Sunday, April 23, 2017

World War III or Perpetual War?

A few years ago, I spoke to a former database administrator for a defense contractor to the CIA from the 1970s to the late 1990s who had to prepare reports for the Joint Chiefs every morning. He said, over the course of that time, there wasn't a day that went by that we weren't at war with someone, somewhere in the world. And this was before 9/11.

Take the philosophical thought experiment, "If a tree falls in a forest and no one is around to hear it, does it make a sound?" and replace it with, "If one nation makes war upon another, and no one reports on it, did that war really happen?" The modern science of mass manipulation through mainstream mesmerizing media and the distortions, lies and fabrications, incessantly pouring out of this media, has ensured that it hasn't, or if it has, it's not even close to what really occurred.  

WWIII is a loaded term. It assumes that these mass murders that humanity calls war are isolated events with distinct beginnings and ends. This simplification obscures the multi-generational chain reactions that lead up to that moment when swords are drawn or missiles fly.
Of course, there is another reason that the public is rarely conscious of these chain reactions. The ruling class has learned long ago that the best way to take a nation to war is to trick them into it."

Remember, proxy wars are still wars.


The Elite, the ‘Great Game’ and World War III
The control of the US, and of global politics, by the wealthiest families of the planet is exercised in a powerful, profound and clandestine manner. This control began in Europe and has a continuity that can be traced back to the time when the bankers discovered it was more profitable to give loans to governments than to needy individuals.

These banking families and their subservient beneficiaries have come to own most major businesses over the two centuries during which they have secretly and increasingly organized themselves as controllers of governments worldwide and as arbiters of war and peace.


Friday, April 14, 2017

Natural Cancer Bullets A - Z

There are many silver bullets that you can use to fight cancer. I will post some of these bullets (alphabetically) along with sources and brief explanations over the next several months.

Acai Berries

Source: Fruits from the Açaí Palm.

Brazilian berry destroys cancer cells in lab, UF study shows
Published today in the Journal of Agricultural and Food Chemistry, the study showed extracts from acai (ah-SAH’-ee) berries triggered a self-destruct response in up to 86 percent of leukemia cells tested, said Stephen Talcott, an assistant professor with UF’s Institute of Food and Agricultural Sciences. “Acai berries are already considered one of the richest fruit sources of antioxidants,” Talcott said. “This study was an important step toward learning what people may gain from using beverages, dietary supplements or other products made with the berries.”


Sources: Aloe Vera Plant, Aloe Vera Juice

Aloe-Emodin Induces Apoptosis in T24 Human Bladder Cancer Cells

AE inhibited cell viability, and induced G2/M arrest and apoptosis in T24 cells. AE increased the levels of Wee1 and cdc25c, and may have led to inhibition of the levels of cyclin-dependent kinase 1 and cyclin B1, which cause G2/M arrest. AE induced p53 expression and was accompanied by the induction of p21 and caspase-3 activation, which was associated with apoptosis. In addition, AE was associated with a marked increase in Fas/APO1 receptor and Bax expression but it inhibited Bcl-2 expression.

Anticancer effect of aloe-emodin on cervical cancer cells involves G2/M arrest and induction of differentiation.
Aloe-emodin inhibited the growth of HeLa cells in a dose-dependent manner at concentrations ranging between 2.5 and 40 micromol/L. The flow cytometric analysis showed that HeLa cells were arrested at the G2/M phase. This effect was associated with the decrease in cyclin A and CDK2, and the increase in cyclin B1 and CDK1. More importantly, the ALP activity was found to be increased by aloe-emodin treatment, and accompanied by the inhibition of PCNA expression. In addition, aloe-emodin suppressed the expression of PKCalpha and c-myc.

Aloe-emodin suppresses prostate cancer by targeting the mTOR complex 2
Our results herein are noteworthy in that prostate cancer cell growth is suppressed by aloe-emodin in vivo. Moreover, the low in vivo toxicity and tumor inhibitory activity of aloe-emodin observed in nude mice suggest that aloe-emodin is an effective chemopreventive agent against prostate cancer (Figure 6A and B). In conclusion, we showed here that mTORC2 is closely associated with prostate cancer cell growth. We also provided clear evidence showing that aloe-emodin effectively suppresses anchorage-independent cell growth and in vivo tumor growth in PC3 cancer cell-bearing nude mice by inhibiting Akt activity. Collectively, these findings support the anticancer efficacy of aloe-emodin through its targeting of mTORC2 for the inhibition of prostate cancer progression.
Protein kinase C involvement in aloe-emodin- and emodin-induced apoptosis in lung carcinoma cell
This study demonstrated aloe-emodin- and emodin-induced apoptosis in lung carcinoma cell lines CH27 (human lung squamous carcinoma cell) and H460 (human lung non-small cell carcinoma cell). Aloe-emodin- and emodin-induced apoptosis was characterized by nuclear morphological changes and DNA fragmentation.

