HonCode

Go Back   HER2 Support Group Forums > Articles of Interest
Register Gallery FAQ Members List Calendar Search Today's Posts Mark Forums Read

Reply
 
Thread Tools Display Modes
Old 10-08-2008, 03:40 PM   #1
Rich66
Senior Member
 
Rich66's Avatar
 
Join Date: Feb 2008
Location: South East Wisconsin
Posts: 3,431
Ip6

(reverts cancer cells to normal, Telomerase, angiogenesis, inflammation, PI3k-Akt, EGFR, IGF-1R, cyclin D1, VEGF, Hif-1alpha, anti-proliferation, p53, caspase, w/Doxo,W/TAM, w/resveratrol, w/Irinotecan, immune enhancing, dietary sources, supplements better w/o food, reduces chemo side fx, w/Pac, w/green tea)


IP6+Inositol from Cell Forte

Other sources

MD Anderson link:


IP-6

Background and Health Claims
IP-6, also known as inositol hexophosphate or phytic acid, is a sugar molecule with six phosphate groups attached. Naturally present in whole grains and high fiber foods, IP-6 recently has gained popularity as a cancer fighter. Experts feel that it also may play a role in the prevention and treatment of heart disease, kidney stones and liver disease.

At this time, the exact mechanism through which IP-6 works is not known. It may decrease the proliferation of cancer cells, act as an antioxidant, enhance the immune system by boosting the activity of natural killer cells (which destroy abnormal cells), or influence cells’ ability to dedicate themselves to a particular function.
Much of the scientific research completed with IP-6 has been done by Abulkalam Shamsuddin, a scientist at the University of Maryland School of Medicine. Several of Dr. Shamsuddin’s animal and human cancer cell line studies have shown promising results with colon, prostate, liver and breast cancer. Epidemiological studies show that people who eat lots of foods that contain IP-6 have lower incidences of cancer of the breast, colon and prostate. Foods that are significant sources of IP-6 include soybeans, rice, sesame, beans, legumes, corn and cereals.
Precautions
I
P-6 reduces platelet activity; therefore, people with low blood cell counts, or who are taking aspirin or other blood thinning medications, may want to avoid using IP-6. Because of its antioxidant properties, IP-6 may not be appropriate for patients receiving radiation or chemotherapy. Supplemental forms of IP-6 may also bind with calcium, magnesium, copper, iron and zinc and should therefore not be taken with food.

Dose
Although Dr. Shamsuddin indicates that further research must be completed before making more specific dosage recommendations, he gives the following guidelines: 1-2 g of IP-6 daily for cancer prevention, 4 g daily for people with an increased cancer risk, and up to 8 g daily for those with cancer. Patients who are considering an IP-6 supplement should consult with their physician or dietician.

Obtaining IP-6 from natural food sources is likely very safe. The following table shows the amount of IP-6 in various foods.
Food
Serving Size
Amount of IP-6
Beans½ cup250 mg
Brown rice½ cup uncooked220 mg
Cornbread3 ½ ounces130 mg
Sesame seeds¾ cup530 mg
Wheat bran1 ¾ cups460 mg
Corn, whole kernel ½ cup650 mg






IP6 Shines Brightly as an Alternative Cancer Treatment and Preventive
Originally published October 29 2008

http://www.naturalnews.com/z024635.html


by Barbara L. Minton (see all articles by this author)


(NaturalNews) The anticancer effects of IP6 are turning out to be nothing short of astounding. Research is showing that besides reducing cell proliferation and increasing the differentiation of malignant cells, IP6 can often restore cancerous cells to normality.

What is IP6?

IP6, also known as inositol hexophosphate or phytic acid, is a sugar molecule with six phosphate groups attached. It is composed of inositol (one of the B vitamins) bound with six molecules of phosphorous. IP6 was first identified in 1855, but has only recently been researched as a preventative and cure for cancer as well as heart and liver diseases, kidney stones, Parkinson's disease, and more. It is also a powerful antioxidant, immune system enhancer, and booster of natural killer cells. Foods that are significant sources of IP6 include dried beans, whole grains, nuts, seeds, rice, wheat germ, corn and sesame.

Dr. Abulkalam Shamsuddin, a scientist at the University of Maryland School of medicine has been the pioneer researcher of IP6, beginning his work on the compound in the late 1980's. He discovered the ability of IP6 to control the rate of abnormal cell division even when administered long after cancer was induced. He then proved that IP6 normalized the sugar production of cancerous cells, thereby altering the gene expression toward a more healthful state. This proven ability to change cancer cell physiology had major implications, since cancer cells that are well behaved have far less negative impact on health.

Although IP6 has been proven to boost Natural Killer (NK) cell activity, for Shamsuddin the value of IP6 lies not in its ability to augment the immune system, but rather its ability to directly affect the physiology of cancerous cells. Whereas most cancer research has focused on killing or destroying cancer cells, Shamsuddin's research focused on taming or controlling the condition to the point where normality could be restored.

How IP6 works to Protect Against Cancer

Here are several ways IP6 is known to prevent and fight against cancer. IP6 is a very common intracellular messenger, meaning that it controls and influences many cellular activities:

Normalizes the Rate of Cell Growth � Cancer cells lose their control mechanisms and typically divide too rapidly, resulting in great numbers of cells that have a devastating impact on health. IP6 slows or normalizes the rate at which cancer cells divide. It reestablishes control in cells that by definition have lost their control mechanisms due to gene mutation. (does this mean reducing chemo effectiveness since most chemos destroy fast growing cells? Rich66)

Helps to normalize cell physiology � How a cancer cell expresses itself largely determines how threatening it is. Experiments have shown that IP6 normalizes several aspects of cell physiology in spite of the fact that these cells have altered DNA. In many instances, DNA repair is achieved.

Enhances NK cells � NK cells are white blood cells that help to protect against virally infected or cancerous cells. Researchers believe that the higher the NK activity, the lower the incidence of some cancers. The healthy human produces 500 to 1000 cancer cells daily. NK cells and programmed cell death (apoptosis) result in the vast majority of these cells being destroyed and removed. During time of stress, NK activity is compromised, and this is why there is a link between stress levels and cancer. IP6 is able to increase NK cells during these periods. Although many supplements claim to increase NK activity, for IP6 these claims have been documented and proven.

