techniques from both labs in the broad areas of enzymology, protein biochemistry, computational and structural bioinformatics. |
Collaborator Contribution | By using state-of-the-art computational methods at the University of Georgia, I am investigating how point mutations in ABL and EGFR directly influence the conformation of the proteins, including how they transition from active to inactive states, and how resistant mutations perturb inhibitor binding |
Impact | The specific research I propose to pursue in Kannan's lab at UoG involves characterizing effects of mutations found in the ABL and EGFR tyrosine kinases associated with patient drug relapse. This will allow us to understand how these mutations directly influence the structure of these kinases, and the binding and efficacy of FDA-approved drugs for the treatment of chronic myeloid leukaemia (CML) and non-small cell lung cancer (NSCLC). |
Start Year | 2018 |