The antiproliferative activity of aloe-emodin is through p53-dependent and p21-dependent apoptotic pathway in human hepatoma cell lines

The aim of this study is to investigate the anticancer effect of aloe-emodin in two human liver cancer cell lines, Hep G2 and Hep 3B. We observed that aloe-emodin inhibited cell proliferation and induced apoptosis in both examined cell lines, but with different the antiproliferative mechanisms.
Aloe-emodin Is a New Type of Anticancer Agent with Selective Activity against Neuroectodermal Tumors
Here we report that aloe-emodin (AE), a hydroxyanthraquinone present in Aloe vera leaves, has a specific in vitro and in vivo antineuroectodermal tumor activity. The growth of human neuroectodermal tumors is inhibited in mice with severe combined immunodeficiency without any appreciable toxic effects on the animals. The compound does not inhibit the proliferation of normal fibroblasts nor that of hemopoietic progenitor cells. The cytotoxicity mechanism consists of the induction of apoptosis, whereas the selectivity against neuroectodermal tumor cells is founded on a specific energy-dependent pathway of drug incorporation. Taking into account its unique cytotoxicity profile and mode of action, AE might represent a conceptually new lead antitumor drug.
Aloe-emodin induced in vitro G2/M arrest of cell cycle in human promyelocytic leukemia HL-60 cells.
Aloe-emodin inhibited cell proliferation and induced G2/M arrest and apoptosis in HL-60 cells. Investigation of the levels of cyclins B1, E and A by immunoblot analysis showed that cyclin E level was unaffected, whereas cyclin B1 and A levels increased with aloe-emodin in HL-60 cells. Investigation of the levels of cyclin-dependent kinases, Cdk1 and 2, showed increased levels of Cdk1 but the levels of Cdk2 were not effected with aloe-emodin in HL-60 cells. The levels of p27 were increased after HL-60 cells were cotreated with various concentrations of aloe-emodin.
Aloe-emodin-induced apoptosis in human gastric carcinoma cells
The purpose of this study was to investigate the anticancer effect of aloe-emodin, an anthraquinone compound present in the leaves of Aloe vera, on two distinct human gastric carcinoma cell lines, AGS and NCI-N87. We demonstrate that aloe-emodin induced cell death in a dose- and time-dependent manner. Noteworthy is that the AGS cells were generally more sensitive than the NCI-N87 cells. Aloe-emodin caused the release of apoptosis-inducing factor and cytochrome c from mitochondria, followed by the activation of caspase-3, leading to nuclear shrinkage and apoptosis.

Aloe-emodin induces in vitro G2/M arrest and alkaline phosphatase activation in human oral cancer KB cells
Aloe-emodin is a natural anthraquinone compound from the root and rhizome of Rheum palmatum. In this study, KB cells were treated with 2.5, 5, 10, 20, and 40 microM aloe-emodin for 1 to 5 days. The results showed that aloe-emodin inhibited cancer cells in a dose-dependent manner. Treatment with aloe-emodin at 10 to 40 microM resulted in cell cycle arrest at G2/M phase. The alkaline phosphatase (ALP) activity in KB cells increased upon treatment with aloe-emodin when compared to controls. This is one of the first studies to focus on the expression of ALP in human oral carcinomas cells treated with aloe-emodin. These results indicate that aloe-emodin has anti-cancer effect on oral cancer, which may lead to its use in chemotherapy and chemo preventment of oral cancer.


Source: Cannabis

Anandamide May Fight Aggressive Skin Cancer
According to the study’s results, anandamide may be involved in a complex mechanism that includes the CB1 receptor, and possibly GPR55 – a cannabinoid receptor in its own right. Although not much is known about GPR55, it is sometimes referred to as the CB3 receptor, because it responds to both endogenous and plant-derived cannabinoids.
The endogenous cannabinoid anandamide inhibits human breast cancer cell proliferation
Anandamide was the first brain metabolite shown to act as a ligand of “central” CB1 cannabinoid receptors. Here we report that the endogenous cannabinoid potently and selectively inhibits the proliferation of human breast cancer cells in vitro. Anandamide dose-dependently inhibited the proliferation of MCF-7 and EFM-19 cells with IC50 values between 0.5 and 1.5 μM and 83–92% maximal inhibition at 5–10 μM. The proliferation of several other nonmammary tumoral cell lines was not affected by 10 μM anandamide. The anti-proliferative effect of anandamide was not due to toxicity or to apoptosis of cells but was accompanied by a reduction of cells in the S phase of the cell cycle. ...These data suggest that anandamide blocks human breast cancer cell proliferation through CB1-like receptor-mediated inhibition of endogenous prolactin action at the level of prolactin receptor.

