Tomas Lindahl

Tomas Lindahl
Born Tomas Robert Lindahl
28 January 1938[1]
Nationality Sweden
Fields Cancer research
Institutions
Alma mater
Thesis On the structure and stability of nucleic acids in solution (1967)
Known for Clarification of cellular resistance to carcinogens
Notable awards
Website
www.london-research-institute.org.uk/research/past-researchers/tomas-lindahl

Tomas Robert Lindahl FRS FMedSci (born 28 January 1938) is a Swedish scientist specialising in cancer research.[3][4][5][6][7][8][9][10][11]

Education

Lindahl was awarded a PhD in 1967[12] and a Doctor of Medicine qualification in 1970 from the Karolinska Institutet in Stockholm,[1]

Career

Following his PhD, Lindahl did postdoctoral research at Princeton University and Rockefeller University.[13] After moving to the United Kingdom he joined the Imperial Cancer Research Fund (now Cancer Research UK) as a researcher in 1981.[13]

Awards and honours

Lindahl won the Royal Medal for "making fundamental contributions to our understanding of DNA repair. His achievements stand out for their great originality, breadth and lasting influence."[14] He is a member of the Norwegian Academy of Science and Letters.[15] He was awarded the Royal Society's Royal Medal in 2007 and the Copley Medal in 2010. He was elected a founding Fellow of the Academy of Medical Sciences in 1998. His nomination for the Royal Society reads

“ Dr. Tomas Lindahl is noted for his contributions to the comprehension of DNA repair at the molecular level in bacterial and mammalian cells. He was the first to isolfiate a mammalian DNA ligase and to describe a totally unanticipated novel group of DNA glycosylases as mediators of DNA excision repair. He has also discovered a unique class of enzymes in mammalian cells, namely the methyltransferases, which mediate the adaptive response to alkylation of DNA and has shown that the expression of these enzymes is regulated by the ada gene. More recently he has elucidated the molecular defect in Blooms syndrome to be the lack of DNA ligase I. Apart from providing profound insights into the nature of the DNA repair process his very important contributions promise to facilitate the design of more selective chemotherapeutic drugs for the treatment of cancer. Lindahl has also made a number of significant contributions to understanding at the DNA level the mechanism of transformation of B-lymphocytes by the Epstein-Barr virus. The most notable of these was the first description of the occurrence in lymphoid cells of closed circular duplex viral DNA.[2] ”

References

  1. ↑ 1.0 1.1 LINDAHL, Tomas Robert. Who's Who 2014 (online Oxford University Press ed.). A & C Black, an imprint of Bloomsbury Publishing plc. (subscription required)
  2. ↑ 2.0 2.1 "Lindahl, Tomas Robert: EC/1988/20". London: The Royal Society. Archived from the original on 2014-11-21.
  3. ↑ Gerken, T.; Girard, C. A.; Tung, Y. -C. L.; Webby, C. J.; Saudek, V.; Hewitson, K. S.; Yeo, G. S. H.; McDonough, M. A.; Cunliffe, S.; McNeill, L. A.; Galvanovskis, J.; Rorsman, P.; Robins, P.; Prieur, X.; Coll, A. P.; Ma, M.; Jovanovic, Z.; Farooqi, I. S.; Sedgwick, B.; Barroso, I.; Lindahl, T.; Ponting, C. P.; Ashcroft, F. M.; O'Rahilly, S.; Schofield, C. J. (2007). "The Obesity-Associated FTO Gene Encodes a 2-Oxoglutarate-Dependent Nucleic Acid Demethylase". Science 318 (5855): 1469–1472. doi:10.1126/science.1151710. PMC 2668859. PMID 17991826.
  4. ↑ Tomas Lindahl's publications indexed by the Scopus bibliographic database, a service provided by Elsevier.
  5. ↑ Lindahl, T. (1993). "Instability and decay of the primary structure of DNA". Nature 362 (6422): 709–15. doi:10.1038/362709a0. PMID 8469282.
  6. ↑ Wood, R. D. (2001). "Human DNA Repair Genes". Science 291 (5507): 1284–9. doi:10.1126/science.1056154. PMID 11181991.
  7. ↑ Satoh, M. S.; Lindahl, T. (1992). "Role of poly(ADP-ribose) formation in DNA repair". Nature 356 (6367): 356. doi:10.1038/356356a0.
  8. ↑ Trewick, S. C.; Henshaw, T. F.; Hausinger, R. P.; Lindahl, T; Sedgwick, B (2002). "Oxidative demethylation by Escherichia coli AlkB directly reverts DNA base damage". Nature 419 (6903): 174–8. doi:10.1038/nature00908. PMID 12226667.
  9. ↑ Barnes, D. E.; Lindahl, T (2004). "Repair and genetic consequences of endogenous DNA base damage in mammalian cells". Annual Review of Genetics 38: 445–76. doi:10.1146/annurev.genet.38.072902.092448. PMID 15568983.
  10. ↑ Yang, Y. G.; Lindahl, T; Barnes, D. E. (2007). "Trex1 exonuclease degrades ssDNA to prevent chronic checkpoint activation and autoimmune disease". Cell 131 (5): 873–86. doi:10.1016/j.cell.2007.10.017. PMID 18045533.
  11. ↑ Crow, Y. J.; Hayward, B. E.; Parmar, R; Robins, P; Leitch, A; Ali, M; Black, D. N.; Van Bokhoven, H; Brunner, H. G.; Hamel, B. C.; Corry, P. C.; Cowan, F. M.; Frints, S. G.; Klepper, J; Livingston, J. H.; Lynch, S. A.; Massey, R. F.; Meritet, J. F.; Michaud, J. L.; Ponsot, G; Voit, T; Lebon, P; Bonthron, D. T.; Jackson, A. P.; Barnes, D. E.; Lindahl, T (2006). "Mutations in the gene encoding the 3'-5' DNA exonuclease TREX1 cause Aicardi-Goutières syndrome at the AGS1 locus". Nature Genetics 38 (8): 917–20. doi:10.1038/ng1845. PMID 16845398.
  12. ↑ Lindahl, Tomas (1967). On the structure and stability of nucleic acids in solution. Stockholm.
  13. ↑ 13.0 13.1 "Cancer Research UK Grants & Research - Tomas Lindahl". Retrieved 2008-11-10.
  14. ↑ "Royal recent winners". Retrieved 2008-11-10.
  15. ↑ "Gruppe 6: Cellebiologi og molekylærbiologi" (in Norwegian). Norwegian Academy of Science and Letters. Retrieved 7 October 2010.