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Caffeine As A Potential Treatment For Cancer

haidut

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Mar 18, 2013
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18,214
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USA / Europe
Ray has written many times about the anti-cancer properties of substances like caffeine and aspirin, but official research has been lagging behind in explaining how these substances work. A few months ago, I posted another study showing that adenosine antagonism reduces hypoxia in cancer cells and can be a viable treatment of cancer.
Caffeine as a potential cancer treatment

This study shows that another one of the primary mechanisms of caffeine - inhibiting phosphodiesterase 4 (PDE4) - is also highly therapeutic for lung cancer and there is close relationship between PDE4 and the overexpression of HIF in cancer cells that Ray has also written about. Btw, virtually all xanthines are PDE inhibitors and even though there are pharma drugs with similar effects, the advantage of xanthines like caffeine is that they are non-specific, so they act on the entire PDE and not just PDE4.

Scientists aim to starve lung tumours

"...New blood vessels form to ensure an adequate supply of nutrients to the growing tumour. The growing tissue is immediately penetrated by blood vessels. The growth of the blood vessels is regulated by the tumour cells using a complex signal cascade, which is triggered initially by a low oxygen content (hypoxia) in the tumour tissue. “This state, which is known as hypoxia prompts the activation of around 100 genes in the tumour cells,” explains Rajkumar Savai, research group leader at the Max Planck institute. “In addition to the growth of blood vessels, hypoxia also stimulates the proliferation of lung cancer cells.” Three molecules play a particularly important role in this process. The activation of the genes at the beginning of the cascade is triggered by the transcription factor HIF and a messenger molecule, cAMP, is involved again at the end of the cascade. The researchers examined the third molecule that acts as a link between these two molecules in detail. The molecule in question is a phosphodiesterase, PDE4. The scientists from Bad Nauheim and Giessen were able to demonstrate in their study that various sections of PDE4 have binding sites for HIF. The researchers then tested the influence of a PDE4 blockade on the cells from ten different cell lines, which are characteristic of around 80 percent of lung cancers, in the laboratory. The rate of cell division in the cells treated with a PDE4 inhibitor was significantly lower and the HIF level also declined as a result. The effect in the tumour bearing mice was particularly obvious. To observe this, the Max Planck researchers implanted a human tumour cell line under the skin of nude mice and treated the animals with the phosphodiesterase 4 inhibitor. Tumour growth in these animals declined by around 50 percent. “Our microscopic analysis revealed that the blood vessel growth in the tumours of the mice that had been treated with the inhibitor was significantly reduced. We also observed indicators of decelerated cell division in the tumour cells. Overall, the tumour growth was strongly curbed.”
 

High_Prob

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Joined
Mar 23, 2016
Messages
332
Ray has written many times about the anti-cancer properties of substances like caffeine and aspirin, but official research has been lagging behind in explaining how these substances work. A few months ago, I posted another study showing that adenosine antagonism reduces hypoxia in cancer cells and can be a viable treatment of cancer.
Caffeine as a potential cancer treatment

This study shows that another one of the primary mechanisms of caffeine - inhibiting phosphodiesterase 4 (PDE4) - is also highly therapeutic for lung cancer and there is close relationship between PDE4 and the overexpression of HIF in cancer cells that Ray has also written about. Btw, virtually all xanthines are PDE inhibitors and even though there are pharma drugs with similar effects, the advantage of xanthines like caffeine is that they are non-specific, so they act on the entire PDE and not just PDE4.

Scientists aim to starve lung tumours

"...New blood vessels form to ensure an adequate supply of nutrients to the growing tumour. The growing tissue is immediately penetrated by blood vessels. The growth of the blood vessels is regulated by the tumour cells using a complex signal cascade, which is triggered initially by a low oxygen content (hypoxia) in the tumour tissue. “This state, which is known as hypoxia prompts the activation of around 100 genes in the tumour cells,” explains Rajkumar Savai, research group leader at the Max Planck institute. “In addition to the growth of blood vessels, hypoxia also stimulates the proliferation of lung cancer cells.” Three molecules play a particularly important role in this process. The activation of the genes at the beginning of the cascade is triggered by the transcription factor HIF and a messenger molecule, cAMP, is involved again at the end of the cascade. The researchers examined the third molecule that acts as a link between these two molecules in detail. The molecule in question is a phosphodiesterase, PDE4. The scientists from Bad Nauheim and Giessen were able to demonstrate in their study that various sections of PDE4 have binding sites for HIF. The researchers then tested the influence of a PDE4 blockade on the cells from ten different cell lines, which are characteristic of around 80 percent of lung cancers, in the laboratory. The rate of cell division in the cells treated with a PDE4 inhibitor was significantly lower and the HIF level also declined as a result. The effect in the tumour bearing mice was particularly obvious. To observe this, the Max Planck researchers implanted a human tumour cell line under the skin of nude mice and treated the animals with the phosphodiesterase 4 inhibitor. Tumour growth in these animals declined by around 50 percent. “Our microscopic analysis revealed that the blood vessel growth in the tumours of the mice that had been treated with the inhibitor was significantly reduced. We also observed indicators of decelerated cell division in the tumour cells. Overall, the tumour growth was strongly curbed.”


As far as Xanthines acting on the entire PDE, what do you think about the suggestion that PDE5 may be implicated in the development of malignant melanoma? I recall you talking about this on an episode of Generative Energy, you weren't talking about PDE5 specifically but a drug that happens to have PDE5 inhibition as one of it's properties. I think your main point in the episode was about the drugs effect on NO (increasing). Hopefully caffeine doesn't even have a really strong effect on PDE5 and maybe the effect that it does have is balanced out by the other good effects that it has on NO inhibition...

http://jama.jamanetwork.com.proxy1.athensams.net/article.aspx?articleid=2338254
 
Last edited:

haidut

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Thread starter
Joined
Mar 18, 2013
Messages
18,214
Location
USA / Europe
As far as Xanthines acting on the entire PDE, what do you think about the suggestion that PDE5 may be implicated in the development of malignant melanoma? I recall you talking about this on an episode of Generative Energy, you weren't talking about PDE5 specifically but a drug that happens to have PDE5 inhibition as one of it's properties. I think your main point in the episode was about the drugs effect on NO (increasing). Hopefully caffeine doesn't even have a really strong effect on PDE5 and maybe the effect that it does have is balanced out by the other good effects that it has on NO inhibition...

http://jama.jamanetwork.com.proxy1.athensams.net/article.aspx?articleid=2338254

Caffeine is also an inhibitor of iNOS, so its net effects on NO are lowering it as opposed to increasing its effects like the PDE5-specific inhibitors. I think there are also studies showing Viagra directly stimulates iNOS, thus having even stronger pro-NO effect.
 
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