Anti-proliferative and apoptotic effects of anandamide in human prostatic cancer cell lines
ANA induced a decrease of EGFR levels on LNCaP, DU145, and PC3 prostatic cancer cells by acting through cannabinoid CB1 receptor subtype and this leaded to an inhibition of the EGF-stimulated growth of these cells. Moreover, the G1 arrest of metastatic DU145 and PC3 growth was accompanied by a massive cell death by apoptosis and/or necrosis while LNCaP cells were less sensitive to cytotoxic effects of ANA. The apoptotic/necrotic responses induced by ANA on these prostatic cancer cells were also potentiated by the acidic ceramidase inhibitor, N-oleoylethanolamine and partially inhibited by the specific ceramide synthetase inhibitor, fumonisin B1 indicating that these cytotoxic actions of ANA might be induced via the cellular ceramide production. The potent anti-proliferative and cytotoxic effects of ANA on metastatic prostatic cancer cells might provide basis for the design of new therapeutic agents for effective treatment of recurrent and invasive prostatic cancers.
Cannabinoids, Endocannabinoids and Cancer
Cannabinoids exert a number of interesting effects that are dependent on the cell line or tumor type. Synthetic cannabinoids and the endocannabinoid system are implicated in inhibiting cancer cell proliferation and angiogenesis, reducing tumor growth and metastases, and inducing apoptosis.
Anandamide is an endogenous inhibitor for the migration of tumor cells and T lymphocytes
Cell migration is of paramount importance in physiological processes such as immune surveillance, but also in the pathological processes of tumor cell migration and metastasis development. The factors that regulate this tumor cell migration, most prominently neurotransmitters, have thus been the focus of intense investigation. While the majority of neurotransmitters have a stimulatory effect on cell migration, we herein report the inhibitory effect of the endogenous substance anandamide on both tumor cell and lymphocyte migration. ...Using the specific agonist docosatetraenoylethanolamide (DEA), we have observed that the norepinephrine-induced migration of colon carcinoma cells is inhibited by the CB1-R. The SDF-1–induced migration of CD8+ T lymphocytes was, however, inhibited via the CB2-R, as shown by using the specific agonist JWH 133. Therefore, specific inhibition of tumor cell migration via CB1-R engagement might be a selective tool to prevent metastasis formation without depreciatory effects on the immune system of cancer patients.
The endogenous cannabinoid, anandamide, induces cell death in colorectal carcinoma cells
These findings suggest anandamide may be a useful chemopreventive/therapeutic agent for colorectal cancer as it targets cells that are high expressors of COX-2, and may also be used in the eradication of tumour cells that have become resistant to apoptosis.


Sources: Parsley, Celery, Coriander, Licorice, Majoram, Oregano, Rosemary, Tarragon, Citrus, Tea and Wheat.

Breast cancer effectively treated with chemical found in celery, parsley, mouse study suggests
Apigenin, a natural substance found in grocery store produce aisles, shows promise as a non-toxic treatment for an aggressive form of human breast cancer, following a new study. Researchers found apigenin shrank a type of breast cancer tumor that is stimulated by progestin, a synthetic hormone given to women to ease symptoms related to menopause.
Apigenin induces breast cancer cells
Apigenin is a low toxicity and non-mutagenic phytopolyphenol and protein kinase inhibitor. It exhibits anti-proliferating effects on human breast cancer cells. Here we examined several human breast cancer cell lines having different levels of HER2/neu expression and found that apigenin exhibited potent growth-inhibitory activity in HER2/neu-over expressing breast cancer cells but was much less effective for those cells expressing basal levels of HER2/neu
Selective growth-inhibitory, cell-cycle deregulatory and apoptotic response of apigenin in normal versus human prostate carcinoma cells
The growth-inhibitory and apoptotic potential of apigenin was also observed in a variety of prostate carcinoma cells representing different stage and androgen responsiveness. Apigenin may be developed as a promising chemopreventive and/or chemotherapeutic agent against prostate cancer.
Signal pathways involved in apigenin inhibition of growth and induction of apoptosis of human anaplastic thyroid cancer cells
Recently we demonstrated that several flavonoids can inhibit the proliferation of certain human thyroid cancer cell lines. Among the flavonoids tested, apigenin and luteolin are the most effective inhibitors of these tumor cell lines. In the present study, we investigated the signal transduction mechanism associated with the growth inhibitory effect of apigenin, using a human anaplastic thyroid carcinoma cell line, ARO.

5,6-Dichloro-ribifuranosylbenzimidazole- and apigenin-induced sensitization of colon cancer cells to TNF--mediated apoptosis

Here we report that inhibition of CK2 in HCT-116 and HT-29 cells with the use of two specific CK2 inhibitors, 5,6-dichloro-ribifuranosylbenzimidazole (DRB) and apigenin, effected a synergistic reduction in cell survival when used in conjunction with TNF-. Furthermore, there was a demonstrable synergistic reduction in colony formation in soft agar with the use of the same combinations.

