John Angus Hickman
John Angus Hickman (born 10 September 1945) is a British-French cancer pharmacologist who worked in UK and American universities and in the French pharmaceutical industry. He was born in Nottingham, UK, to a Scottish mother and English father. He has two children from his marriage to Jennifer Pullan and a third from his marriage to Nathalie Aveline.
He proposed highly innovative directions for cancer drug discovery, suggesting cell signalling as drug targets in the early 1980s and in the 1990s the investigation of the role of apoptosis (cell death) in determining the sensitivity and resistance of cancer cells to anticancer drugs.[1][2] He led teams that discovered anticancer drugs inhibiting proteins that regulate apoptosis.[3][4]
Education
Hickman was educated at Queen Elizabeth’s Grammar School in Ashbourne, Derbyshire (founded in 1585). He obtained his PhD in heterocyclic organic chemistry in 1971 from Aston University in Birmingham, UK, after obtaining a degree in pharmacy. He was a Medical Research Council postdoctoral fellow at the Chester Beatty Institute in London, working with Professor Tom Connors on the mechanism of action of anticancer alkylating agents. He obtained an MSc in biochemistry from King’s College London in 1974 and a DSc in 1989.
Career
After a lectureship in Liverpool, he returned to Aston University in 1977, where shortly afterwards the UK Cancer Research Campaign (now CRUK) established their Experimental Cancer Chemotherapy Group. The preclinical activity of antitumour drug Temozolomide (Temodal), synthesised by Robert Stone with Malcolm Stevens, was then discovered by Drs. Hickman, Langdon and Gibson.[5] In 1982 he spent 18 months in the Department of Pharmacology at Yale University where, with Tom Tritton, he suggested that cell membrane signalling could be a target for anticancer drugs,[6][7] an iconoclastic idea at that time. In 1989 he co-organised the first foreign American Association for Cancer Research Special Meeting in Cambridge, UK, on anticancer drugs targeting cell signalling.[8] He moved to Manchester University’s School of Biological Sciences in 1989 as the Imperial Chemical Industries (ICI) Professor of Molecular Pharmacology where he directed a research group investigating the role of apoptosis in cancer drug sensitivity and resistance. Hickman initiated and was director of a joint laboratory with ICI Pharmaceuticals (becoming Zeneca) and the School of Biological Sciences. He became head of the Division of Physiology, Pharmacology and Toxicology in the School of Biological Sciences and was a co-founder of the Manchester University Biotechnology Incubator, whose restaurant was called “Hickmans”. After short sabbaticals at Northwestern University in Evanston, Oxford University and two summer periods at Woods Hole Marine Biology Laboratory,[9] Hickman left Manchester for Paris in 1999 to head a new cancer drug discovery group at the private pharmaceutical company Servier, largely focusing on the discovery of drugs inhibiting the anti-apoptotic proteins BCL-2 and MCL-1.[10] Retiring in 2010 he then coordinated a European Union Innovative Medicines project PREDECT investigating preclinical models that better represented the complexity of cancer.[11] He now writes about the challenges of drug therapy for cancer,[12] the limitations of preclinical models[13] and the social hegemony of the pharmaceutical industry.[14] He works with the group Consilium Scientific.[15]
National and international activities
Hickman co-chaired three American Association for Cancer Research special meetings and sat on their annual meeting programme committee. He chaired the 1996 Gordon Conference on Cancer Chemotherapy at Oxford University, initiated the European Association of Cancer Research meeting “Goodbye Flat Biology” and for a decade co-chaired the European School of Haematology’s meetings on apoptosis. He presented his teams’ work at The Royal Society in London, the Nobel Forum at the Karolinska Institute in Stockholm and at many international venues. He is currently a Board Member of Consilium Scientific.[15] Living in Paris and Montpellier he divides his time between his family, writing, attending classical music concerts and being a Parisian “flaneur”.
References
- ↑ Dive, Caroline (1991). "Drug-target interactions: only the first step in the commitment to a programmed cell death?". Br. J. Cancer. 64 (1): 192–196. doi:10.1038/bjc.1991.269. PMC 1977304. PMID 1854622.
- ↑ Hickman, John A. (1992). "Apoptosis induced by anticancer drugs". Cancer Metastasis Rev. 11 (2): 121–139. doi:10.1007/BF00048059. PMID 1327566. Unknown parameter
|s2cid=ignored (help) - ↑ Kotschy, A. (2016). "The MCL1 inhibitor S63845 is tolerable and effective in diverse cancer models". Nature. 538 (7626): 477–482. Bibcode:2016Natur.538..477K. doi:10.1038/nature19830. PMID 27760111. Unknown parameter
|s2cid=ignored (help) - ↑ Casara, P. (2018). "S55746 is a novel orally active BCL-2 selective and potent inhibitor that impairs hematological tumor growth". Oncotarget. 9 (28): 20075–20088. doi:10.18632/oncotarget.24744. PMC 5929447. PMID 29732004.
- ↑ Stevens, Malcolm F.G. (1987). "Antitumor Activity and Pharmacokinetics in Mice of 8-Carbamoyl-3-methyl-imidazo[5,1-d]-1,2,3,5-tetrazin-4(3H)-one (CCRG 81045; M & B 39831), a Novel Drug with Potential as an Alternative to Dacarbazine". Cancer Research. 47 (22): 5846–5852. PMID 3664486.
- ↑ Hickman, John A. (1984). "Membrane targets in cancer chemotherapy". Trends Pharmacol. Sci. 5: 15 and 17.
- ↑ Hickman, John A. (Aug 1988). "Membrane targets in cancer chemotherapy". Eur J Cancer Clin Oncol. 24 (8): 1385–1389. doi:10.1016/0277-5379(88)90236-2. PMID 3181263.
- ↑ Powis, Garth (1990). "The Cell Membrane and Cell Signals as Targets in Cancer Chemotherapy AACR, EORTC, and BACR Special Conference in Cancer Research". Cancer Research. 50: 2203 and 2211.
- ↑ Jonas, E.A. (2004). "Proapoptotic N-truncated BCL-xL protein activates endogenous mitochondrial channels in living synaptic terminals". Proc. Natl. Acad. Sci. (USA). 101 (37): 13590–13595. Bibcode:2004PNAS..10113590J. doi:10.1073/pnas.0401372101. PMC 518799. PMID 15342906.
- ↑ Casara, P. (2018). "S55746 is a novel orally active BCL-2 selective and potent inhibitor that impairs hematological tumor growth". Oncotarget. 9 (28): 20075–20088. doi:10.18632/oncotarget.24744. PMC 5929447. PMID 29732004.
- ↑ Hickman, John A. (2014). "Three‐dimensional models of cancer for pharmacology and cancer cell biology: capturing tumor complexity in vitro/ex vivo". Biotechnol. J. 9 (9): 1115–1128. doi:10.1002/biot.201300492. PMID 25174503. Unknown parameter
|s2cid=ignored (help) - ↑ Tannock, Ian F. (2016). "Limits to personalized cancer medicine". New Eng. J. Med. 375 (13): 1289–1294. doi:10.1056/NEJMsb1607705. PMID 27682039.
- ↑ Scannell, J.W. "Predictive Validity in Drug Discovery: What it is, Why it Matters, and How to Improve it". Nature Rev. Drug Disc.
- ↑ Hickman, John A. (2021). "The European Union and personalised cancer medici". Eur J Cancer. 150: 95–98. doi:10.1016/j.ejca.2021.03.013. PMID 33892410 Check
|pmid=value (help). Unknown parameter|s2cid=ignored (help) - ↑ 15.0 15.1 "HOME". Consilium-Scientific.
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