Is there a role for carbohydrate restriction in the treatment and prevention of cancer?
http://www.ncbi.nlm....les/PMC3267662/
[Full Article]
LongeCityAdvocacy & Research for Unlimited Lifespans
Cancer Knowledge
Started by
davidd
, Nov 24 2008 04:47 PM
268 replies to this topic
#212
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Posted 22 February 2013 - 02:34 PM
Thank you. I was curious and did a bit of research I wish to log here. How many compounds scientists found promising on mice which then failed on humans trials, 9 out of 10, someone quotes below! Let's hope not for this new one!TIC10 induces apoptosis in cancer cells and stimulates immune response in neighbouring healthy cells.
http://www.nature.co...suicide-1.12385
Dual Inactivation of Akt and ERK by TIC10 Signals Foxo3a Nuclear Translocation, TRAIL Gene Induction, and Potent Antitumor Effects.
http://www.ncbi.nlm..../?term=23390247
Small-molecule drug drives cancer cells to suicide. Studies in mice show therapy is effective even in hard-to-treat brain tumours. The molecule, TIC10, activates the gene for a protein called TRAIL (tumour-necrosis-factor-related apoptosis-inducing ligand), which has long been a target for cancer researchers looking for drugs that would avoid the debilitating effects of conventional therapies.
http://www.nature.co...suicide-1.12385
TIC10 is a potent, stable, and orally active antitumor agent that crosses the blood-brain barrier and transcriptionally induces TRAIL and TRAIL-mediated cell death in a p53-independent manner.
http://repository.up...ons/AAI3542769/
Last year Dr Allen secured a $1.3m grant from Pennsylvania's department of health to begin clinical trials. These will be carried out in collaboration with Oncoceutics, a drug company. Nine out of ten promising molecules which work in mice fail in humans, so "Cure for cancer" headlines must wait.
http://www.economist...02/cancer-drugs
Oncoceutics Inc. announced the publication in the journal Science Translational Medicine of a report that the company’s ONC201 compound is a potent, orally active, and stable small molecule that demonstrates significant antitumor activity in a number of different types of human cancer through a novel mechanism.
http://oncoceutics.c...ional-medicine/
The TIC10 patent application
http://www.freepaten...20120276088.pdf
#213
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Posted 01 March 2013 - 11:13 AM
Scientists cure cancer with dichloroacetate, which is currently used to treat metabolic disorders.
"...Canadian scientists tested this dichloroacetate (DCA) on human’s cells; it killed lung, breast and brain cancer cells and left the healthy cells alone. It was tested on Rats inflicted with severe tumors; their cells shrank when they were fed with water supplemented with DCA. The drug is widely available and the technique is easy to use, why the major drug companies are not involved? Or the Media interested in this find?
In human bodies there is a natural cancer fighting human cell, the mitochondria, but they need to be triggered to be effective. Scientists used to think that these mitochondria cells were damaged and thus ineffective against cancer. So they used to focus on glycolysis, which is less effective in curing cancer and more wasteful. The drug manufacturers focused on this glycolysis method to fight cancer. This DCA on the other hand doesn’t rely on glycolysis instead on mitochondria; it triggers the mitochondria which in turn fights the cancer cells.
The side effect of this is it also reactivates a process called apoptosis. You see, mitochondria contain an all-too-important self-destruct button that can’t be pressed in cancer cells. Without it, tumors grow larger as cells refuse to be extinguished. Fully functioning mitochondria, thanks to DCA, can once again die..."
http://www.drzarkov.com/blog/?p=1789
"...Canadian scientists tested this dichloroacetate (DCA) on human’s cells; it killed lung, breast and brain cancer cells and left the healthy cells alone. It was tested on Rats inflicted with severe tumors; their cells shrank when they were fed with water supplemented with DCA. The drug is widely available and the technique is easy to use, why the major drug companies are not involved? Or the Media interested in this find?
In human bodies there is a natural cancer fighting human cell, the mitochondria, but they need to be triggered to be effective. Scientists used to think that these mitochondria cells were damaged and thus ineffective against cancer. So they used to focus on glycolysis, which is less effective in curing cancer and more wasteful. The drug manufacturers focused on this glycolysis method to fight cancer. This DCA on the other hand doesn’t rely on glycolysis instead on mitochondria; it triggers the mitochondria which in turn fights the cancer cells.
The side effect of this is it also reactivates a process called apoptosis. You see, mitochondria contain an all-too-important self-destruct button that can’t be pressed in cancer cells. Without it, tumors grow larger as cells refuse to be extinguished. Fully functioning mitochondria, thanks to DCA, can once again die..."
http://www.drzarkov.com/blog/?p=1789
#214
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Posted 13 March 2013 - 07:59 PM
http://www.vhio.net/news/75/
08/03/2013
VHIO scientists eradicate lung tumours in a pre-clinical mouse model
Previous studies had already shown that Myc was a key protein in tumour development and had established how to inhibit Myc through gene therapy
This protein is involved in the development of diverse tumours and so Myc-targeted therapy could make a positive contribution to the therapeutic options for different types of cancer
The study, led by the Vall d’Hebron Institute of Oncology (VHIO), has managed to eliminate mouse lung tumours by inhibiting Myc, a protein that plays a key role in the development of many different tumours. The results, published in the journal Genes & Development, confirm that repeated, long-term treatment does not cause side effects. Even more importantly, no resistance to treatment has been encountered, which is one of the biggest concerns with anticancer therapies. These results show that anticancer therapies based on Myc inhibition are a safe, effective therapeutic option in new drug development.
Myc is a protein that plays a big role in regulating gene transcription and it is involved in cell processes such as proliferation, differentiation and apoptosis (programmed cell death - an essential part of regenerating tissues and eliminating damaged cells). It acts as a regulator gene that controls the expression of some 15% of human genes. However, imbalances in this protein bring about uncontrolled cell growth which in turn can lead to the onset of cancer in different tissues. In fact, deregulated Myc is found in most tumours, including cervical, breast, colon, lung and stomach cancer.
From protein to therapy: a long haul
The work conducted by the Mouse Models of Cancer Therapy group at the VHIO, led by Dr Laura Soucek, shows that Myc can be controlled and inhibited through a mutant called Omomyc that hijacks Myc and prevents it from acting. “Even if we clearly identify a mechanism behind tumour development, it is still extremely complex to pinpoint how to intervene in cells' internal machinery or modify genetic processes,” explained Dr Soucek. “We have found a way to inhibit Myc through Omomyc,” she continued. “We induced Omomyc expression in mice through gene therapy and managed to activate and deactivate it by administering an antibiotic to the mice in their drinking water.”