Induction of apoptosis by apigenin in leukaemia HL-60 cells
The potency of these flavonoids on these features of apoptosis were in the order of: apigenin>quercetin>myricetin>kaempferol in HL-60 cells treated with 60μM flavonoids. These results suggest that flavonoid-induced apoptosis is stimulated by the release of cytochrome c to the cytosol, by procaspase-9 processing, and through a caspase-3-dependent mechanism. The induction of apoptosis by flavonoids may be attributed to their cancer chemopreventive activity. Furthermore, the potency of flavonoids for inducing apoptosis may be dependent on the numbers of hydroxyl groups in the 2-phenyl group and on the absence of the 3-hydroxyl group. This provides new information on the structure–activity relationship of flavonoids.
Arachidonyl Ethanolamide

Source: Cannabis

Arachidonyl ethanolamide induces apoptosis of uterine cervix cancer cells via aberrantly expressed vanilloid receptor-1
The major finding was that AEA induced apoptosis of CxCa cell lines via aberrantly expressed vanilloid receptor-1, whereas AEA binding to the classical CB1 and CB2 cannabinoid receptors mediated a protective effect. Furthermore, unexpectedly, a strong expression of the three forms of AEA receptors was observed in ex vivo CxCa biopsies.

Sources: wormwood plant

Artemisinin Induces Apoptosis in Human Cancer Cells
Artemisinin is a chemical compound extracted from the wormwood plant, Artemisia annua L. It has been shown to selectively kill cancer cells in vitro and retard the growth of implanted fibrosarcoma tumors in rats. In the present research, we investigated its mechanism of cytotoxicity to cancer cells. ...This rapid induction of apoptosis in cancer cells after treatment with DHA indicates that artemisinin and its analogs may be inexpensive and effective cancer agents.
Effects of artemisinin and its derivatives on growth inhibition and apoptosis of oral cancer cells
Artemisinin is of special biological interest because of its outstanding antimalarial activity. Recently, it was reported that artemisinin has antitumor activity. Its derivatives, artesunate, arteether, and artemeter, also have antitumor activity against melanoma, breast, ovarian, prostate, CNS, and renal cancer cell lines. Recently, monomer, dimer, and trimer derivatives were synthesized from deoxoartemisinin, and the dimers and the trimers were found to have much more potent antitumor activity than the monomers. ...The deoxoartemisinin trimer was found to have greater antitumor effect on tumor cells than other commonly used chemotherapeutic drugs, such as 5-FU, cisplatin, and paclitaxel. Furthermore, the ability of artemisinin and its derivatives to induce apoptosis highlights their potential as chemotherapeutic agents, for many anticancer drugs achieve their antitumor effects by inducing apoptosis in tumor cells.
Transferrin overcomes drug resistance to artemisinin in human small-cell lung carcinoma cells
Multiple drug resistance is a significant problem in small-cell lung cancer (SCLC). Artemisinin (ART) is a natural product used to treat drug-resistant malaria. The drug is effective because the Fe2+ present in infected erythrocytes acts non-enzymatically to convert ART to toxic products. We tested the effects of ART on drug-sensitive (H69) and multi-drug-resistant (H69VP) SCLC cells, pretreated with transferrin (TF) to increase the intracellular Fe2+ level. ...These data indicate the potential use of ART and TF in drug-resistant SCLC.
Dihydroartemisinin induces apoptosis and sensitizes human ovarian cancer cells to carboplatin therapy
The present study was designed to determine the effects of artemisinin (ARS) and its derivatives on human ovarian cancer cells, to evaluate their potential as novel chemotherapeutic agents used alone or in combination with a conventional cancer chemotherapeutic agent, and to investigate their underlying mechanisms of action. Human ovarian cancer cells (A2780 and OVCAR-3), and immortalized non-tumourigenic human ovarian surface epithelial cells (IOSE144), were exposed to four ARS compounds for cytotoxicity testing. The in vitro and in vivo antitumour effects and possible underlying mechanisms of action of dihydroartemisinin (DHA), the most effective compound, were further determined in ovarian cancer cells. ...These effects were also observed in in vivo ovarian A2780 and OVCAR-3 xenograft tumour models. In conclusion, ARS derivatives, particularly DHA, exhibit significant anticancer activity against ovarian cancer cells in vitro and in vivo, with minimal toxicity to non-tumourigenic human OSE cells, indicating that they may be promising therapeutic agents for ovarian cancer, either used alone or in combination with conventional chemotherapy.


Natural Cancer Bullets A - Z

Natural cancer bullets A - Z continued:


Source: Ginger Root

Antitumor effect of β-elemene in non-small-cell lung cancer cells is mediated via induction of cell cycle arrest and apoptotic cell death
Beta-elemene is a novel anticancer drug, which was extracted from the ginger plant. However, the mechanism of action of beta-elemene in non-small-cell lung cancer (NSCLC) remains unknown. Here we show that beta-elemene had differential inhibitory effects on cell growth between NSCLC cell lines and lung fibroblast and bronchial epithelial cell lines. ...These data indicate that the effect of beta-elemene on lung cancer cell death may be through a mitochondrial release of the cytochrome c-mediated apoptotic pathway.

