Conclusion
The specific antitumour effect of FSC involves DNA damage; apoptosis and oncogene alteration. Apparently p53 could induce apoptosis by at least two distinct pathways. Namely, opposite to wp53 mutant of p53 is a potent inducer of apoptosis. In considering drug therapy, the question as to whether a given apoptotic stimulus might trigger more than one apoptotic pathways is of great importance. Selective inhibition of growth and viability seems possible that FSC-iron could act through the mechanism of the cellular growth regulation that differ between normal and malignant cells. It is well know that malignant cells are less able to inactivate the oxygen radicals, because the activities of cellular antioxidants that protect normal cells against oxidative damage may be decreased in cancer cells. Thus FSC-iron (iron from Jectofer) might work through the toxicity of reactive oxygen species (ROS) or through perturbation of cellular iron metabolism. It could be important in strategy in the treatment of cancer and thus warrants continued investigation.
Keywords
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.
This is a preview of subscription content, log in via an institution.
Buying options
Tax calculation will be finalised at checkout
Purchases are for personal use only
Learn about institutional subscriptionsPreview
Unable to display preview. Download preview PDF.
References
Flajsig, I. and Poljak-Blazi, M., 1990, Influence of iron on proliferation and cell cycle kinetics on cultured malignant and non-malignant cells. Oncology47:443–446.
Herrmann, M., Lorenz, H.M., Voll, R., et al., 1994, Rapid and simple method for the isolation of apoptotic DNA fragments. Nuc. Acid Res.22:5506–5507.
Kranz, B.R., Thiel, E., and Thierfelder, S., 1989, Immunocytochemical identification of meningeal leukaemia and lymphoma: Polly-L-lysine-coated slides permit multimarker analysis even with minute cerebrospinal fluid cell specimens. Blood73:194–213.
Poljak-Blazi, M., Stancic-Rokotov, D., and Ferle-Vidovic, A., 1985, Inhibitory effect of iron on melanoma B16 growth. Period. Biol.87:17–21.
Poljak-Blazi, M., ••arkovic, N., and Schaur, R.J., 1998, Impaired proliferation and DNA synthesis of a human tumour cell line (HeLa) caused by a short treatment with FSC and the lipid peroxidation product 4-hydroxinonenal. Cancer Biother. Radioph.13:395–402.
Author information
Authors and Affiliations
Editor information
Editors and Affiliations
Rights and permissions
Copyright information
© 2002 Kluwer Academic Publishers
About this chapter
Cite this chapter
Poljak-Blazi, M., Kralj, M., Popovic-Hadzija, M. (2002). Oncogene Activation and Apoptosis as Possible Mechanism of Antitumour Effect of Ferric-Sorbitol-Citrate. In: Roussel, A.M., Anderson, R.A., Favier, A.E. (eds) Trace Elements in Man and Animals 10. Springer, New York, NY. https://doi.org/10.1007/0-306-47466-2_24
Download citation
DOI: https://doi.org/10.1007/0-306-47466-2_24
Published:
Publisher Name: Springer, New York, NY
Print ISBN: 978-0-306-46378-5
Online ISBN: 978-0-306-47466-8
eBook Packages: Springer Book Archive