Increases tumor suppressor P53 gene activity - DNA contains tumor suppressor genes that inhibit pathways or processes that allow cells to become cancerous. The p53 gene acts as a control to preventing genetically damaged or cancerous cells from growing and propagating. If the p53 gene becomes damaged or compromised, cancers can establish themselves more readily. IP6 has been shown to greatly increase the amount of p53 gene activity, up to 17 times. When augmented by IP6, "standard of care" treatments become more effective due to this increase in p53 gene activity.

Inhibits inflammation � The level of systemic inflammation is an important indicator in determining cancer survival prognosis. Inflammation results in the release of cytokines, chemical messengers that trigger reactions that enable normal cells to grow and repair themselves. Cytokines can also cause cancer cells to grow. IP6 has been shown to significantly inhibit inflammation.

Exhibits potent antioxidant activity � Antioxidants are known to protect against various disease states and aging in general. Oxidative damage to DNA leaves cells susceptible to mutation that can result in cancerous cells being produced. IP6 has been shown to be a significantly more potent antioxidant than green tea.

Enhances apoptosis (programmed cell death) � Programmed cell death is orderly and results in the removal of individual cells without affecting the surrounding cells. It is a normal part of growth and the maintenance of healthy tissues. It removes unwanted cells so that inflammation or immunological reactions do not result. Cancerous cells are resistive to normal cell apoptosis. This is one mechanism of tumor formation. IP6 has been shown to enhance the natural apoptosis of cancer cells.

Affects angiogenesis � Angiogenesis is the process by which tumors set up their own blood supply, assuring the nutrients necessary to fuel their growth. Once this blood supply is set up, tumor growth spirals as more growth leads to more establishment of blood supply. IP6 inhibits this process, resulting in the starvation of cancer cells.

Inhibits metastasis � IP6 inhibits the adhesion of cancer cells to the extra-cellular matrix proteins, thereby leading to an inhibition of cell migration and invasion. Limiting adhesion is very important after surgeries and biopsies, as these procedures can cause cancer cells to become dislodged. One reason that so many breast cancer patients are found to have lymph nodes containing cancer cells is that mammography can dislodge cancer cells which then migrate to the lymph nodes.

Pharmaceutical research is geared to the development of drugs to treat cancer utilizing these mechanisms. Many of the substances being developed and tested are newly created molecules, having never before appeared in nature. As a result, severe side effects are common place. IP6 already exists in human cells and is easily recognized by the body, so side effects, if any, are rare.

Recent research findings document these mechanisms

The frequency and depth of research into IP6 is expanding at a rapid rate. Here are some of the most recent findings.

The Journal of Clinical Cancer Research, reports a study evaluation the in vivo cancer preventative efficacy of IP6 against prostate tumor growth and progression. Prostate cancer was induced in male mice that were then given either water containing IP6 or plain water. IP6 inhibited prostate cancer progression at the neoplasia state and strongly reduced the incidence of adenocarginoma. The incidence of well-differentiated and poorly differentiated adenocarcinomas in the IP6-fed group were reduced by 44% and 62% respectively. Analysis of the prostate tissue showed a 3.5-fold increase in apoptotic cells. The researchers concluded that these findings are highly significant in establishing for the first time that oral IP6, without toxicity, suppresses prostate tumor growth and progression at the neoplastic state, the state of abnormal or uncontrolled growth.

A study conducted in China and reported in Wei Sheng Yan Jiu explored the effect and mechanism of IP6 on cell proliferation in human gastric carcinoma. They found that IP6 inhibited malignant cell growth in a dose and time dependent manner. The proliferation of gastric carcinoma cells inhibited by IP6 was associated with apoptosis through altered gene expression.

The Brazilian journal, Acta Cirurgica Brasilerira reported a study to determine the modulation effect of IP6 in the biological immunohistochemistry expression of cellular signaling marker apoptosis in a model of induced colon cancer. They found that IP6 was effective in promoting modulation of biological markers in colon cancer.

Another study reported in Acta Cirurgica Brasilerira analyzed of the influence of IP6 on the transcription of genes coding for tumor necrosis factor-alpha and its receptors in a human colon cancer cell line. The results showed that IP6 modulated the expression of the listed genes at transcription level in a dose and time dependent manner.

The journal Neurochemistry Research reported a study of the impact of IP6 as a therapeutic agent on glioblastoma, the deadliest brain tumor in humans and the one currently being battled by Senator Kennedy. Researchers found that the viability of glioblastoma cells decreased following treatment with increasing doses of IP6. The treated cells showed morphological and biochemical features of apoptosis.

Laryngoscope reports a study that found IP6 effective at promoting nuclear factor-kappa B, an early response gene that is associated with head and neck squamous cell cancer. This increased gene expression resulted in reduced cell proliferation and increased cell death.

IP6 is more than a cancer treatment

In addition to the anti-cancer benefits of IP6, ongoing research is revealing its promise as a treatment for diabetes, depression, osteoporosis, heart disease, and kidney stones.

A very recent study reported in the Journal of Toxicology considered the effect of IP6 on Parkinson's Disease. Disrupted iron metabolism and excess iron accumulation has been reported in the brains of Parkinson's patients. Because excessive iron can induce oxidative stress and result in neuronal degradation in Parkinson patients, researchers sought to determine the protective effect of IP6, a natural chelator of iron. They found a 45% reduction in DNA fragmentation with the use of IP6, and protection in the differentiated cells. They concluded that IP6 offered a significant neuro-protective effect.

Supplementing with IP6

IP6 has been shown to be quite safe to use. It is naturally present in mammalian cells, and it is obtainable from food. However, in food, IP6 is bound to protein. Before it can be absorbed it must be freed from this protein. An enzyme called phytase that is present in both food and the intestinal tract performs this function. The problem is that the power of the phytase enzyme is damaging to the IP6 and renders much of it inactive and therefore less effective. Pure IP6 from a supplement is not protein-bound and is easily absorbed in tact, and able to provide its complete medicinal properties. Research has shown that when fiber from All Bran was added to the diet of rats with mammary cancer it was much less effective than the equivalent amount of IP6 added to their drinking water.

Many holistic healers and naturopaths recommend IP6 as both a preventative and treatment for cancer. It is becoming standard alternative treatment to recommend it for anyone with a high risk of cancer or who has had cancer and is looking to prevent a recurrence. Some traditional physicians are also becoming aware of the potential of this compound and although they are loath to abandon their traditional treatments, they are adding IP6 to their protocols.

IP6 is available in capsules or powered form. The capsules provide what is considered to be a maintenance or preventive dose of 2 capsules twice a day. The powered form allows for easy dosing at the therapeutic level which is one scoop mixed with water twice a day. IP6 should be taken on an empty stomach. IP6+Inositol from Cell Forte is the most economical and readily available brand. It is sold online at Vitacost.