Elemene displays anti-cancer ability on laryngeal cancer cells in vitro and in vivo
Elemene inhibited the growth of HEp-2 cells in vitro in a dose- and time-dependent manner with an IC50 of 346.5 μM (24 h incubation). Increased apoptosis was observed in elemene-administered cells. Elemene is suspected to enhance caspase-3 activity, and thus inhibit protein expression of eIFs (4E, 4G), bFGF, and VEGF. In vivo, the growth of HEp-2 cell-transplanted tumors in nude mice was inhibited by intraperitoneal injection of elemene. Compared with control groups, elemene significantly inhibited the protein expression of eIFs (4E and 4G), bFGF, and VEGF and decreased the MVD. Conclusions: Elemene inhibits the growth of HEp-2 cells in vitro and in vivo. These data provide useful information for further clinical study on the treatment of LSCC by elemene.

Antiproliferative effect of β-elemene in chemoresistant ovarian carcinoma cells

In this study, we show that beta-elemene inhibited the proliferation of cisplatin-resistant human ovarian cancer cells and their parental cells, but had only a marginal effect in human ovary cells, indicating differential inhibitory effects on cell growth between ovarian cancer cells and normal ovary cells.
Effect of Local Arterial Infusion of β_elemene on Breast Cancer Tissue Inhibition and Cell Apoptosis and Proliferation
The effect of local arterial infusion of β_elemene on breast cancer tissue inhibition and cell apoptosis and proliferation was observed.
N-(beta-Elemene-13-yl)tryptophan methyl ester induces apoptosis in human leukemia cells
Beta-elemene is an active component of herb medicine Curcuma Wenyujin and N-(beta-elemene-13-yl)tryptophan methyl ester (ETME) was synthesized for increasing its antitumor activity. ETME induced apoptosis in human leukemia HL-60 and NB4 cells at concentrations less than 40 microM. The apoptosis induction ability of ETME was associated with the production of hydrogen peroxide (H(2)O(2)), the decrease of mitochondrial membrane potential, and the activation of caspase-3 that was blocked by catalase. ETME in combination with arsenic trioxide (As(2)O(3)), an agent used to treat acute promyelocytic leukemia, synergistically induced apoptosis in both cell lines by enhanced production of H(2)O(2). These data suggest that ETME induces apoptosis and synergizes with As(2)O(3) in leukemia cells through a H(2)O(2)-dependent pathway.


Foods: Mushrooms, Grains & Yeast.
Mushrooms: Shiitake (Lentinula edodes), Reishi (Ganoderma lucidum & Ganoderma tsugae), Maitake (Grifola frondosa), Oyster Mushroom (Pleurotus ostreatus), Cauliflower Mushroom (Sparassis). Grains: Oats, Barley.

Fights cancer and eases the effects of radiation.

NOTE: Literally all of the listed mushrooms above have other important anti-cancer effects not necessarily specified here

ß-Glucan...Uses Antibodies to Target Tumors for Cytotoxic Recognition by Leukocyte Complement Receptor Type 3

ß-Glucans were identified 36 years ago as a biologic response modifier that stimulated tumor rejection. In vitro studies have shown that ß-glucans bind to a lectin domain within complement receptor type 3 (CR3; known also as Mac-1, CD11b/CD18, or Mß2-integrin, that functions as an adhesion molecule and a receptor for factor I-cleaved C3b, i.e., iC3b) resulting in the priming of this iC3b receptor for cytotoxicity of iC3b-opsonized target cells. This investigation explored mechanisms of tumor therapy with soluble ß-glucan in mice. Normal mouse sera were shown to contain low levels of Abs reactive with syngeneic or allogeneic tumor lines that activated complement, depositing C3 onto tumors. Implanted tumors became coated with IgM, IgG, and C3, and the absent C3 deposition on tumors in SCID mice was reconstituted with IgM or IgG isolated from normal sera. Therapy of mice with glucan- or mannan-rich soluble polysaccharides exhibiting high affinity for CR3 caused a 57–90% reduction in tumor weight. In young mice with lower levels of tumor-reactive Abs, the effectiveness of ß-glucan was enhanced by administration of a tumor-specific mAb, and in SCID mice, an absent response to ß-glucan was reconstituted with normal IgM or IgG. The requirement for C3 on tumors and CR3 on leukocytes was highlighted by therapy failures in C3- or CR3-deficient mice. Thus, the tumoricidal function of CR3-binding polysaccharides such as ß-glucan in vivo is defined by natural and elicited Abs that direct iC3b deposition onto neoplastic cells, making them targets for circulating leukocytes bearing polysaccharide-primed CR3. Therapy fails when tumors lack iC3b, but can be restored by tumor-specific Abs that deposit iC3b onto the tumors.