In the study, multiple lung tumours were induced in the mouse (up to 200 tumours in each individual) and Myc inhibition episodes were achieved by activating Omomyc expression for 4-weeks, followed by 4-week rest periods. This therapy - known as metronomic therapy - was maintained for more than a year, regularly checking tumour progress in each mouse. All mice became tumour free after the first inhibition period, but 63% of cases then relapsed. After the second Myc inhibition period, only 11% of the initial tumours reappeared. According to Dr Soucek, “the most important finding was that there were no signs of resistance to treatment. This is one of the biggest disadvantages of many anticancer therapies: the disease develops resistance and can return even more aggressively.”
Finally, only two remaining tumours were found after more than one year of treatment among the mice that received eight inhibition and rest cycles. Dr Soucek found that Omomyc expression had been suppressed in these tumours, and this was the only adaptive mechanism that mice developed to treatment. “These results are hugely positive for us, because one year of life in a mouse is equivalent to almost 40 human years. The fact that the results are maintained over time, that there is no tumour relapse and no resistance, suggests that Myc-targeted therapy may offer an unprecedented way forward."
A study full of surprises
Previous studies conducted by Dr Soucek had already shown that Myc inhibition could halt tumour processes, making it an interesting therapeutic target for new drug development. However, in view of the protein's major role as a regulator gene, there was concern that long-term treatment could cause significant and uncontrollable side effects, such as epithelial tissue or bone marrow atrophy.
The potential for resistance was also questioned, since this occurs in many other similar treatments. The results of this latest study confirm that after multiple and periodic applications of Omomyc (the Myc inhibitor), tumours do not develop any resistance, side effects are mild and completely reversible, and almost all initial tumours are eradicated, even in advanced disease. “To make sure resistance was really non-existent, we applied the worst case scenario,” said Dr Soucek, “which was to assess the effect of Myc inhibition while suppressing p53 (a cell cycle regulator protein), because without p53, a tumour can accumulate a large number of mutations. If there were any chance of a mutation appearing and managing to resist Myc inhibition, this would have happened in the absence of p53. So we have now demonstrated that long-term Myc inhibition not only stops lung tumour growth indefinitely, but also progressively eradicates tumour growth, without side effects or resistance. These results confirm that Myc is a firm target for new cancer drugs,” she asserted.
These encouraging results provide sufficient scientific evidence to consider taking the next step: inhibiting Myc in patients. “Now our challenge for the future is to make Myc inhibition feasible from a pharmacological point of view, so that it can be administered, and done so safely. This will be the last step before designing clinical trials with Myc inhibitors,” explained Dr Soucek. “We're so excited about reaching this turning point and I am quite certain that it will change the course of cancer therapy, despite there being a long road ahead.”
08/03/2013
VHIO scientists eradicate lung tumours in a pre-clinical mouse model
Previous studies had already shown that Myc was a key protein in tumour development and had established how to inhibit Myc through gene therapy
This protein is involved in the development of diverse tumours and so Myc-targeted therapy could make a positive contribution to the therapeutic options for different types of cancer
The study, led by the Vall d’Hebron Institute of Oncology (VHIO), has managed to eliminate mouse lung tumours by inhibiting Myc, a protein that plays a key role in the development of many different tumours. The results, published in the journal Genes & Development, confirm that repeated, long-term treatment does not cause side effects. Even more importantly, no resistance to treatment has been encountered, which is one of the biggest concerns with anticancer therapies. These results show that anticancer therapies based on Myc inhibition are a safe, effective therapeutic option in new drug development.
Myc is a protein that plays a big role in regulating gene transcription and it is involved in cell processes such as proliferation, differentiation and apoptosis (programmed cell death - an essential part of regenerating tissues and eliminating damaged cells). It acts as a regulator gene that controls the expression of some 15% of human genes. However, imbalances in this protein bring about uncontrolled cell growth which in turn can lead to the onset of cancer in different tissues. In fact, deregulated Myc is found in most tumours, including cervical, breast, colon, lung and stomach cancer.
From protein to therapy: a long haul
The work conducted by the Mouse Models of Cancer Therapy group at the VHIO, led by Dr Laura Soucek, shows that Myc can be controlled and inhibited through a mutant called Omomyc that hijacks Myc and prevents it from acting. “Even if we clearly identify a mechanism behind tumour development, it is still extremely complex to pinpoint how to intervene in cells' internal machinery or modify genetic processes,” explained Dr Soucek. “We have found a way to inhibit Myc through Omomyc,” she continued. “We induced Omomyc expression in mice through gene therapy and managed to activate and deactivate it by administering an antibiotic to the mice in their drinking water.”
In the study, multiple lung tumours were induced in the mouse (up to 200 tumours in each individual) and Myc inhibition episodes were achieved by activating Omomyc expression for 4-weeks, followed by 4-week rest periods. This therapy - known as metronomic therapy - was maintained for more than a year, regularly checking tumour progress in each mouse. All mice became tumour free after the first inhibition period, but 63% of cases then relapsed. After the second Myc inhibition period, only 11% of the initial tumours reappeared. According to Dr Soucek, “the most important finding was that there were no signs of resistance to treatment. This is one of the biggest disadvantages of many anticancer therapies: the disease develops resistance and can return even more aggressively.”
Finally, only two remaining tumours were found after more than one year of treatment among the mice that received eight inhibition and rest cycles. Dr Soucek found that Omomyc expression had been suppressed in these tumours, and this was the only adaptive mechanism that mice developed to treatment. “These results are hugely positive for us, because one year of life in a mouse is equivalent to almost 40 human years. The fact that the results are maintained over time, that there is no tumour relapse and no resistance, suggests that Myc-targeted therapy may offer an unprecedented way forward."
A study full of surprises
Previous studies conducted by Dr Soucek had already shown that Myc inhibition could halt tumour processes, making it an interesting therapeutic target for new drug development. However, in view of the protein's major role as a regulator gene, there was concern that long-term treatment could cause significant and uncontrollable side effects, such as epithelial tissue or bone marrow atrophy.
The potential for resistance was also questioned, since this occurs in many other similar treatments. The results of this latest study confirm that after multiple and periodic applications of Omomyc (the Myc inhibitor), tumours do not develop any resistance, side effects are mild and completely reversible, and almost all initial tumours are eradicated, even in advanced disease. “To make sure resistance was really non-existent, we applied the worst case scenario,” said Dr Soucek, “which was to assess the effect of Myc inhibition while suppressing p53 (a cell cycle regulator protein), because without p53, a tumour can accumulate a large number of mutations. If there were any chance of a mutation appearing and managing to resist Myc inhibition, this would have happened in the absence of p53. So we have now demonstrated that long-term Myc inhibition not only stops lung tumour growth indefinitely, but also progressively eradicates tumour growth, without side effects or resistance. These results confirm that Myc is a firm target for new cancer drugs,” she asserted.