Sources:

"Complementary Therapies", University of Texas MD Anderson Cancer Center.

Dr. Kim Vanderlinden, Dr. Ivana Vucenik, Too Good to be True?




Breast Cancer Res Treat. 2003 Jun;79(3):301-12.
Inositol hexaphosphate (IP6) enhances the anti-proliferative effects of adriamycin and tamoxifen in breast cancer.

Tantivejkul K, Vucenik I, Eiseman J, Shamsuddin AM.
Department of Pathology, University of Maryland School of Medicine, Baltimore, MD 21201, USA.
The current treatment of breast carcinomas recognizes the importance of combination therapy in order to increase efficacy and decrease side effects of conventional chemotherapy. Inositol hexaphosphate (IP6), a naturally occurring polyphosphorylated carbohydrate, has shown a significant anti-cancer effect in various in vivo and in vitro models, including breast cancer. In this study, we investigated the in vitro growth inhibitory activity of IP6 in combination with adriamycin or tamoxifen, against three human breast cancer cell lines: estrogen receptor (ER) alpha-positive MCF-7, ER alpha-negative MDA-MB 231 and adriamycin-resistant MCF-7 (MCF-7/Adr) using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. Much lower concentrations of IP6 were required after 96 h of treatment to inhibit the growth of MCF-7/Adr cells than MCF-7 cells; the IC50 for MCF-7/Adr cells was 1.26 mM compared to 4.18 mM for MCF-7 cells. The ER-negative MDA-MB 231 cells were also highly sensitive to IP6 with IC50 being 1.32 mM. To determine the effects of IP6 in combination with either adriamycin or tamoxifen, the median effect principle and Webb's fraction method were used to determine the combination index (CI) and the statistical differences. Growth suppression was markedly increased when IP6 was administered prior to the addition of adriamycin, especially against MCF-7 cells (CI = 0.175 and p < 0.0001). Synergism was also observed when IP6 was administered after tamoxifen in all three cell lines studied (CI = 0.343, 0.701 and 0.819; p < 0.0001, p = 0.0003 and 0.0241 for MCF-7/Adr, MCF-7 and MDA-MB 231, respectively). The growth of primary culture of breast cancer cells from patients was inhibited by IP6 with LC50 values ranging from 0.91 to 5.75 mM (n = 10). Our data not only confirm that IP6 alone inhibits the growth of breast cancer cells; but it also acts synergistically with adriamycin or tamoxifen, being particularly effective against ER alpha-negative cells and adriamycin-resistant cell lines.

PMID: 12846414 [PubMed - indexed for MEDLINE]





J Surg Res. 2005 Jun 15;126(2):199-203. Links
Inositol hexaphosphate (IP6): a novel treatment for pancreatic cancer.

Somasundar P, Riggs DR, Jackson BJ, Cunningham C, Vona-Davis L, McFadden DW.
Louis A. Johnson VA Medical Center, Clarksburg, West Virginia; Department of Surgery, West Virginia University, Morgantown, West Virginia, USA.
BACKGROUND: Inositol hexaphosphate (IP6) is a naturally occurring polyphosphorylated carbohydrate found in food sources high in fiber content. IP6 has been reported to have significant inhibitory effects against a variety of primary tumors including breast and colon. The effects of IP6 have not been evaluated in pancreatic cancer. We hypothesized that IP6 would significantly inhibit cell growth and increase the apoptotic rate of pancreatic cancer in vitro. MATERIALS AND METHODS: Two pancreatic cancer cell lines (MIAPACA and PANC1) were cultured using standard techniques and treated with IP6 at doses of 0.5, 1.0, and 5.0 mm. Cell viability was measured by MTT at 24 and 72 h. Apoptosis was evaluated by Annexin V-FITC and results calculated using FACS analysis. Statistical analysis was performed by ANOVA. RESULTS: Significant reductions (P < 0.01) in cellular proliferation were observed with all IP6 concentrations tested in both cell lines and at both time points. Reductions in cell proliferation ranged from 37.1 to 91.5%. IP6 increased early and late apoptotic activity (P < 0.01). CONCLUSIONS: Treatment of pancreatic cancer with the common dietary polyphosphorylated carbohydrate IP6 significantly decreased cellular growth and increased apoptosis. Our findings suggest that IP6 has the potential to become an effective adjunct for pancreatic cancer treatment. Further in vivo and human studies are needed to evaluate safety and clinical utility of this agent in patients with pancreatic cancer.


J Nutr. 2003 Nov;133(11 Suppl 1):3778S-3784S. Links
Cancer inhibition by inositol hexaphosphate (IP6) and inositol: from laboratory to clinic.


FULL TEXT


Vucenik I, Shamsuddin AM.
Department of Medical and Research Technology, University of Maryland School of Medicine, Baltimore, MD 21201, USA. ivucenik@umaryland.edu
Inositol hexaphosphate (IP6) is a naturally occurring polyphosphorylated carbohydrate that is present in substantial amounts in almost all plant and mammalian cells. It was recently recognized to possess multiple biological functions. A striking anticancer effect of IP6 was demonstrated in different experimental models. Inositol is also a natural constituent possessing moderate anticancer activity. The most consistent and best anticancer results were obtained from the combination of IP6 plus inositol. In addition to reducing cell proliferation, IP6 increases differentiation of malignant cells, often resulting in a reversion to normal phenotype. Exogenously administered IP6 is rapidly taken into the cells and dephosphorylated to lower-phosphate inositol phosphates, which further interfere with signal transduction pathways and cell cycle arrest. Enhanced immunity and antioxidant properties can also contribute to tumor cell destruction. However, the molecular mechanisms underlying this anticancer action are not fully understood. Because it is abundantly present in regular diet, efficiently absorbed from the gastrointestinal tract, and safe, IP6 holds great promise in our strategies for the prevention and treatment of cancer. IP6 plus inositol enhances the anticancer effect of conventional chemotherapy, controls cancer metastases, and improves the quality of life, as shown in a pilot clinical trial. The data strongly argue for the use of IP6 plus inositol in our strategies for cancer prevention and treatment. However, the effectiveness and safety of IP6 plus inositol at therapeutic doses needs to be determined in phase I and phase II clinical trials in humans.



Carcinogenesis. 2004 Nov;25(11):2115-23. Epub 2004 Aug 5.
Anti-angiogenic activity of inositol hexaphosphate (IP6).

