Antitumour Ether Lipids and Platelet-Activating Factor Analogues Have Different Cytotoxic Profiles and Calcium Mobilizing Effects — a Structure-Activity Study

  • M. Lohmeyer
  • P. Workman
Part of the Developments in Oncology book series (DION, volume 71)


We have examined the structure-activity relationships governing the cytotoxicity and calcium- mobilizing potentials of a number of synthetic antitumour ether lipids (AELs) and related natural ether lipid counterparts such as platelet-activating factor (PAF). We have found wide variation in the cytotoxic potency of AELs between different cell lines, with murine EMT6/VJ mammary tumour cells being markedly more resistant to lipid exposure than human HT29 colon carcinoma or HL 60 promyelocytic leukemia cells. In the human cell lines, AELs were far more cytotoxic than PAF, lyso-PAF or arachidonoyl- PAF. Hexadecylphosphocholine (HPC), proved intermediate in toxicity. In terms of calcium mobilization, AELs were weaker calcium agonists than PAF, lyso-PAF or HPC. The kinetics of AEL-induced elevations in intracellular calcium were similar to those for lyso-PAF and HPC, but different from responses obtained with the natural lipid mediator PAF.


HT29 Cell Calcium Mobilization Mammary Tumour Cell Ether Lipid Full Medium 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.



antitumour ether lipid


1-O-alkyl-2-0-acetyl-sn -glycero-3-phosphocholine;


1-O-alkyl-sn-glycero-3-phosphocholine (octadecyl and hexadecyl analogues of PAF and Iyso-PAF are identified by (C18) and (C16) suffixes, respectively)







SRI 62-834

[tetrahydro-2-(octadecyloxy) methylfuran-2-yl] methoxyl-phosphocholine






Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.


  1. 1.
    Berdel, W.E. Onkologie 13: 245–250, 1990.PubMedCrossRefGoogle Scholar
  2. 2.
    Vogler, W.R., Olson, A.C., Berdel, W.E., Okamoto, S., and Glasser, L. Prag. Clin. Biol. Res. 333:1–20, 1990.Google Scholar
  3. 3.
    Powis, G. Trends Pharmacol. sci. 12:188–194, 1991.PubMedCrossRefGoogle Scholar
  4. 4.
    Workman, P. Annals of Oncology 1:100–111, 1990.PubMedCrossRefGoogle Scholar
  5. 5.
    Daniel, L.W., Etkin, L.A., Morrison, B.T., Parker, J., Morris, N.S., Surles, J.R., and Piantadosi, C. Lipids 22:851–855, 1987.PubMedCrossRefGoogle Scholar
  6. 6.
    Houlihan, WJ., Lee, M.L., Munder, P.G., Nemecek, G.M., Handley, D.A., Winslow, C.M., Happy, J., and Jaeggi, C. Lipids 22:884–890, 1987.PubMedCrossRefGoogle Scholar
  7. 7.
    Seewald, M.J., Olsen, R.A., Sehgal, I., Melder, D.C., Modest, E.J., and Powis, G. Cancer Res. 50:4458–4463, 1990.PubMedGoogle Scholar
  8. 8.
    Coley, H.M., Twentyman, P.R., and Workman, P. Cancer Chemother. Pharmacol. 24:284–290, 1989.PubMedCrossRefGoogle Scholar
  9. 9.
    Lazenby, C.M., Thompson, M.G., and Hickman, J.A. Cancer Res., 50:4458–4463, 1990.Google Scholar

Copyright information

© Springer Science+Business Media New York 1993

Authors and Affiliations

  • M. Lohmeyer
    • 1
  • P. Workman
    • 1
  1. 1.MRC Clinical Oncology and Radiotherapeutics UnitCambridgeUK

Personalised recommendations