These encouraging results provide sufficient scientific evidence to consider taking the next step: inhibiting Myc in patients. “Now our challenge for the future is to make Myc inhibition feasible from a pharmacological point of view, so that it can be administered, and done so safely. This will be the last step before designing clinical trials with Myc inhibitors,” explained Dr Soucek. “We're so excited about reaching this turning point and I am quite certain that it will change the course of cancer therapy, despite there being a long road ahead.”
#216
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Posted 29 March 2013 - 10:22 AM
http://www.pnas.org/...nas;109/17/6662
The CD47-signal regulatory protein alpha (SIRPa) interaction is a therapeutic target for human solid tumors PNAS 2012 109 (17) 6662-6667; published ahead of print March 26, 2012, doi:10.1073/pnas.1121623109
Abstract
Full Text (HTML)
Full Text (PDF)
Figures Only
Supporting Information
OPEN ACCESS ARTICLE
Abstract 1 of 1Biological Sciences / Medical Sciences
The CD47-signal regulatory protein alpha (SIRPa) interaction is a therapeutic target for human solid tumors
CD47, a “don't eat me” signal for phagocytic cells, is expressed on the surface of all human solid tumor cells. Analysis of patient tumor and matched adjacent normal (nontumor) tissue revealed that CD47 is overexpressed on cancer cells. CD47 mRNA exp<b></b>ression levels correlated with a decreased probability of survival for multiple types of cancer. CD47 is a ligand for SIRPα, a protein expressed on macrophages and dendritic cells. In vitro, blockade of CD47 signaling using targeted monoclonal antibodies enabled macrophage phagocytosis of tumor cells that were otherwise protected. Administration of anti-CD47 antibodies inhibited tumor growth in orthotopic immunodeficient mouse xenotransplantation models established with patient tumor cells and increased the survival of the mice over time. Anti-CD47 antibody therapy initiated on larger tumors inhibited tumor growth and prevented or treated metastasis, but initiation of the therapy on smaller tumors was potentially curative. The safety and efficacy of targeting CD47 was further tested and validated in immune competent hosts using an orthotopic mouse breast cancer model. These results suggest all human solid tumor cells require CD47 exp<b></b>ression to suppress phagocytic innate immune surveillance and elimination. These data, taken together with similar findings with other human neoplasms, show that CD47 is a commonly expressed molecule on all cancers, its function to block phagocytosis is known, and blockade of its function leads to tumor cell phagocytosis and elimination. CD47 is therefore a validated target for cancer therapies.
Freely available online through the PNAS open access option.
---
This looks very effective, although healthy cells are also damaged in the treatment.
The CD47-signal regulatory protein alpha (SIRPa) interaction is a therapeutic target for human solid tumors PNAS 2012 109 (17) 6662-6667; published ahead of print March 26, 2012, doi:10.1073/pnas.1121623109
Abstract
Full Text (HTML)
Full Text (PDF)
Figures Only
Supporting Information
OPEN ACCESS ARTICLE
Abstract 1 of 1Biological Sciences / Medical Sciences
The CD47-signal regulatory protein alpha (SIRPa) interaction is a therapeutic target for human solid tumors
CD47, a “don't eat me” signal for phagocytic cells, is expressed on the surface of all human solid tumor cells. Analysis of patient tumor and matched adjacent normal (nontumor) tissue revealed that CD47 is overexpressed on cancer cells. CD47 mRNA exp<b></b>ression levels correlated with a decreased probability of survival for multiple types of cancer. CD47 is a ligand for SIRPα, a protein expressed on macrophages and dendritic cells. In vitro, blockade of CD47 signaling using targeted monoclonal antibodies enabled macrophage phagocytosis of tumor cells that were otherwise protected. Administration of anti-CD47 antibodies inhibited tumor growth in orthotopic immunodeficient mouse xenotransplantation models established with patient tumor cells and increased the survival of the mice over time. Anti-CD47 antibody therapy initiated on larger tumors inhibited tumor growth and prevented or treated metastasis, but initiation of the therapy on smaller tumors was potentially curative. The safety and efficacy of targeting CD47 was further tested and validated in immune competent hosts using an orthotopic mouse breast cancer model. These results suggest all human solid tumor cells require CD47 exp<b></b>ression to suppress phagocytic innate immune surveillance and elimination. These data, taken together with similar findings with other human neoplasms, show that CD47 is a commonly expressed molecule on all cancers, its function to block phagocytosis is known, and blockade of its function leads to tumor cell phagocytosis and elimination. CD47 is therefore a validated target for cancer therapies.
Freely available online through the PNAS open access option.
---
This looks very effective, although healthy cells are also damaged in the treatment.
Edited by MrHappy, 29 March 2013 - 10:25 AM.
#217
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Posted 29 March 2013 - 11:19 AM
http://www.pnas.org/gca?allch=citmgr&submit=Go&gca=pnas;109/17/6662
The CD47-signal regulatory protein alpha (SIRPa) interaction is a therapeutic target for human solid tumors PNAS 2012 109 (17) 6662-6667; published ahead of print March 26, 2012, doi:10.1073/pnas.1121623109
Abstract
Full Text (HTML)
Full Text (PDF)
Figures Only
Supporting Information
OPEN ACCESS ARTICLE
Abstract 1 of 1Biological Sciences / Medical Sciences
The CD47-signal regulatory protein alpha (SIRPa) interaction is a therapeutic target for human solid tumors
CD47, a “don't eat me” signal for phagocytic cells, is expressed on the surface of all human solid tumor cells. Analysis of patient tumor and matched adjacent normal (nontumor) tissue revealed that CD47 is overexpressed on cancer cells. CD47 mRNA exp<b></b>ression levels correlated with a decreased probability of survival for multiple types of cancer. CD47 is a ligand for SIRPα, a protein expressed on macrophages and dendritic cells. In vitro, blockade of CD47 signaling using targeted monoclonal antibodies enabled macrophage phagocytosis of tumor cells that were otherwise protected. Administration of anti-CD47 antibodies inhibited tumor growth in orthotopic immunodeficient mouse xenotransplantation models established with patient tumor cells and increased the survival of the mice over time. Anti-CD47 antibody therapy initiated on larger tumors inhibited tumor growth and prevented or treated metastasis, but initiation of the therapy on smaller tumors was potentially curative. The safety and efficacy of targeting CD47 was further tested and validated in immune competent hosts using an orthotopic mouse breast cancer model. These results suggest all human solid tumor cells require CD47 exp<b></b>ression to suppress phagocytic innate immune surveillance and elimination. These data, taken together with similar findings with other human neoplasms, show that CD47 is a commonly expressed molecule on all cancers, its function to block phagocytosis is known, and blockade of its function leads to tumor cell phagocytosis and elimination. CD47 is therefore a validated target for cancer therapies.
