John Angus Hickman

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John A. Hickman (born 10 September 1945) is a British-French cancer pharmacologist.

Career[edit]

Professor at Manchester University, he received his Doctor of Science (DSc) in 1990 for his work in Experimental Cancer Chemotherapy. Jointly establishing and directing the Cancer Research Campaign's (now CRUK) Experimental Cancer Chemotherapy Group at Aston University (UK), the antitumour drug Temozolomide (Temodal), used to treat brain cancers, was discovered there by Dr. Hickman with Drs. Langdon and Gibson.[1]

In 1982 he spent 18 months in the Department of Pharmacology at Yale University where with Thomas R. Tritton he suggested that cell membrane signalling could be a target for anticancer drugs,[2][3] 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.[4] 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. After short sabbaticals at Northwestern University in Evanston, Oxford University and two summers periods at Woods Hole Marine Biology Laboratory,[5] Hickman left Manchester for Paris in 1999 to head a new cancer drug discovery group at the private pharmaceutical company Servier, largely focussing on the discovery of drugs inhibiting the anti-apoptotic proteins BCL-2 and MCL-13,14. Retiring in 2010 he then coordinated a European Union Innovative Medicines project PREDECT investigating preclinical models that better represented the complexity of cancer.[6] He now writes about the challenges of drug therapy for cancer,[7] the limitations of preclinical models[8] and the social hegemony of the pharmaceutical industry.[9] He works with the group Consilium Scientific.[10]

Research work[edit]

He proposed novel 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.[11][12] In addition to the discovery of Temodal, he led teams that discovered anticancer drugs inhibiting proteins that regulate apoptosis.[13][14] He has an H-index of 68 in Google Scholar and more than 20,000 citations.

Books[edit]

  • Apoptosis and cancer chemotherapy. Totowa, N.J.: Humana Press. 1999. ISBN 9780896037434.[15]
  • Cancer chemotherapy. Oxford: Blackwell Scientific Publications. 1993. ISBN 9780632034413.[16][17]

References[edit]

  1. ^ 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.
  2. ^ Hickman, John A. (1984). "Membrane targets in cancer chemotherapy". Trends Pharmacol. Sci. 5: 15 and 17. doi:10.1016/0165-6147(84)90352-3.
  3. ^ 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.
  4. ^ 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.
  5. ^ 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.
  6. ^ 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. S2CID 2517208.
  7. ^ Tannock, Ian F. (2016). "Limits to personalized cancer medicine". N. Engl. J. Med. 375 (13): 1289–1294. doi:10.1056/NEJMsb1607705. PMID 27682039.
  8. ^ Scannell, J.W. "Predictive Validity in Drug Discovery: What it is, Why it Matters, and How to Improve it". Nature Rev. Drug Disc. 21 (12): 915–931.
  9. ^ 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. S2CID 233382086.
  10. ^ "HOME". Consilium-Scientific.
  11. ^ 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.
  12. ^ Hickman, John A. (1992). "Apoptosis induced by anticancer drugs". Cancer Metastasis Rev. 11 (2): 121–139. doi:10.1007/BF00048059. PMID 1327566. S2CID 23716134.
  13. ^ 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. S2CID 4472590.
  14. ^ 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.
  15. ^ McConkey, David J. (1 September 2000). "Apoptosis and Cancer Chemotherapy. John A. Hickman , Caroline Dive". The Quarterly Review of Biology. 75 (3): 367–368. doi:10.1086/393618. ISSN 0033-5770.
  16. ^ Coleman, R. E. (1993). "Review of Cancer Chemotherapy". BMJ: British Medical Journal. 307 (6910): 1014. ISSN 0959-8138. JSTOR 29721440.
  17. ^ Newlands, E S (1994). "Cancer Chemotherapy". Journal of Pharmacy and Pharmacology. 46 (2): 158. doi:10.1111/j.2042-7158.1994.tb03765.x.

External links[edit]

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