Vucenik I, Passaniti A, Vitolo MI, Tantivejkul K, Eggleton P, Shamsuddin AM.
Department of Medical and Research Technology, University of Maryland School of Medicine, Baltimore, MD, USA.
A significant anticancer activity of the naturally occurring carbohydrate inositol hexaphosphate (IP(6)) has been reported against numerous cancer models. Since tumors require angiogenesis for growth and metastasis, we hypothesize that IP(6) reduces tumor growth by inhibiting angiogenesis. Because angiogenesis depends on the interaction between endothelial and tumor cells, we investigated the effect of IP(6) on both. IP(6) inhibited the proliferation and induced the differentiation of endothelial cells in vitro; the growth of bovine aortic endothelial cells (BAECs) evaluated by MTT proliferation assay was inhibited in a dose-dependent manner (IC(50) = 0.74 mM). The combination of IP(6) and vasostatin, a calreticulin fragment with anti-angiogenic activity, was synergistically superior in growth inhibition than either compound. IP(6) inhibited human umbilical vein endothelial cell (HUVEC) tube formation (in vitro capillary differentiation) on a reconstituted extracellular matrix, Matrigel, and disrupted pre-formed tubes. IP(6) significantly reduced basic fibroblast growth factor (bFGF)-induced vessel formation (P < 0.01) in vivo in Matrigel plug assay. Exposure of HepG2, a human hepatoma cell line, to IP(6) for 8 h, resulted in a dose-dependent decrease in the mRNA levels of vascular endothelial growth factor (VEGF), as assessed by RT-PCR. IP(6) treatment of HepG2 cells for 24 h also significantly reduced the VEGF protein levels in conditioned medium, in a concentration-dependent manner (P = 0.012). Thus, IP(6) has an inhibitory effect on induced angiogenesis.

PMID: 15297368 [PubMed - indexed for MEDLINE]




Cancer Res. 2009 Dec 15;69(24):9465-72.
Inositol hexaphosphate suppresses growth and induces apoptosis in prostate carcinoma cells in culture and nude mouse xenograft: PI3K-Akt pathway as potential target.

Gu M, Roy S, Raina K, Agarwal C, Agarwal R.
Department of Pharmaceutical Sciences, School of Pharmacy, and University of Colorado Cancer Center, University of Colorado-Denver, Aurora, Colorado 80045, USA.
Constitutive activation of phosphoinositide 3-kinase (PI3K)-Akt pathway transmits growth-regulatory signals that play a central role in promoting survival, proliferation, and angiogenesis in human prostate cancer cells. Here, we assessed the efficacy of inositol hexaphosphate (IP6) against invasive human prostate cancer PC-3 and C4-2B cells and regulation of PI3K-Akt pathway. IP6 treatment of cells suppressed proliferation, induced apoptosis along with caspase-3 and poly(ADP-ribose) polymerase (PARP) cleavage, and inhibited constitutive activation of Akt and its upstream regulators PI3K, phosphoinositide-dependent kinase-1 and integrin-linked kinase-1 (ILK1). Downstream of Akt, IP6 inhibited the phosphorylation of glycogen synthase kinase-3alpha/beta at Ser(21/9) and consequently reduced cyclin D1 expression. Efficacy studies employing PC-3 tumor xenograft growth in nude mice showed that 2% (w/v) IP6 feeding in drinking water inhibits tumor growth and weight by 52% to 59% (P < 0.001). Immunohistochemical analysis of xenografts showed that IP6 significantly reduces the expression of molecules associated with cell survival/proliferation (ILK1, phosphorylated Akt, cyclin D1, and proliferating cell nuclear antigen) and angiogenesis (platelet endothelial cell adhesion molecule-1 or CD31, vascular endothelial growth factor, endothelial nitric oxide synthase, and hypoxia-inducible factor-1alpha) together with an increase in apoptotic markers (cleaved caspase-3 and PARP). These findings suggest that, by targeting the PI3K-ILK1-Akt pathway, IP6 suppresses cell survival, proliferation, and angiogenesis but induces death in prostate cancer cells, which might have translational potential in preventing and controlling the growth of advanced and aggressive prostate cancer for which conventional chemotherapy is not effective.

PMID: 19920184 [PubMed - indexed for MEDLINE]




Mol Carcinog. 2010 Jan;49(1):1-12.
Inositol hexaphosphate downregulates both constitutive and ligand-induced mitogenic and cell survival signaling, and causes caspase-mediated apoptotic death of human prostate carcinoma PC-3 cells.

Gu M, Raina K, Agarwal C, Agarwal R.
Department of Pharmaceutical Sciences, University of Colorado Denver, Aurora, 80045, USA.
Constitutively active mitogenic and prosurvival signaling cascades due to aberrant expression and interaction of growth factors and their receptors are well documented in human prostate cancer (PCa). Epidermal growth factor (EGF) and insulin-like growth factor-1 (IGF-1) are potent mitogens that regulate proliferation and survival of PCa cells via autocrine and paracrine loops involving both mitogen-activated protein kinase (MAPK)- and Akt-mediated signaling. Accordingly, here we assessed the effect of inositol hexaphosphate (IP6) on constitutive and ligand (EGF and IGF-1)-induced biological responses and associated signaling cascades in advanced and androgen-independent human PCa PC-3 cells. Treatment of PC-3 cells with 2 mM IP6 strongly inhibited both growth and proliferation and decreased cell viability; similar effects were also observed in other human PCa DU145 and LNCaP cells. IP6 also caused a strong apoptotic death of PC-3 cells together with caspase 3 and PARP cleavage. Mechanistic studies showed that biological effects of IP6 were associated with inhibition of both constitutive and ligand-induced Akt phosphorylation together with a decrease in total Akt levels, but a differential inhibitory effect on MAPKs extra cellular signal-regulated kinase 1/2 (ERK1/2), c-Jun N-terminal protein kinase (JNK1/2), and p38 under constitutive and ligand-activated conditions. Under similar condition, IP6 also inhibited AP-1 DNA-binding activity and decreased nuclear levels of both phospho and total c-Fos and c-Jun. Together, these findings for the first time establish IP6 efficacy in inhibiting aberrant EGF receptor (EGFR) or IGF-1 receptor (IGF-1R) pathway-mediated sustained growth promoting and survival signaling cascades in advanced and androgen-independent human PCa PC-3 cells, which might have translational implications in advanced human PCa control and management. 2009 Wiley-Liss, Inc.