Freely available online through the PNAS open access option.
---
This looks very effective, although healthy cells are also damaged in the treatment.
Unfortunately it seems to be the trend.
At least we are moving in the right direction.
#220
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Posted 03 April 2013 - 09:39 AM
http://www.hngn.com/...cancer-mice.htm
A team of UC Davis scientists has found that a product resulting from a metabolized omega-3 fatty acid helps combat cancer by cutting off the supply of oxygen and nutrients that fuel tumor growth and spread of the disease.
The scientists report their discovery in the Proceedings of the National Academy of Sciences (PNAS). The groundbreaking study was a collaboration among multiple UC Davis laboratories and Harvard University.
The metabolite is epoxy docosapentaenoic acid (EDP), an endogenous compound produced by the human body from the omega-3 fatty acid named docosahexaenoic acid (DHA), which is found in fish oil and breast milk. In animal studies, the UC Davis scientists found that EDP inhibits angiogenesis, the formation of new blood vessels in the body.
<more>..
Actual article:
http://www.pnas.org/...ed-1f1b713a7b02
A team of UC Davis scientists has found that a product resulting from a metabolized omega-3 fatty acid helps combat cancer by cutting off the supply of oxygen and nutrients that fuel tumor growth and spread of the disease.
The scientists report their discovery in the Proceedings of the National Academy of Sciences (PNAS). The groundbreaking study was a collaboration among multiple UC Davis laboratories and Harvard University.
The metabolite is epoxy docosapentaenoic acid (EDP), an endogenous compound produced by the human body from the omega-3 fatty acid named docosahexaenoic acid (DHA), which is found in fish oil and breast milk. In animal studies, the UC Davis scientists found that EDP inhibits angiogenesis, the formation of new blood vessels in the body.
<more>..
Actual article:
http://www.pnas.org/...ed-1f1b713a7b02
#221
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Posted 04 April 2013 - 05:14 AM
http://www.hngn.com/...cancer-mice.htm
A team of UC Davis scientists has found that a product resulting from a metabolized omega-3 fatty acid helps combat cancer by cutting off the supply of oxygen and nutrients that fuel tumor growth and spread of the disease.
http://www.ucdmc.ucd...s/research/7671
#223
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Posted 26 May 2013 - 03:53 PM
Cancer cell enzymes shown to act as 'good cops'
"...Enzymes released by cancerous cells have a protective function and are not one of the "bad guys", say researchers from the University of East Anglia.
Their study found the MMP-8 enzyme sent a signal to the immune system to attack the tumour..."
http://www.bbc.co.uk...health-22645780
"...Enzymes released by cancerous cells have a protective function and are not one of the "bad guys", say researchers from the University of East Anglia.
Their study found the MMP-8 enzyme sent a signal to the immune system to attack the tumour..."
http://www.bbc.co.uk...health-22645780
#224
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Posted 14 June 2013 - 08:04 PM
Question, I apologize if it is answered someplace in the thread, there was alot to read.
Do Antioxidants work against the Natural Killer T cells?
I have read mixed things about it. My concern is that antioxidants are protecting the cancer cells. Forgive me I am new to all of this. Below Is out new regimen based on a new diagnosis.
8am - mini breakfast - warm - .6u Lantus
> Avemar 1/4tsp
> Ahcc ~ 150 mg
> Superfood Immunity 1/8 tsp
> Now Foods Sipalina 73 MG
> Tumeric 200mg
> Quercatin 200mg
> CoQ10 19.5 MG
> Coconut oil 1/16 tsp
>
>
> 10am - full breakfast - room temp
> Carnosine 131.5MG
> Resveratrol 199 MG
> Ester-c 53.5MG
> Benadyrl 3MG
> Tagamet 25MG
> Cell Advantage 1/2 CAP
> Bilberry 120MG
>
>
>
>
>
> 12 - 1/3 lunch - chilled
>
>
> 2pm - 1/3 lunch if needed
>
>
> 6pm - 1/3 lunch
> Ocuglo 1cap
> Milk thistle 83mg
> K9 Transfer Factor 1/4 tab
> Benadyrl 3MG
> Tagamet 25MG
>
>
> 8pm - mini dinner - .8u lantus
> Avemar 1/4tsp
> Ahcc ~ 150 mg
> K9 Immunity 1/2 cap
> Tumeric 200mg
> Quercatin 200mg
>
Thank you everyone for you feedback!!
Do Antioxidants work against the Natural Killer T cells?
I have read mixed things about it. My concern is that antioxidants are protecting the cancer cells. Forgive me I am new to all of this. Below Is out new regimen based on a new diagnosis.
8am - mini breakfast - warm - .6u Lantus
> Avemar 1/4tsp
> Ahcc ~ 150 mg
> Superfood Immunity 1/8 tsp
> Now Foods Sipalina 73 MG
> Tumeric 200mg
> Quercatin 200mg
> CoQ10 19.5 MG
> Coconut oil 1/16 tsp
>
>
> 10am - full breakfast - room temp
> Carnosine 131.5MG
> Resveratrol 199 MG
> Ester-c 53.5MG
> Benadyrl 3MG
> Tagamet 25MG
> Cell Advantage 1/2 CAP
> Bilberry 120MG
>
>
>
>
>
> 12 - 1/3 lunch - chilled
>
>
> 2pm - 1/3 lunch if needed
>
>
> 6pm - 1/3 lunch
> Ocuglo 1cap
> Milk thistle 83mg
> K9 Transfer Factor 1/4 tab
> Benadyrl 3MG
> Tagamet 25MG
>
>
> 8pm - mini dinner - .8u lantus
> Avemar 1/4tsp
> Ahcc ~ 150 mg
> K9 Immunity 1/2 cap
> Tumeric 200mg
> Quercatin 200mg
>
Thank you everyone for you feedback!!
#225
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Posted 01 July 2013 - 05:57 PM
Your regimen looks good. Continue with it.
It would be preferable to add in pterostilbene or replace resveratrol
with it, and replace turmeric with curcumin.
Resveratrol has an extremely short half-life of just 15 minutes,
a bioavailability of only 20 per cent, and penetrates the blood-brain
barrier poorly, in contrast to pterostilbene.
Moreover, resveratrol inhibits PPAR gamma, unlike pterostilbene
which activates it, which is what you want against cancer.
Vitamin C and its physiological role with respect to the components
of the immune system
" Vitamin C inhibits excessive activation of the immune system to prevent
tissue damage, but also supports antibacterial activity, stimulates NK cells .... "
http://www.ncbi.nlm....pubmed/23121060
Polyphenols inhibit indoleamine 3,5-dioxygenase-1 enzymatic activity --
a role of immunomodulation in chemoprevention.
