Ervaringen van kankerpatienten met complementaire aanpak zijn te vinden onder ervaringsverhalen en er zijn op onze website ook een aantal video's van ervaringen van kankerpatienten met complementaire aanpak te zien. Aan te klikken via videoknop linksbovenaan op deze pagina. Of ga naar de website van het SNFK waar voorlichtingsfilmpjes zijn te zien over complementaire aanpak bij kanker.

 
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46. Medicijn voor suikerziekte zou ook remmend werken bij kankergroei, aldus onderzoekers in The Scientist. 

 

In The Scientist van vandaag d.d. 26 september 2003 wordt melding gemaakt van een onverwachte ontdekking dat bepaalde medicijnen voor suikerziekte - diabetici - ook remmend zouden werken op kankergroei. Ik moet eerlijk zeggen dat onderstaande artikel mijn wetenschappelijke petje te boven gaat dus ga ook maar niet proberen dit te vertalen, maar wellicht dat sommigen onder u wel precies hieruit af kunnen leiden wat nu precies het goede aan dit bericht is. Wat ik eruit begrijp is dat bepaalde eiwitten in bepaalde genen wel bij suikerziekte en kanker voorkomen maar niet bij gezonde mensen en/of dat die eiwitten wel of niet een rol spelen in het opruimen door het immuunsysteem van beschadigde cellen (kankercellen), maar verder durf ik dat niet uit te leggen. Als een arts of medisch deskundige dit wel kan voelen we ons aanbevolen voor zijn/haar uitleg. Dat het in The Scientist wordt gemeld geeft wel aan dat dit een belangrijke ontdekking kan zijn.

Bron: The Scientist

Diabetes and cancer: an unexpected link may also help in the treatment of some forms of cancer | By Andrea Rinaldi

An intriguing study in the September 24 Journal of Biology—published by BioMed Central, a sister company of The Scientist—suggests there could be a previously unrecognized anticancer benefit from treatment with some common antidiabetic drugs. Simon A. Hawley and colleagues at the University of Dundee show how the tumor suppressor protein kinase LKB1 is linked to AMP-activated protein kinase (AMPK), the target enzyme for several drugs commonly used to treat type 2 diabetes (Journal of Biology, 2:28, September 24, 2003). 

AMPK acts as a "metabolic master switch," reducing glucose levels and inhibiting biosynthetic pathways and cell proliferation. A lack of, or a mutation in, the LKB1 gene gives rise to Peutz-Jeghers syndrome, an autosomal dominant human disorder in which the risk of developing malignant tumors in some tissues is 15-fold higher than normal. Both the activation pattern of AMPK and the LKB1 substrate have been poorly understood, but recent observations suggest that the latter is associated with a group of accessory proteins known as STRADa/ß and MO25a/ß, which increase the kinase activity of LKB1.

Hawley et al. purified two forms of AMPK from rat liver and observed that both fractions contained LKB1, STRADa, and MO25a and that the AMPK activity could be immunoprecipitated using anti-LKB1 antibodies. Recombinant LKB1–STRADa/ß –MO25a/ß complexes fully activated AMPK in cell-free assays, providing further support for the idea that the link between AMPK and LKB1 has a functional background. In addition, the authors demonstrated that LKB1-mediated activation of AMPK also takes place in vivo in HEK-293T cells, but not in HeLa cells (which don't express LKB1 and therefore represents a natural knockout cell line). In HeLa cells, activation was achieved by stably expressing recombinant LKB1. This suggests that the tumor-suppressing properties of LKB1 may depend on its ability to activate AMPK.

"Our findings provide strong evidence that LKB1–STRAD–MO25 complexes represent the major upstream kinases acting on AMPK, although they do not rule out the possibility that the complex might contain additional components," conclude the authors.

Having established the LKB1–AMPK connection, Hawley et al. attempted to verify if antidiabetic drugs targeting AMPK by increasing its enzymatic activity could be affected by LKB1 in vivo. They observed that metformin—the most widely used diabetes drug in the world—could not activate AMPK in HeLa cells, presumably since they lack LKB1, and that expression of recombinant LKB1 restored the ability of HeLa cells to respond to the drug. The authors speculate that metformin, and possibly other diabetes drugs, may work by directly activating LKB1, which in turn activates AMPK, leading to glucose sequestration—with immediate benefits for those with diabetes—and to inhibition of cell growth and division, which ultimately prevent tumor development and proliferation.

Links for this article
S.A. Hawley et al., "Complexes between the LKBI tumor suppressor, STRADa/ß and MO25a/ß are upstream kinases in the AMP-activated protein kinase cascade," Journal of Biology, 2:28, September 24, 2003.
http://jbiol.com/content/2/4/28 

University of Dundee
http://www.dundee.ac.uk/ 

A. Hemminki, "The molecular basis and clinical aspects of Peutz-Jeghers syndrome," Cellular and Molecular Life Sciences, 55:735-750, May 1999.
[PubMed Abstract] 

J. Boudeau et al., "MO25a/ß interact with STRADa/ß enhancing their ability to bind, activate and localise LKB1 in the cytoplasm," European Molecular Biology Organization Journal, 22:5102-5114, October 1, 2003.
http://emboj.oupjournals.org/