Yeast ß-Glucan Amplifies Phagocyte Killing of iC3b-Opsonized Tumor Cells

Anti-tumor mAbs hold promise for cancer therapy, but are relatively inefficient. Therefore, there is a need for agents that might amplify the effectiveness of these mAbs. One such agent is -glucan, a polysaccharide produced by fungi, yeast, and grains, but not mammalian cells. -Glucans are bound by C receptor 3 (CR3) and, in concert with target-associated complement fragment iC3b, elicit phagocytosis and killing of yeast. -Glucans may also promote killing of iC3b-opsonized tumor cells engendered by administration of anti-tumor mAbs. In this study, we report that tumor-bearing mice treated with a combination of -glucan and an anti-tumor mAb show almost complete cessation of tumor growth.

Chemosensitization of Carmustine with Maitake β-Glucan on Androgen-Independent Prostatic Cancer Cells
This study demonstrates a sensitized cytotoxic effect of BCNU with β-glucan in PC-3 cells, which was associated with a drastic (~80%) inactivation of Gly-I. Therefore, the BCNU/β-glucan combination may help to improve current treatment efficacy by targeting Gly-I, which appears to be critically involved in prostate cancer viability.

Beta glucan induces proliferation and activation of monocytes in peripheral blood of patients with advanced breast cancer

Glucans are glucose polymers that constitute a structural part of fungal cell wall. They can stimulate the innate immunity by activation of monocytes/macrophages. In human studies it has been shown that beta glucan has an immunomodulatory effect and can increase the efficacy of the biological therapies in cancer patients. In this prospective clinical trial we assessed in vivo effects of short term oral beta glucan administration on peripheral blood monocytes and their expression of activation markers in patients with advanced breast cancer. ...Oral beta glucan administration seems to stimulate proliferation and activation of peripheral blood monocytes in vivo in patients with advanced breast cancer.


Source: Lithospermum (herbs).

ß-Hydroxyisovalerylshikonin Inhibits the Cell Growth of Various Cancer Cell Lines and Induces Apoptosis in Leukemia HL–60 Cells
ß-Hydroxyisovalerylshikonin (ß-HIVS), which was isolated from the plant, Lithosper-mium radix, inhibited the growth of various lines of cancer cells derived from human solid, tumors at low concentrations between 10-8 and 10-6 M. When HL-60 cells were treated with 10-6 M ß-HIVS for 3 h, characteristic features of apoptosis, such as DNA fragmentation, nuclear fragmentation, and activation of caspase-3–like activity, were observed.

β-Hydroxyisovalerylshikonin and Cisplatin Act Synergistically to Inhibit Growth and to Induce Apoptosis of Human Lung Cancer DMS114 Cells

beta-Hydroxyisovalerylshikonin (beta-HIVS) and cisplatin (CDDP) had a synergistic growth-inhibitory effect on cultured human small-cell lung carcinoma DMS114 cells, as well as on human leukemia U937 and epidermoid carcinoma A431 cells, while beta-HIVS and CDDP alone at the same respective concentrations had little effect.


Source: The bark of Red Alder trees & White Birch trees, and the mushroom Chaga that grows on White Birch.

Anti-Cancer Effect of Betulin on a Human Lung Cancer Cell Line
Betulin is a representative compound of Betula platyphylla, a tree species belonging to the Betulaceae family. In this investigation, we revealed that betulin showed anticancer activity on human lung cancer A549 cells by inducing apoptosis and changes in protein expression profiles were observed.

Betulinic Acid Inhibits Prostate Cancer Growth

Betulinic acid is a pentacyclic triterpene natural product initially identified as a melanoma-specific cytotoxic agent that exhibits low toxicity in animal models. Subsequent studies show that betulinic acid induces apoptosis and antiangiogenic responses in tumors derived from multiple tissues;
Betulinic acid induces apoptosis in human neuroblastoma cell lines
Neuroblastoma has long been recognized to show spontaneous regression during fetal development and in the majority of stage 4s infants
Apoptotic activity of betulinic acid derivatives on murine melanoma B16 cell line
Exposure of B16 cells to betulinic acid, 23-hydroxybetulinic acid and 3-oxo-23-hydroxybetulinic acid caused a rapid increase in reactive oxidative species production and a concomitant dissipation of mitochondrial membrane potential in a dose- and time-dependent manner, which resulted in cell apoptosis, as demonstrated by fluorescence microscopy, gel electrophoresis and flow-cytometric analysis. Cell cycle analysis further demonstrated that both 3-oxo-23-hydroxybetulinic acid and 23-hydroxybetulinic acid dramatically increased DNA fragmentation at the expense of G1 cells at doses as low as 12.5 and 25 microg/ml, respectively, thereby showing their potent apoptotic properties. Our results showed that hydroxylation at the C3 position of betulinic acid is likely to enhance the apoptotic activity of betulinic acid derivatives (23-hydroxybetulinic acid and 3-oxo-23-hydroxybetulinic acid) on murine melanoma B16 cells.