PMID: 19544333 [PubMed - indexed for MEDLINE]




Am J Surg. 2009 Nov;198(5):679-84.
Effects of pterostilbene (resveratrol) on melanoma alone and in synergy with inositol hexaphosphate.

Schneider JG, Alosi JA, McDonald DE, McFadden DW.
Department of Surgery, University of Vermont, Burlington, VT, USA.
BACKGROUND: Pterostilbene and inositol-6-phosphate (IP6) have been shown to inhibit melanoma growth in vitro. However, pterostilbene's mechanism of action has not been clearly demonstrated. We aimed to further investigate the mechanism of action for pterostilbene and to determine whether combination treatment with IP6 produced synergistic growth inhibition. METHODS: Melanoma cells were treated with increasing doses of pterostilbene, IP6, or combinations thereof. Cell viability was measured at 24 hours, 48 hours, and 72 hours using a MTT assay. Caspase activity and vascular endothelial growth factor (VEGF) production were measured using enzyme-linked immunosorbent assay (ELISA). Analysis of variance (ANOVA) and t tests were used for statistical analysis. RESULTS: Pterostilbene inhibits melanoma growth in vitro in association with increased effector caspase activity. Combination treatment with inositol hexaphosphate produces synergistic growth inhibition, greater than either treatment alone. CONCLUSIONS: Pterostilbene produces caspase-dependent apoptosis in melanoma cell lines. Combination treatment with IP6 produces synergistic growth inhibition. Both compounds have significant potential for a therapeutic role in the treatment of melanoma.

PMID: 19887199 [PubMed - indexed for MEDLINE]





(Irinotecan/camptosar is a Topo 1 inhibitor chemotherapy)


J Control Release. 2009 May 21;136(1):30-7. Epub 2009 Jan 24.
Novel irinotecan-loaded liposome using phytic acid with high therapeutic efficacy for colon tumors.

Hattori Y, Shi L, Ding W, Koga K, Kawano K, Hakoshima M, Maitani Y.
Department of Fine Drug Targeting Research, Institute of Medicinal Chemistry, Hoshi University, Ebara 2-4-41, Shinagawa-ku, Tokyo 142-8501, Japan. yhattori@hoshi.ac.jp
Phytic acid (IP-6) is a polyphosphorylated carbohydrate with antitumor activity for many kinds of tumors. In this study, we developed a novel method of loading irinotecan (CPT-11) into liposomes using IP-6, and evaluated its antitumor effect on colon tumors in vivo. Liposomal CPT-11 was prepared by loading CPT-11 to distearoylphosphatidylcholine/cholesterol/methoxy-poly(ethyleneglycol)-distearylphosphatidylethanolamine liposomes prepared in IP-6 solution, CuSO(4) solution and citrate buffer, respectively (IP6-, Cu- and Cit-L). CPT-11 loading efficiency for IP6-L (90-100%) was higher than that for Cit-L (less than 40%), and similar to Cu-L when CPT-11 to total lipid weight ratio was increased from 0.2 to 0.6. Plasma elimination and biodistribution of liposomal CPT-11 and its metabolite SN-38 were measured after intravenous administration. IP6-L following i.v. injection showed 1.3- and 1.7-fold higher plasma area under the curves of CPT-11 and SN-38, respectively, than Cu-L. Finally, therapeutic activity was determined in mouse Colon 26 and human COLO 320DM tumor xenografts in mice. IP6-L significantly exhibited superior anticancer activity to Cu-L and free CPT-11 in Colon 26 tumor. Using IP-6 as a drug-trapping agent in liposome, IP6-L improved CPT-11 pharmacokinetics and increased antitumor activity in colon tumors.

PMID: 19331859 [PubMed - indexed for MEDLINE]




Nutr Cancer. 2006;55(2):109-25.Links
Protection against cancer by dietary IP6 and inositol.

Vucenik I, Shamsuddin AM.
Department of Pathology, University of Maryland School of Medicine, MD 21201, USA. ivucenik@umaryland.edu
Inositol hexaphosphate (IP(6)) is a naturally occurring polyphosphorylated carbohydrate, abundantly present in many plant sources and in certain high-fiber diets, such as cereals and legumes. In addition to being found in plants, IP(6) is contained in almost all mammalian cells, although in much smaller amounts, where it is important in regulating vital cellular functions such as signal transduction, cell proliferation, and differentiation. For a long time IP(6) has been recognized as a natural antioxidant. Recently IP(6) has received much attention for its role in cancer prevention and control of experimental tumor growth, progression, and metastasis. In addition, IP(6) possesses other significant benefits for human health, such as the ability to enhance immune system, prevent pathological calcification and kidney stone formation, lower elevated serum cholesterol, and reduce pathological platelet activity. In this review we show the efficacy and discuss some of the molecular mechanisms that govern the action of this dietary agent. Exogenously administered IP(6) is rapidly taken up into cells and dephosphorylated to lower inositol phosphates, which further affect signal transduction pathways resulting in cell cycle arrest. A striking anticancer action of IP(6) was demonstrated in different experimental models. In addition to reducing cell proliferation, IP(6) also induces differentiation of malignant cells. Enhanced immunity and antioxidant properties also contribute to tumor cell destruction. Preliminary studies in humans show that IP(6) and inositol, the precursor molecule of IP(6), appear to enhance the anticancer effect of conventional chemotherapy, control cancer metastases, and improve quality of life. Because it is abundantly present in regular diet, efficiently absorbed from the gastrointestinal tract, and safe, IP(6) + inositol holds great promise in our strategies for cancer prevention and therapy. There is clearly enough evidence to justify the initiation of full-scale clinical trials in humans.


1: J Environ Pathol Toxicol Oncol. 2008;27(3):209-17. Links
Inositol hexaphosphate induces apoptosis by coordinative modulation of P53, Bcl-2 and sequential activation of caspases in 7,12 dimethylbenz[a]anthracene exposed mouse epidermis.

