Drug Target Optimization in Chronic Myeloid Leukemia Using Innovative Computational Platform
- Submitting institution
-
University College London
- Unit of assessment
- 11 - Computer Science and Informatics
- Output identifier
- 13991
- Type
- D - Journal article
- DOI
-
10.1038/srep08190
- Title of journal
- SCIENTIFIC REPORTS
- Article number
- ARTN 8190
- First page
- -
- Volume
- 5
- Issue
- 1
- ISSN
- 2045-2322
- Open access status
- Out of scope for open access requirements
- Month of publication
- February
- Year of publication
- 2015
- URL
-
-
- Supplementary information
-
https://acm-prod-cdn.literatumonline.com/2785956.2787495/3b814e12-3fcc-4537-b440-4d0f17195b31/p15-hartert.webm?b92b4ad1b4f274c70877518315abb28be831d54738a81f1de54388f7ef00efe69476506f9779c01589746dee76c7772beaf4bc1209f31f6121c73aae30c72d609232138b96895e972a6019f8ce27a112ed4879dac8fd999a9e87d0dbcb5dacfe363108c1d3
- Request cross-referral to
- -
- Output has been delayed by COVID-19
- No
- COVID-19 affected output statement
- -
- Forensic science
- No
- Criminology
- No
- Interdisciplinary
- Yes
- Number of additional authors
-
10
- Research group(s)
-
-
- Citation count
- 8
- Proposed double-weighted
- No
- Reserve for an output with double weighting
- No
- Additional information
- Chronic Myeloid Leukemia (CML) patients face high risk drug resistance, caused by mutations and/or activation of alternative cellular pathways. To develop drugs that avoid this problem, we must systematically test all possible combinations of drug targets within the genetic network that regulates the disease. This paper solves the problem using termination proving techniques, based on the observation that cancer is a termination bug in the body. This technique probed previously unseen interactions between pathways and cellular outcomes, suggesting new therapeutic targets, and highlighting unexplored sensitivities to Interleukin-3. This work is now used commercially by Astra-Zeneca.
- Author contribution statement
- -
- Non-English
- No
- English abstract
- -