" Metastasis is one of the cancer hallmarks described by Hanahan and Weinberg.
Emerging evidence shows that it requires interplays between cancer cells
and micro-environmental biofactors. Indoleamine 3,5-dioxygenase-1 (IDO-1)
produced by cancer, local lymph nodes, and satellite cells have been
demonstrated as one of the biofactors. "
" Aberrant IDO-1 activity has partially contributed to immunosuppressive
environment by repressing T lymphocyte and natural killer cell activities,
and activating regulatory T cells (Treg, CD4+CD25+). "
" These results suggest that attenuation of immune suppression via inhibition
of IDO-1 enzyme activity may be one of the important mechanisms of
polyphenols in chemoprevention or combinatorial cancer therapy. "
http://www.discovery...hemoprevention/
Resveratrol diminishes platelet aggregation and increases susceptibility
of K562 tumor cells to natural killer cells.
" At the same concentration, it increased the NKCs cytotoxic activity ....."
http://www.ncbi.nlm....pubmed/23617069
The antitumoral effect of the American mistletoe Phoradendron serotinum
(Raf.) M.C. Johnst. (Viscaceae) is associated with the release of immunity-
related cytokines.
In addition, PSE stimulated the proliferation of murine splenocytes and
induced the NK cell activity.
http://www.ncbi.nlm....pubmed/22732726
Phytic acid--anticancer nutriceutic
." Antioxidant properties, participation in signal transduction,
ability to enhance NK-cells ..... "
http://www.ncbi.nlm....pubmed/22993910
Morpho-functional reaction of spleen natural killer cells and macrophages to
melatonin administration to the animals kept on different illumination regimens
" It was shown that long-term administration of melatonin under conditions
of natural illumination had an immunosuppressive effect ..... "
" However, long-term hormone administration under conditions of
artificial darkening had an immunostimulatory effect as evidenced by
the increased inflow of immunocompetent cells into the spleen, "
http://www.ncbi.nlm....pubmed/22724333
In other words, take melatonin only at night.
Quercetin enhances susceptibility to NK cell-mediated lysis of tumor cells
through induction of NKG2D ligands and suppression of HSP70.
" It is known that treatments with heat shock, some anticancer drugs, and
ionizing radiation increase the expression of heat-shock proteins (HSPs)
and natural killer group 2D (NKG2D) ligands in tumor cells. The increased
HSPs may make the tumor cells resistant to apoptosis and reduction of
HSPs may make the tumor cells more susceptible to natural killer (NK)-cell
mediated lysis of tumor cells."
" ..... induced NKG2D ligands with the decrease of HSP70 protein by quercetin
may provide an attractive strategy to improve the effectiveness of NK cell-
based cancer immunotherapy. "
http://www.ncbi.nlm....pubmed/20386467
It would be preferable to add in pterostilbene or replace resveratrol
with it, and replace turmeric with curcumin.
Resveratrol has an extremely short half-life of just 15 minutes,
a bioavailability of only 20 per cent, and penetrates the blood-brain
barrier poorly, in contrast to pterostilbene.
Moreover, resveratrol inhibits PPAR gamma, unlike pterostilbene
which activates it, which is what you want against cancer.
Vitamin C and its physiological role with respect to the components
of the immune system
" Vitamin C inhibits excessive activation of the immune system to prevent
tissue damage, but also supports antibacterial activity, stimulates NK cells .... "
http://www.ncbi.nlm....pubmed/23121060
Polyphenols inhibit indoleamine 3,5-dioxygenase-1 enzymatic activity --
a role of immunomodulation in chemoprevention.
" Metastasis is one of the cancer hallmarks described by Hanahan and Weinberg.
Emerging evidence shows that it requires interplays between cancer cells
and micro-environmental biofactors. Indoleamine 3,5-dioxygenase-1 (IDO-1)
produced by cancer, local lymph nodes, and satellite cells have been
demonstrated as one of the biofactors. "
" Aberrant IDO-1 activity has partially contributed to immunosuppressive
environment by repressing T lymphocyte and natural killer cell activities,
and activating regulatory T cells (Treg, CD4+CD25+). "
" These results suggest that attenuation of immune suppression via inhibition
of IDO-1 enzyme activity may be one of the important mechanisms of
polyphenols in chemoprevention or combinatorial cancer therapy. "
http://www.discovery...hemoprevention/
Resveratrol diminishes platelet aggregation and increases susceptibility
of K562 tumor cells to natural killer cells.
" At the same concentration, it increased the NKCs cytotoxic activity ....."
http://www.ncbi.nlm....pubmed/23617069
The antitumoral effect of the American mistletoe Phoradendron serotinum
(Raf.) M.C. Johnst. (Viscaceae) is associated with the release of immunity-
related cytokines.
In addition, PSE stimulated the proliferation of murine splenocytes and
induced the NK cell activity.
http://www.ncbi.nlm....pubmed/22732726
Phytic acid--anticancer nutriceutic
." Antioxidant properties, participation in signal transduction,
ability to enhance NK-cells ..... "
http://www.ncbi.nlm....pubmed/22993910
Morpho-functional reaction of spleen natural killer cells and macrophages to
melatonin administration to the animals kept on different illumination regimens
" It was shown that long-term administration of melatonin under conditions
of natural illumination had an immunosuppressive effect ..... "
" However, long-term hormone administration under conditions of
artificial darkening had an immunostimulatory effect as evidenced by
the increased inflow of immunocompetent cells into the spleen, "
http://www.ncbi.nlm....pubmed/22724333
In other words, take melatonin only at night.
Quercetin enhances susceptibility to NK cell-mediated lysis of tumor cells
through induction of NKG2D ligands and suppression of HSP70.
" It is known that treatments with heat shock, some anticancer drugs, and
ionizing radiation increase the expression of heat-shock proteins (HSPs)
and natural killer group 2D (NKG2D) ligands in tumor cells. The increased
HSPs may make the tumor cells resistant to apoptosis and reduction of
HSPs may make the tumor cells more susceptible to natural killer (NK)-cell
mediated lysis of tumor cells."
" ..... induced NKG2D ligands with the decrease of HSP70 protein by quercetin
may provide an attractive strategy to improve the effectiveness of NK cell-
based cancer immunotherapy. "
http://www.ncbi.nlm....pubmed/20386467
Edited by tham, 01 July 2013 - 06:00 PM.
#227
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Posted 06 July 2013 - 06:44 PM
This research is in vitro on mouse cells, but increasing information with those already available in human in vivo, can not we improve supplementation?