Singh J, Gupta KP.
Environmental Carcinogenesis Division, Industrial Toxicology Research Center, Mahatma Gandhi Marg, Lucknow-226001, India.
Inositol hexaphosphate (IP6) is a major constituent of most cereals, legumes, nuts, oil seeds, and soybean. Anticancer effects of IP6 have been demonstrated in different experimental models. Besides reducing cell proliferation, IP6 increases differentiation of malignant cells, often resulting in restoring the normal phenotype. Exogenously administered IP6 is rapidly taken into the cells and dephosphorylated to lower-phosphate, inositol phosphates, which further interfere with signal transduction pathways and cell cycle arrest. Enhanced immunity and antioxidant properties could also contribute to tumor cell destruction. However, the molecular mechanisms underlying this anticancer action are not fully understood. The present study deals with the effect of topical application of IP6 on some of the selective and critical events of apoptosis in DMBA exposed mouse epidermis. IP6 showed an inhibition of DMBA-induced mutant (mt) p53 expression. Similarly, DMBA induced over expression of Bcl-2 was also reversed by topical treatment of IP6. In addition to the modulation of mt p53 and Bcl-2 expressions, IP6 brought the DMBA-inhibited activity of caspases back to the normal or induced it above the normal levels. The effects of IP6 appeared to be the function of its dose and the duration of its exposure. These results suggested that topically applied IP6 directly induces apoptotic machinery by modulating the expression of mt p53, Bcl-2, and caspase activity.

1: Neurochem Res. 2007 Dec;32(12):2094-102. Epub 2007 Jul 7. Links
Molecular mechanism of inositol hexaphosphate-mediated apoptosis in human malignant glioblastoma T98G cells.

Karmakar S, Banik NL, Ray SK.
Department of Neurosciences, Medical University of South Carolina, Charleston, SC 29425, USA.
Glioblastoma is the deadliest brain tumor in humans. Current therapies are mostly ineffective and new agents need to be explored for controlling this devastating disease. Inositol hexaphosphate (IP6) is a phytochemical that is widely found in corns, cereals, nuts, and high fiber-content foods. Previous studies demonstrated anti-cancer properties of IP6 in several in vitro and in vivo tumor models. However, therapeutic efficacy of IP6 has not yet been evaluated in glioblastoma. Here, we explored the molecular mechanism of action of IP6 in human malignant glioblastoma T98G cells. The viability of T98G cells decreased following treatment with increasing doses of IP6. T98G cells exposed to 0.25, 0.5, and 1 mM IP6 for 24 h showed morphological and biochemical features of apoptosis. Western blotting indicated changes in expression of Bax and Bcl-2 proteins resulting in an increase in Bax:Bcl-2 ratio and upregulation of cytosolic levels of cytochrome c and Smac/Diablo, suggesting involvement of mitochondria-dependent caspase cascade in apoptosis. IP6 downregulated cell survival factors such as baculovirus inhibitor-of-apoptosis repeat containing-2 (BIRC-2) protein and telomerase to promote apoptosis. Upregulation of calpain and caspase-9 occurred in course of apoptosis. Increased activities of calpain and caspase-3 cleaved 270 kD alpha-spectrin at specific sites generating 145 kD spectrin break down product (SBDP) and 120 kD SBDP, respectively. Increased caspase-3 activity also cleaved inhibitor of caspase-3-activated DNase and poly(ADP-ribose) polymerase. Collectively, our results demonstrated that IP6 down regulated the survival factors BIRC-2 and telomerase and upregulated calpain and caspase-3 activities for apoptosis in T98G cell



A very long, detailed exploration from '04:

Anti-angiogenic activity of inositol hexaphosphate (IP6)


http://carcin.oxfordjournals.org/cgi...ull/25/11/2115

The last two paragraphs:

Cancer therapy that combines distinct inhibitors of angiogenesis is a novel, effective strategy for the experimental treatment of cancer. To develop more successful anti-angiogenic therapy, combined treatment, directed to different cellular compartments may be important. It is hoped that the combination of these angiogenesis inhibitors with cytotoxic and differentiating chemotherapeutic agents will significantly improve survival and quality of life for not just cancer patients, but also of others affected by enhanced angiogenesis.
In conclusion, this study shows that IP6 has inhibitory action on several angiogenic responses, including growth and differentiation of endothelial cells, as well as inhibitory effects on the secretion of VEGF, a key angiogenic cytokine. This anti-angiogenic activity, combined with the previously known potential of IP6 as a strong anti-proliferative and differentiation-inducing agent, provides evidence that IP6 is useful for prevention and therapy of cancers and other conditions of excessive angiogenesis in humans, and merits further investigation.



Another extended paper from '03. At time, thought to be synergistic with chemo and Tamoxifen. Mentions some sort of of trial at Mayo in combination with chemo. Mentions doxo resistant bc.

http://jn.nutrition.org/cgi/content/full/133/11/3778S


excerpt:

P6 acts synergistically with standard chemotherapeutics. Current cancer treatment recognizes the importance of using combination therapy to increase efficacy and decrease side effects of conventional chemotherapy. Another important aspect of cancer treatment is overcoming acquired drug resistance. Our recent data demonstrate that IP6 acts synergistically with doxorubicin and tamoxifen, being particularly effective against estrogen receptor–negative and doxorubicin-resistant cell lines, both conditions that are challenging to treat (67). These data are particularly important because tamoxifen is usually given as a chemopreventive agent in the posttreatment period and doxorubicin has enormous cardiotoxicity and its use is associated with doxorubicin resistance. IP6 affects principal pathways of malignancy. Our goal is to identify agents that can target tumors at vulnerable sites and interrupt specific pathways of carcinogenesis. From the behavior and characteristics of malignant cells, several principal pathways of malignancy have been established, such as proliferation, cell cycle progression, metastases and invasion, angiogenesis, and apoptosis; interestingly, IP6 targets and acts on all of them.
Uncontrolled proliferation is a hallmark of malignant cells, and IP6 can reduce the cell proliferation rate of many different cell lines of different lineage and of both human and rodent origin (35,26,28,3133,38). Although normal cells divide at a controlled and limited rate, malignant cells escape from the control mechanisms that regulate the frequency of cell multiplication and usually have lost the checkpoint controls that prevent replication of defective cells. IP6 can regulate the cell cycle to block uncontrolled cell division and force malignant cells either to differentiate or go into apoptosis. IP6 induces G1 phase arrest and a significant decrease of the S phase of human breast (68,69), colon (69), and prostate (34) cancer cell lines. However, IP6 causes the accumulation of human leukemia cells in the G2M phase of the cell cycle; a cDNA microarray analysis showed a down-modulation of multiple genes involved in transcription and cell-cycle regulation by IP6 (27).
One important characteristic of malignancy is the ability of tumor cells to metastasize and infiltrate normal tissue. A significant reduction in the number of lung metastatic colonies by IP6 was observed in a mouse metastatic tumor model using FSA-1 cells (39). Using highly invasive MDA-MB 231 human breast cancer cells, we demonstrated that IP6 inhibits metastasis in vitro through effects on cancer cell adhesion, migration, and invasion (70,71). Tumor cells emit substances known as matrix metalloproteinases that allow metastatic cells to pass into the blood vessels; IP6 significantly inhibited secretion of MMP-9 from MDA-MB 231 cells (70).
Tumors depend on the formation of new blood vessels to support their growth and metastasis. Many tumors produce large amounts of vascular endothelial growth factor, a cytokine that signals normal blood vessels to grow. IP6 inhibited the growth and differentiation of endothelial cells (66,72) and inhibited the secretion of vascular endothelial growth factor from malignant cells (27,66,72). IP6 can also adversely affect angiogenesis as antagonist of fibroblast growth factor (58).
Apoptosis is a hallmark of action of many anticancer drugs. It has been reported that IP6 induces apoptosis in vivo (45) and in vitro in prostate (34) and cervical cancer (25) cell lines, involving cleavage of caspase 3, caspase 9, and poly ADP-ribose polymerase, an apoptotic substrate, in a time- and dose-dependent manner.
Effectiveness of IP6 as a cancer preventive agent. Possible mechanisms of the cancer preventive action of IP6 include carcinogen blocking activities, antioxidant activities, and antiproliferation and antiprogression activities (73). Therefore, the strategy of chemoprevention is to use agents that will inhibit mutagenesis, induce apoptosis, induce maturation and differentiation, and inhibit proliferation (74). The antioxidant activity of IP6 is widely accepted and indisputable (11), and IP6 possesses antiproliferative and antiprogression activities. Its induction of terminal differentiation (26,28,29,32,33,38), restoration of immune response (59), modulation of growth factors (58), modulation of signal transduction pathways (15,16,35,57), induction of apoptosis (25,34,45), and possibly inhibition of oncogene activity and restoration of tumor suppressor function are well documented. IP6 not only inhibits the activities of some liver enzymes (75,76) but also significantly increases the hepatic levels of glutathione S-transferase (44,77), both of which indicate its possible role in carcinogen-blocking activities and cancer protection.
Although IP6 may belong to almost all previously mentioned categories of cancer preventive drugs, affecting almost all phases of cancer prevention, it still appears that IP6 is not a direct antagonist to the carcinogen because of its moderate efficacy in vitro when tested and compared with other chemopreventive agents (30) and a lack of dramatic decrease in cancer incidence when tested in vivo. However, because cancer prevention is a long process, a long administration of cancer preventive agent is generally needed, requiring usually 10–40 y of continuous treatment (2,73), and, therefore, it is very important that cancer preventive agents have low or almost no toxicity. IP6, a natural compound with virtually no toxicity, can satisfy this special and very important requirement for cancer prevention.
IP6 plus inositol and patients
An enhanced antitumor activity without compromising the patient's quality of life was demonstrated in a pilot clinical trial involving six patients with advanced colorectal cancer (Dukes C and D) with multiple liver and lung metastasis (78). IP6 plus inositol was given as an adjuvant to chemotherapy according to Mayo protocol. One patient with liver metastasis refused chemotherapy after the first treatment, and she was treated only with IP6 plus inositol; her control ultrasound and abdominal computed tomography scan 14 mo after surgery showed a significantly reduced growth rate. A reduced tumor growth rate was noticed overall and in some cases a regression of lesions was noted.
Additionally, when IP6 plus inositol was given in combination with chemotherapy, side effects of chemotherapy
__________________



High-Fiber Foods Block Cancer Pathways

LINK

February 26, 2010

Why do people who eat high-fiber diets typically have lower incidence of certain cancers? Researchers at the Univ. of Colorado Cancer Center may have an explanation after discovering that a nutrient called inositol hexaphosphate (IP-6) blocks a pathway some cancer cells use to multiply, recruit blood vessels and keep from dying.
IP-6, also commonly known as phytic acid, is found in high concentrations in whole grains and legumes. It’s also a currently available nutritional supplement.
Mallikarjuna Gu, a research associate of Pharmaceutical Sciences Dept. at the Univ. of Colorado School of Pharmacy, discovered that treating prostate cancer cells in a Petri dish and those transplanted into mice with IP-6 stopped the cancer from growing.
Upon further investigation, he discovered that IP-6 disrupts the P13K-Akt pathway, which is shown to play a major role in the development and progression of prostate cancer, breast cancer and colorectal cancer.
“P13K-Akt is a master regulator of carcinogenesis,” Gu says. “It’s a cascade pathway, so if we can block its action, we stop many processes from starting. We showed that IP-6 inhibits the pathway not only in cells, but also in mice transplanted with human prostate cancer cells. That’s very exciting news, because in cancer we are looking for targets. We found a major target.”
Gu works in the lab of Rajesh Agarwal, co-leader of UCCC’s AMC Cancer Prevention and Control Program and professor of Pharmaceutical Sciences at the Univ. of Colorado School of Pharmacy. Agarwal studies natural substances that can prevent cancer from happening or keep it from returning once treatment is complete.
Agarwal says the research points out how IP-6 works in cells, and may explain why people who eat diets high in fiber—and specifically high in legumes—seem to have a lower risk of cancer.
“If IP-6 blocks the mechanism that certain cancers use to stay alive, it makes sense that people who eat a lot of it would block that same mechanism,” Agarwal says. “Now, we have to do clinical trials to find out how much IP-6 is needed to have both preventive and therapeutic effects.”
Agarwal is collaborating with UCCC prostate cancer physicians Michael Glodé and Thomas Flaig to design clinical trials of various natural products, to test how they work in men with prostate cancer or signs they may develop it.
“We may see if we can alter the speed of prostate cancer development in men who are at high risk by giving them this supplement or having them change to a diet high in fiber and legumes,” Agarwal says. “And we may also explore combining IP-6 with traditional chemotherapy to see if we can get a synergizing effect—if the supplement makes the cancer drugs work better.”
The discovery is published in Cancer Research.
Source: Univ. of Colorado Cancer Center
__________________

Mom's treatment history (link)
Rich66 is offline   Reply With Quote
Old 05-28-2010, 08:42 PM   #2
Rich66
Senior Member
 
Rich66's Avatar
 
Join Date: Feb 2008
Location: South East Wisconsin
Posts: 3,431
Re: Ip6

J Exp Clin Cancer Res. 2010 Feb 12;29:12.
Efficacy of IP6 + inositol in the treatment of breast cancer patients receiving chemotherapy: prospective, randomized, pilot clinical study.