Betulinic acid: A new cytotoxic compound against malignant head and neck cancer cells

In two HNSCC cell lines betulinic acid induced apoptosis, which was characterized by a dose-dependent reduction in cell numbers, emergence of apoptotic cells, and an increase in caspase activity. Western blot analysis of the expression of various Bcl-2 family members in betulinic acid–treated cells showed, surprisingly, a suppression of the expression of the proapoptotic protein Bax but no changes in Mcl-1 or Bcl-2 expression.


Evidence for anti-cancer properties of blueberries: a mini-review.
Blueberries are amongst the most commonly consumed berries in the United States. Berries in general are rich in phenolic compounds, which are known for their high antioxidant capacity. Specifically, evidence from in vitro, in vivo and a few clinical studies suggest that blueberries and their active constituents show promise as effective anti-cancer agents, both in the form of functional foods and as nutritional supplements. Some of the mechanisms by which blueberries have been shown to prevent carcinogenesis include inhibition of the production of pro-inflammatory molecules, oxidative stress and products of oxidative stress such as DNA damage, inhibition of cancer cell proliferation and increased apoptosis. This review will focus on the preclinical and clinical evidence that supports blueberries as an anti-cancer fruit, as well as expressing the need for more preclinical studies and the conduction of clinical studies with respect to the cancer preventive ability of blueberries.

Effect of Anthocyanin Fractions from Selected Cultivars of Georgia-Grown Blueberries on Apoptosis and Phase II Enzymes

The response correlated positively with dose. The QR activity was lower in all cells treated with an anthocyanin fraction from Tifblue, Powderblue, Brightblue, and Brightwell cultivars than in control cells (P < 0.05). The activity decreased gradually when treated with increased concentrations of anthocyanin fractions (50−150 μg/mL) in the Tifblue and Powderblue cultivars. The GST activity was lower (P < 0.05) in cells treated with anthocyanin fractions from all of the cultivars and at all concentrations. These results indicated that apoptosis was confirmed in HT-29 cells when treated with anthocyanins from blueberry cultivars at 50−150 μg/mL concentrations, but these same concentrations decrease QR and GST activities rather than induce them.
Availability of blueberry phenolics for microbial metabolism in the colon and the potential inflammatory implications
Blueberries are a rich source of phenylpropanoid-derived phytochemicals, widely studied for their potential health benefits. Of particular interest for colonic health are the lower molecular weight phenolic acids and their derivatives, as these are the predominant phenolic compounds detected in the colon. Blueberries contained a wide variety of phenolic acids, the majority of which (3371.14 ± 422.30 mg/kg compared to 205.06 ± 45.34 mg/kg for the free phenolic acids) were attached to other plant cell-wall components and therefore, likely to become available in the colon. Cytokine-induced stimulation of the inflammatory pathways in colon cells was four-fold up-regulated in the presence of the free phenolic acid fraction. Incubation of the bound phenolic acids with human faecal slurries resulted in qualitative and quantitative differences in the phenolic compounds recovered. The metabolites obtained by incubation with faecal slurries from one volunteer significantly decreased (1.67 ± 0.69 ng/cm3) prostanoid production, whereas an increase (10.78 ± 5.54 ng/cm3) was obtained with faecal slurries from another volunteer. These results suggest that any potential protective effect of blueberry phenolics as anti-inflammatory agents in the colon is a likely result of microbial metabolism. Studies addressing a wide-range of well-characterised human volunteers will be required before such health claims can be fully established.


Relatives: Romanesco, Broccoflower, Cauliflower, Kale, Raab, Brussel Sprouts, Cabbage, Collards and Kohl Rabi.

Natural Compound in Broccoli Slows Breast Cancer Stem Cells
In lab studies, when breast cancer cells were exposed to sulforaphane extract from broccoli, the growth of cancer stems cells slowed down and tumors shrank. The researchers speculate about the possible use of sulforaphane extract to prevent as well as treat breast cancer, someday.
Broccoli Sprouts contain 3X the amount of Sulforaphane Glucosinolate
Johns Hopkins University researchers found that young broccoli sprouts, in particular, contained high concentrations of SGS. The scientists believe that SGS boosts the body's own antioxidant defense system, including Phase 2 detoxification enzymes, which promote long-lasting antioxidant activity in the body.

Diindolylmethane (DIM)
At the University of California at Berkeley, the Chairman of the Nutritional Sciences Department and the Director of the National Institutes of Health Cancer Research Program were studying the biological properties of Diindolylmethane (DIM), a naturally occurring compound found in Brassica vegetables (broccoli, cauliflower, cabbage, kale, brussels sprouts), when they made a remarkable discovery: DIM is a potent activator of the immune response system. They patented their discovery and ActivaMune was launched as a first-in-class nutritional supplement to enhance the immune system and support multiple organs throughout the body: breast, prostate, cardiovascular, vision, skin and colon health. ActivaMune's unique and patented formula combines multiple nutrients for maximum effectiveness: Diindolylmethane (DIM), Sulforaphane, Selenium, Lycopene, Lutein, Zeaxanthin, Calcium and Vitamins C, D3 & E.