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2650746/#!po=17.3077
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2957567/#!po=32.1429
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2650746/#!po=17.3077
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2957567/#!po=32.1429
#228
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Posted 08 July 2013 - 09:02 AM
Selenium Compounds Activate Early Barriers of Tumorigenesis
" ..... selenium induces an ATM-dependent senescence response via redox
regulation in non-cancerous but not in cancerous cells, suggesting a novel
mechanism of selenium in counteracting tumorigenesis. "
" The observation that selenium specifically induces senescence response
in non-cancerous cells suggests a cost-effective scenario by which
tumorigenesis can be stifled at the very beginning in individuals who
consume selenium with a cancer prevention perspective. "
http://www.ncbi.nlm....les/PMC2852943/
Selenium is a modulator of circadian clock that protects mice from
the toxicity of a chemotherapeutic drug via upregulation of the
core clock protein, BMAL1
http://www.impactjou...le&op=view[]=411&path[]=681
" ..... selenium induces an ATM-dependent senescence response via redox
regulation in non-cancerous but not in cancerous cells, suggesting a novel
mechanism of selenium in counteracting tumorigenesis. "
" The observation that selenium specifically induces senescence response
in non-cancerous cells suggests a cost-effective scenario by which
tumorigenesis can be stifled at the very beginning in individuals who
consume selenium with a cancer prevention perspective. "
http://www.ncbi.nlm....les/PMC2852943/
Selenium is a modulator of circadian clock that protects mice from
the toxicity of a chemotherapeutic drug via upregulation of the
core clock protein, BMAL1
http://www.impactjou...le&op=view[]=411&path[]=681
#229
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Posted 25 July 2013 - 07:15 PM
"Scientists develop ground-breaking new method of ‘starving’ cancer cell"
"...Chris Proud, Professor of Cellular Regulation in Biological Sciences at the University of Southampton says: “Cancer cells grow and divide much more rapidly than normal cells, meaning they have a much higher demand for and are often starved of, nutrients and oxygen. We have discovered that a cellular component, eEF2K, plays a critical role in allowing cancer cells to survive nutrient starvation, whilst normal, healthy cells do not usually require eEF2K in order to survive. Therefore, by blocking the function of eEF2K, we should be able to kill cancer cells, without harming normal, healthy cells in the process...”
http://www.southampt...ul/13_129.shtml
The paper is here:
http://www.sciencedi...092867413005321
"...Chris Proud, Professor of Cellular Regulation in Biological Sciences at the University of Southampton says: “Cancer cells grow and divide much more rapidly than normal cells, meaning they have a much higher demand for and are often starved of, nutrients and oxygen. We have discovered that a cellular component, eEF2K, plays a critical role in allowing cancer cells to survive nutrient starvation, whilst normal, healthy cells do not usually require eEF2K in order to survive. Therefore, by blocking the function of eEF2K, we should be able to kill cancer cells, without harming normal, healthy cells in the process...”
http://www.southampt...ul/13_129.shtml
The paper is here:
http://www.sciencedi...092867413005321
#230
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Posted 30 July 2013 - 02:05 PM
Pterostilbene simultaneously induces apoptosis, cell cycle arrest
and cyto-protective autophagy in breast cancer cells.
http://www.ncbi.nlm....les/PMC3276376/
Pterostilbene Exerts Antitumor Activity via the Notch1 Signaling
Pathway in Human Lung Adenocarcinoma Cells.
http://www.plosone.o...al.pone.0062652
#231
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Posted 30 July 2013 - 08:13 PM
The butterfly pea, Clitoria ternatea.
A favourite of the Kelantanese Malays of Malaysia as drinks and natural food coloring.
http://en.wikipedia....itoria_ternatea
http://www.the-herba...toria-ternatea/
IN VITRO CYTOTOXIC ACTIVITY OF CLITORIA TERNATEA
http://ijupls.com/up...10724120752.pdf
AN INVESTIGATION ON CYTOTOXIC AND ANTIOXIDANT PROPERTIES OF
CLITORIA TERNATEA L.
http://www.bioinfo.i...63_1_3_IJDD.pdf
Anticancer Activity of Clitoria ternatea Linn. Against Dalton’s Lymphoma.
http://www.ijppr.com...e4,Article8.pdf
Production of triterpenoid anti-cancer compound taraxerol in
Agrobacterium-transformed root cultures of butterfly pea (Clitoria ternatea L.).
http://www.ncbi.nlm....pubmed/22843061
Discovery and Characterization of Novel Cyclotides Originated from Chimeric Precursors
Consisting of Albumin-1 Chain a and Cyclotide Domains in the Fabaceae Family.
http://www.ncbi.nlm....les/PMC3129208/
A favourite of the Kelantanese Malays of Malaysia as drinks and natural food coloring.
http://en.wikipedia....itoria_ternatea
http://www.the-herba...toria-ternatea/
IN VITRO CYTOTOXIC ACTIVITY OF CLITORIA TERNATEA
http://ijupls.com/up...10724120752.pdf
AN INVESTIGATION ON CYTOTOXIC AND ANTIOXIDANT PROPERTIES OF
CLITORIA TERNATEA L.
http://www.bioinfo.i...63_1_3_IJDD.pdf
Anticancer Activity of Clitoria ternatea Linn. Against Dalton’s Lymphoma.
http://www.ijppr.com...e4,Article8.pdf
Production of triterpenoid anti-cancer compound taraxerol in
Agrobacterium-transformed root cultures of butterfly pea (Clitoria ternatea L.).
http://www.ncbi.nlm....pubmed/22843061
Discovery and Characterization of Novel Cyclotides Originated from Chimeric Precursors
Consisting of Albumin-1 Chain a and Cyclotide Domains in the Fabaceae Family.
http://www.ncbi.nlm....les/PMC3129208/
#232
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Posted 30 July 2013 - 11:41 PM
A Lowering of Breast and Ovarian Cancer Risk in Women with
a BRCA1 Mutation by Selenium Supplementation of Diet.
'' After two years of oral selenium administration the frequency of BRCA1-associated
tumours was two times lower in women who supplemented their diet with selenium,
as compared to women without supplementation. ''
http://www.ncbi.nlm....les/PMC3401925/
a BRCA1 Mutation by Selenium Supplementation of Diet.
'' After two years of oral selenium administration the frequency of BRCA1-associated
tumours was two times lower in women who supplemented their diet with selenium,
as compared to women without supplementation. ''
http://www.ncbi.nlm....les/PMC3401925/
#233
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Posted 31 July 2013 - 05:25 AM
A Lowering of Breast and Ovarian Cancer Risk in Women with
a BRCA1 Mutation by Selenium Supplementation of Diet.
