Richard OdleRichard grew up in Medway and found the prospect of excessive coffee consumption a suitable incentive for studying medicine at Cambridge. He is now undertaking an MB/PhD to spend some time researching with the Cookies. During his undergraduate degree, he developed an interest in cancer research and his third year project with Professor Nick Coleman investigated the signalling networks of the Human Papilloma Virus oncoproteins E6/E7. He has also researched, with Dr Gary Doherty, clinical prognostic indicators in ovarian cancer patients.
His current research focuses on the regulation of Transcription Factor EB (TFEB), in relation to ERK1/2 and the cell cycle. In his spare time, he enjoys attempting (but ultimately failing) to learn Mandarin and cooking (which tends to go wrong as well).
Richard is the first medic to undertake a PhD in the Cook lab and has taken responsibility for our health and wellbeing. He is always on hand with a warm stethoscope, suitable analgesia and an excellent bedside manner.
Myers SM, Miller DC, Molyneux L
European journal of medicinal chemistry
178 1768-3254:530-543 (2019)
MEK1/2 inhibitor withdrawal reverses acquired resistance driven by BRAF amplification whereas KRAS amplification promotes EMT-chemoresistance.
Sale MJ, Balmanno K, Saxena J
10 2041-1723:2030 (2019)
Over-expressed, N-terminally truncated BRAF is detected in the nucleus of cells with nuclear phosphorylated MEK and ERK.
Hey F, Andreadi C, Noble C
4 2405-8440:e01065 (2018)
Targeting IKKβ in Cancer: Challenges and Opportunities for the Therapeutic Utilisation of IKKβ Inhibitors.
Prescott JA, Cook SJ
7 2073-4409: (2018)
Kidger AM, Sipthorp J, Cook SJ
Pharmacology & therapeutics
Kidger AM, Cook SJ
The FEBS journal
285 1742-4658:42-45 (2018)
Calcium phosphate particles stimulate interleukin-1β release from human vascular smooth muscle cells: A role for spleen tyrosine kinase and exosome release.
Dautova Y, Kapustin AN, Pappert K
Journal of molecular and cellular cardiology
ERK1/2 signalling protects against apoptosis following endoplasmic reticulum stress but cannot provide long-term protection against BAX/BAK-independent cell death.
Darling NJ, Balmanno K, Cook SJ
12 1932-6203:e0184907 (2017)
Cook SJ, Stuart K, Gilley R
The FEBS journal
Sipthorp J, Lebraud H, Gilley R
Galloway A, Saveliev A, Łukasiak S
Science (New York, N.Y.)
352 1095-9203:453-9 (2016)
Tumor cells with KRAS or BRAF mutations or ERK5/MAPK7 amplification are not addicted to ERK5 activity for cell proliferation.
Lochhead PA, Clark J, Wang LZ
Cell cycle (Georgetown, Tex.)
15 1551-4005:506-18 (2016)