Bacić I, Druzijanić N, Karlo R, Skifić I, Jagić S.
Department of Surgery, General Hospital Zadar, 23000 Zadar, Croatia.



Abstract

BACKGROUND: Prospective, randomized, pilot clinical study was conducted to evaluate the beneficial effects of inositol hexaphosphate (IP6) + Inositol in breast cancer patients treated with adjuvant therapy. PATIENTS AND METHODS: Patients with invasive ductal breast cancer where polychemotherapy was indicated were monitored in the period from 2005-2007. Fourteen patients in the same stage of ductal invasive breast cancer were involved in the study, divided in two randomized groups. One group was subjected to take IP6 + Inositol while the other group was taking placebo. In both groups of patients the same laboratory parameters were monitored. When the treatment was finished, all patients have filled questionnaires QLQ C30 and QLQ-BR23 to determine the quality of life. RESULTS: Patients receiving chemotherapy, along with IP6 + Inositol did not have cytopenia, drop in leukocyte and platelet counts. Red blood cell counts and tumor markers were unaltered in both groups. However, patients who took IP6 + Inositol had significantly better quality of life (p = 0.05) and functional status (p = 0.0003) and were able to perform their daily activities. CONCLUSION: IP6 + Inositol as an adjunctive therapy is valuable help in ameliorating the side effects and preserving quality of life among the patients treated with chemotherapy.

PMID: 20152024 [PubMed - in process]PMCID: PMC2829500Free PMC Article


Laryngoscope. 2007 Aug;117(8):1381-8.
Inositol hexaphosphate and paclitaxel: symbiotic treatment of oral cavity squamous cell carcinoma.

Janus SC, Weurtz B, Ondrey FG.
Department of Otolaryngology, University of Minnesota, Minneapolis, Minnesota 55455, USA. janu0003@umn.edu
Abstract

OBJECTIVES/HYPOTHESIS: Nuclear factor (NF)-kappaB is an early response gene that has been associated with head and neck squamous cell cancer (HNSCC) progression. NF-kappaB activation is induced by some chemotherapy agents, including paclitaxel. The activation of this gene can be correlated with apoptosis resistance. Inositol hexaphosphate (IP6) is a naturally occurring polyphosphorylated carbohydrate. NF-kappaB levels were evaluated in oral cavity HNSCC lines after treatment with paclitaxel and IP6, alone and in combination. Resulting levels of cell death and apoptosis were assessed, and conclusions are drawn regarding a possible synergistic relationship between paclitaxel and IP6. METHODS: NF-kappaB activation in cancer cells treated with paclitaxel and IP6, alone and in combination, was measured by transient transfection, and results were interpreted by luminometry. Cell proliferation of treated cells was measured by MTT assay. Cell viability and apoptosis of cancer cells treated with paclitaxel and IP6 combinations were quantitated by trypan blue staining and Caspase-Glo 3/7 assay, respectively. RESULTS: IP6 was observed to significantly downregulate NF-kappaB activation in both NA and CA-9-22 oral cavity HNSCC cell lines. Paclitaxel treatments caused increased NF-kappaB activation in the same cell lines. IP6 was observed to mitigate paclitaxel-induced NF-kappaB activation in the CA-9-22 cell line. IP6, when combined with paclitaxel, reduces CA-9-22 cell proliferation, increases cell death, and increases apoptosis, when compared with treatment with paclitaxel alone. CONCLUSIONS: IP6 reduces paclitaxel induced NF-kappaB activation and increases paclitaxel-mediated cell killing and apoptosis. As a well-tolerated and safe supplement, IP6 deserves further study in the treatment of oral cavity squamous cell carcinoma.

PMID: 17607147 [PubMed - indexed for MEDLINE]






J Surg Res. 2007 Jul;141(1):115-9.
Dietary influence on pancreatic cancer growth by catechin and inositol hexaphosphate.

McMillan B, Riggs DR, Jackson BJ, Cunningham C, McFadden DW.
Department Of Surgery, Robert C. Byrd Health Science Center, West Virginia University, Morgantown, West Virginia, USA.
Abstract





INTRODUCTION: Pancreatic cancer is an extremely virulent form of cancer with few effective treatments. We hypothesized that, alone and in combination, IP6 and catechin would be effective against pancreatic cancer. MATERIALS AND METHODS: Pancreatic (PANC-1 and MIAPACA) cancer cell lines were cultured and treated with IP6 (0.8 mM/well), catechin (100 microM/well), and the combination of the two. Cell viability was measured by 3-(4,5-dimethylthiazol-2-y1)-2,5-diphenyltetrazolium bromide (MTT) at 24, 48, and 72 h. Vascular endothelial growth factor (VEGF) was measured in the cell supernatants by ELISA. Apoptosis was evaluated by Annexin V-fluorescein isothiocyanate (FITC). RESULTS: Catechin and inositol hexaphosphate (IP6), two naturally occurring molecules found in green tea and high-fiber foods, respectively, are compounds that have been shown to demonstrate anti-proliferative effects when administered as single therapeutic agents against a number of cancers.The combination of catechin and IP6 significantly inhibited proliferation in the PANC-1 cell line at 24, 48, and 72 h compared to single agents (P < 0.001). Growth of the MIAPACA cell line was inhibited (P < 0.01) by each agent alone, but additive inhibitory effects were not seen. An increase in early apoptosis was attributed to catechin therapy in both cell lines (P < 0.01). The combination of these agents also increased early apoptotic activity when compared to the control (P < 0.001). IP6 reduced VEGF in both cell lines (P < 0.01). In combination, catechin and IP6 amplified VEGF reduction compared to each agent in MIAPACA and control (P < 0.002). CONCLUSIONS: These results, combined with the prevalence of these compounds in safe, naturally occurring foods, make catechin and IP6 attractive therapies for treatment, and possibly in preventative trials, of pancreatic cancer.

PMID: 17574044 [PubMed - indexed for MEDLINE]
__________________

Mom's treatment history (link)
Rich66 is offline   Reply With Quote
Reply

Thread Tools
Display Modes

Posting Rules
You may not post new threads
You may not post replies
You may not post attachments
You may not edit your posts

BB code is On
Smilies are On
[IMG] code is On
HTML code is On

Forum Jump


All times are GMT -7. The time now is 06:25 AM.


Powered by vBulletin® Version 3.8.7
Copyright ©2000 - 2024, vBulletin Solutions, Inc.
Copyright HER2 Support Group 2007 - 2021
free webpage hit counter