'' After two years of oral selenium administration the frequency of BRCA1-associated
tumours was two times lower in women who supplemented their diet with selenium,
as compared to women without supplementation. ''
http://www.ncbi.nlm....les/PMC3401925/
Nitpicking a bit, how can the frequency be "two times lower"? It doesn't make sense to phrase it that way. Are they trying to say "half"?
Edited by joelcairo, 31 July 2013 - 05:27 AM.
#234
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Posted 31 July 2013 - 05:35 AM
I couldn't really figure out what the actual numbers were in the above study (from 2006), so I searched and found a 2009 followup by the same authors. At this point, for all the cancers studied, selenium increased the risk of cancer. However it appears the numbers are still not statistically significant, so make of it what you will.
Selenium and the risk of cancer in BRCA1 carriers
http://www.biomedcen...287-9-S2-A5.pdf
"Selenium supplementation was not associated with a reduction in the risk of primary breast cancer (hazard ratio 1.3; 95% CI: 0.7 to 2.5), of contralateral breast cancer (hazard ratio 1.5; 95% CI: 0.7 to 3.2), or of ovarian cancer (hazard ratio 1.3; 95% CI: 0.6 to 2.7)."
Selenium and the risk of cancer in BRCA1 carriers
http://www.biomedcen...287-9-S2-A5.pdf
"Selenium supplementation was not associated with a reduction in the risk of primary breast cancer (hazard ratio 1.3; 95% CI: 0.7 to 2.5), of contralateral breast cancer (hazard ratio 1.5; 95% CI: 0.7 to 3.2), or of ovarian cancer (hazard ratio 1.3; 95% CI: 0.6 to 2.7)."
Edited by joelcairo, 31 July 2013 - 05:38 AM.
#236
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Posted 20 August 2013 - 07:51 PM
Blocking Telomerase Kills Cancer Cells but Provokes Resistance, Progression.
http://www.mdanderso...rogression.html
Anti-telomerase therapy provokes ALT and mitochondrial adaptive mechanisms in cancer.
'' Cancer cells generally rely more on sugar processing to generate energy.
However, DePinho and colleagues note their genetic evidence suggests
that mitochondria play a role supporting cancer cells. ''
http://www.ncbi.nlm....les/PMC3286017/
http://www.mdanderso...rogression.html
Anti-telomerase therapy provokes ALT and mitochondrial adaptive mechanisms in cancer.
'' Cancer cells generally rely more on sugar processing to generate energy.
However, DePinho and colleagues note their genetic evidence suggests
that mitochondria play a role supporting cancer cells. ''
http://www.ncbi.nlm....les/PMC3286017/
#237
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Posted 07 November 2013 - 04:23 AM
http://www.freepaten...13/0288981.html
BACKGROUND
DNA damage can lead to unrepaired or misrepaired (mutagenic) lesions that can in turn promote aging phenotypes and age-related pathology, including cancer (Vijg, J. et al. Nature 454, 1065-1071 (2008)). The development of cancer from damaged cells in vivo is restricted by two potent tumor suppressive mechanisms: apoptosis (programmed cell death) and cellular senescence (permanent arrest of cell proliferation). Apoptosis produces cross-linked cell fragments, which are cleared from the organism by engulfing macrophages and other cells. Non-dividing senescent cells can also be cleared by immune cells, but this process is inefficient. Consequently, senescent cells can remain in tissues. They have been shown to accumulate with age, and at sites of age-related pathology. Further, senescent cells can acquire secondary mutations that allow them to re-enter a proliferative state. Benign senescent lesions thus retain the capacity to become malignant.
In addition to the cell-autonomous growth arrest, senescent cells also alter the tissue microenvironment and possibly the systemic milieu by secreting pro-inflammatory cytokines, growth factors and matrix degrading proteases, a phenotype termed the senescence-associated secretory phenotype (SASP) (Coppe, J. P. et al. PLoS. Biol. 6, 2853-2868 (2008)). The SASP can accelerate aging phenotypes and cancer progression in a paracrine fashion. Indeed, it was recently shown in a mouse model of progeria that the killing of senescent cells by a suicide gene driven by a senescence-sensitive promoter could reverse certain aging phenotypes in vivo (Baker, D. J. et al. Nature 479, 232-236, (2011)). Thus, removal of senescent cells and senescence-escaped cancer cells by forcing them to undergo apoptosis has tremendous therapeutic potential for treating age-related pathologies, including cancer.
The present invention relates to uses of agents that inhibit Jun kinases and/or FOXO4 in treating cancer and/or removing senescent cells.
All references cited herein, including patent applications and publications, are incorporated by reference in their entirety.
BACKGROUND
DNA damage can lead to unrepaired or misrepaired (mutagenic) lesions that can in turn promote aging phenotypes and age-related pathology, including cancer (Vijg, J. et al. Nature 454, 1065-1071 (2008)). The development of cancer from damaged cells in vivo is restricted by two potent tumor suppressive mechanisms: apoptosis (programmed cell death) and cellular senescence (permanent arrest of cell proliferation). Apoptosis produces cross-linked cell fragments, which are cleared from the organism by engulfing macrophages and other cells. Non-dividing senescent cells can also be cleared by immune cells, but this process is inefficient. Consequently, senescent cells can remain in tissues. They have been shown to accumulate with age, and at sites of age-related pathology. Further, senescent cells can acquire secondary mutations that allow them to re-enter a proliferative state. Benign senescent lesions thus retain the capacity to become malignant.
In addition to the cell-autonomous growth arrest, senescent cells also alter the tissue microenvironment and possibly the systemic milieu by secreting pro-inflammatory cytokines, growth factors and matrix degrading proteases, a phenotype termed the senescence-associated secretory phenotype (SASP) (Coppe, J. P. et al. PLoS. Biol. 6, 2853-2868 (2008)). The SASP can accelerate aging phenotypes and cancer progression in a paracrine fashion. Indeed, it was recently shown in a mouse model of progeria that the killing of senescent cells by a suicide gene driven by a senescence-sensitive promoter could reverse certain aging phenotypes in vivo (Baker, D. J. et al. Nature 479, 232-236, (2011)). Thus, removal of senescent cells and senescence-escaped cancer cells by forcing them to undergo apoptosis has tremendous therapeutic potential for treating age-related pathologies, including cancer.
The present invention relates to uses of agents that inhibit Jun kinases and/or FOXO4 in treating cancer and/or removing senescent cells.
All references cited herein, including patent applications and publications, are incorporated by reference in their entirety.
#238
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Posted 26 November 2013 - 11:38 AM
Dietary bioflavonoids induce cleavage in the MLL gene
and may contribute to infant leukemia.
'' ...... molecular evidence that bioflavonoids induce MLL breakage and
strongly supports the conclusion of Ross et al. that dietary bioflavonoids
could be a causative agent for infant and possibly childhood leukemia.
In a preliminary epidemiological study, it was demonstrated that maternal
consumption of topo II inhibitor-containing foods including bioflavonoids
led to an approximately 10-fold higher risk of infant AML.
Based on data from 1971-1980, the incidence of infant ALL and AML for
several Asian cities, for example, Hong Kong, Osaka, Miyagi, and Kanagawa,
was almost 2-fold higher than in Western countries, where the incidence from
1973-1992 was 37 cases per million per year (United States).
'' This difference in incidence may be because of the high food intake of
bioflavonoids in most Asian countries; for example, the Japanese
consumption of isoflavonoids in the form of soybeans and soybean products
is 1.5-4.1 (genistein) and 6.3-8.3 (genistin) mg per person per day.
For example, 1.5 μM genistein was detected in human blood plasma after the
consumption of 20 g of roasted soybeans. High bioflavonoid concentrations,
which persisted for 2-4 days, were also detected in human milk after
soy consumption.
Using primary and BV173 cells, we detected MLL cleavage with low
concentration levels of 10 μM quercetin or 10 μM fisetin, which were similar
to that with 10 μM VP16 (Fig. 3b). Human plasma levels >1.0 μM of quercetin
alone were detected after a quercetin-free diet followed by a single meal,
corresponding to 200 mg of quercetin. Moreover, the half-life of quercetin
was 25 h, implying that repeated dietary intake of quercetin would lead to
much higher blood concentrations, similar to those used in this study. ''
'' The quercetin concentration in the serum of these patients reached 200-400
μM after administration, which is more than 10-fold higher than the level we
used for the topo II inhibition studies in vivo and therefore could lead to MLL
breakage resulting in therapy-related leukemia. ''
'' In conclusion, although bioflavonoids may be beneficial in certain
circumstances, our studies suggest that high dietary intake of bioflavonoids
could cause DNA breaks in MLL and possibly in other partner genes by
inhibiting topo II. This event could result in chromosome translocations
leading to leukemia in adults, children, and particularly infants,
analogous to t-AML and t-ALL after cancer chemotherapy. ''
http://www.pnas.org/.../97/9/4790.full
and may contribute to infant leukemia.
'' ...... molecular evidence that bioflavonoids induce MLL breakage and
strongly supports the conclusion of Ross et al. that dietary bioflavonoids
could be a causative agent for infant and possibly childhood leukemia.
In a preliminary epidemiological study, it was demonstrated that maternal
consumption of topo II inhibitor-containing foods including bioflavonoids
led to an approximately 10-fold higher risk of infant AML.
Based on data from 1971-1980, the incidence of infant ALL and AML for
several Asian cities, for example, Hong Kong, Osaka, Miyagi, and Kanagawa,
was almost 2-fold higher than in Western countries, where the incidence from
1973-1992 was 37 cases per million per year (United States).
'' This difference in incidence may be because of the high food intake of
bioflavonoids in most Asian countries; for example, the Japanese
consumption of isoflavonoids in the form of soybeans and soybean products
is 1.5-4.1 (genistein) and 6.3-8.3 (genistin) mg per person per day.
For example, 1.5 μM genistein was detected in human blood plasma after the
consumption of 20 g of roasted soybeans. High bioflavonoid concentrations,
which persisted for 2-4 days, were also detected in human milk after
soy consumption.
Using primary and BV173 cells, we detected MLL cleavage with low
concentration levels of 10 μM quercetin or 10 μM fisetin, which were similar
to that with 10 μM VP16 (Fig. 3b). Human plasma levels >1.0 μM of quercetin
alone were detected after a quercetin-free diet followed by a single meal,
corresponding to 200 mg of quercetin. Moreover, the half-life of quercetin
was 25 h, implying that repeated dietary intake of quercetin would lead to
much higher blood concentrations, similar to those used in this study. ''
'' The quercetin concentration in the serum of these patients reached 200-400
μM after administration, which is more than 10-fold higher than the level we
used for the topo II inhibition studies in vivo and therefore could lead to MLL
breakage resulting in therapy-related leukemia. ''
'' In conclusion, although bioflavonoids may be beneficial in certain
circumstances, our studies suggest that high dietary intake of bioflavonoids
could cause DNA breaks in MLL and possibly in other partner genes by
inhibiting topo II. This event could result in chromosome translocations
leading to leukemia in adults, children, and particularly infants,
analogous to t-AML and t-ALL after cancer chemotherapy. ''
http://www.pnas.org/.../97/9/4790.full
Edited by tham, 26 November 2013 - 12:07 PM.
#239
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Posted 27 November 2013 - 12:07 AM
It's not hard to believe that supplementing with high levels of flavonoids would be a bad idea for pregnant women. Anticancer agents such as soy isoflavones and quercetin often target the exact same mechanisms that embryos rely on to grow.
#240
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Posted 01 December 2013 - 01:20 PM
Sea cucumbers are cancer fighters.
In Vitro Antioxidant and Antiproliferative Activities of Three Malaysian
Sea Cucumber Species.
https://www.academia...ucumber_Species
Antioxidant and cytotoxic properties of two sea cucumbers,
Holothuria edulis lesson and Stichopus horrens Selenka
Stichopus horrens is the common sea cucumber species used in the
local Malaysian supplements, wound healing extracts and cosmetic products.
'' ...... the organic extract of S. horrens exhibited the highest cytotoxic effects
against A549 and TE1 cancer cells giving IC50 at 15.5 and 4.0 μg/ml, respectively.
http://www.ncbi.nlm....ubmed/23567827/
http://www.researchg...cc2fb0d9f6f.pdf
Structure elucidation, protein profile and the antitumor effect of the
biological active substance extracted from sea cucumber Holothuria polii.
http://www.ncbi.nlm....ubmed/23188650/
In Vitro Antioxidant and Antiproliferative Activities of Three Malaysian
Sea Cucumber Species.
https://www.academia...ucumber_Species
Antioxidant and cytotoxic properties of two sea cucumbers,
Holothuria edulis lesson and Stichopus horrens Selenka
Stichopus horrens is the common sea cucumber species used in the
local Malaysian supplements, wound healing extracts and cosmetic products.
'' ...... the organic extract of S. horrens exhibited the highest cytotoxic effects
against A549 and TE1 cancer cells giving IC50 at 15.5 and 4.0 μg/ml, respectively.
http://www.ncbi.nlm....ubmed/23567827/
http://www.researchg...cc2fb0d9f6f.pdf
Structure elucidation, protein profile and the antitumor effect of the
biological active substance extracted from sea cucumber Holothuria polii.
http://www.ncbi.nlm....ubmed/23188650/
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