Surprising Discovery Reveals How Broccoli Fights Cancer

Broccoli — and to an even greater degree broccoli sprouts — has gained a reputation as a potent cancer-fighter, and recent research sheds new light on the actual mechanics behind its chemoprotective abilities.

One of the compounds in broccoli known to have anti-cancer activity is sulforaphane, a naturally occurring organic sulfur.

Studies have shown sulforaphane supports normal cell function and division while causing apoptosis (programmed cell death) in colon,1 prostate,2 breast3 and tobacco-induced lung cancer4 cells, and reducing the number of cancerous liver tumors in mice.5

Three servings of broccoli per week may reduce your risk of prostate cancer by more than 60 percent.6 Now, Oregon State University (OSU) researchers believe they've discovered yet another way sulforaphane works to protect you against cancer.


Natural Cancer Bullets A - Z

Caffeic Acid

Sources: Sweetpotato Leaves, Propolis, Apples, White Grapes, White Wine, Olives, Olive Oil, Spinach, Cabbage, Turnips, Radish, Cauliflower, Bok Choy, Arugula, Kale, Asparagus, and Coffee. 

Growth Suppression of Human Cancer Cells by Polyphenolics from Sweetpotato (Ipomoea batatas L.) Leaves
Sweetpotato leaves (Ipomoea batatas L.) contain a high content of polyphenolics that consist of caffeic acid, chlorogenic acid, 3,4-di-O-caffeoylquinic acid, 3,5-di-O-caffeoylquinic acid, 4,5-di-O-caffeoylquinic acid, and 3,4,5-tri-O-caffeoylquinic acid. We investigated the suppression of the proliferation of selected human cancer cells by phenolic compounds isolated from sweetpotato leaf. ...Growth suppression of HL-60 cells by 3,4,5-tri-O-caffeoylquinic acid was determined to be the result of apoptotic death of the cells. These results indicate that 3,4,5-tri-O-caffeoylquinic acid may have potential for cancer prevention.
Caffeic acid phenethyl ester induces mitochondria-mediated apoptosis in human myeloid leukemia U937 cells
Caffeic acid phenyl ester (CAPE), a biologically active ingredient of propolis, has several interesting biological properties including antioxidant, anti-inflammatory, antiviral, immunostimulatory, anti-angiogenic, anti-invasive, anti-metastatic and carcinostatic activities. Recently, several groups have reported that CAPE is cytotoxic to tumor cells but not to normal cells. In this study, we investigated the mechanism of CAPE-induced apoptosis in human myeloid leukemia U937 cells. Treatment of U937 cells with CAPE decreased cell viability in a dose-dependent and time-dependent manner.

Caffeic Acid Phenethyl Ester Induces Apoptosis by Inhibition of NFκB and Activation of Fas in Human Breast Cancer MCF-7 Cells

Our findings demonstrate that NFκB inhibition is sufficient to induce apoptosis and that Fas activation plays a role in NFκB inhibition-induced apoptosis in MCF-7 cells.

The antioxidant caffeic acid phenethyl ester induces apoptosis associated with selective scavenging of hydrogen peroxide in human leukemic HL-60 cells

These results suggest that apoptosis induced by CAPE is associated with mitochondrial dysfunction, GSH depletion and selective scavenging of H2O2 in human leukemic HL-60 cells.
Effect of caffeic acid phenethyl ester on proliferation and apoptosis of colorectal cancer cells in vitro
After HCT116 cells were exposed to CAPE (80, 40, 20, 10, 5, and 2.5 mg/L) for 24, 48, 72, 96 h, CAPE displayed a strong growth inhibitory effect in a dose- and time-dependent manner against HCT116 cells. FCM analysis showed that the ratio of G(0)/G(1) phase cells increased, S phase ratio decreased and apoptosis rate increased after HCT116 cells were exposed to CAPE (10, 5, and 2.5 mg/L) for 24 h. CAPE treatment was associated with decreased cytoplasmic beta-catenin, nuclear beta-catenin and a concurrent increase in beta-catenin protein expression at cell-cell junctions.


Foods: Hot Peppers.

Sources: Pepper Spray (It's probably a very bad idea to try and breath this stuff). Capsaicin (what makes peppers "hot") has been proven to trigger apoptosis in multiple lines of cancer.

Capsaicin Displays Anti-Proliferative Activity against Human Small Cell Lung Cancer in Cell Culture and Nude Mice Models via the E2F Pathway
BrdU assays and PCNA ELISAs showed that capsaicin displays robust anti-proliferative activity in four human SCLC cell lines. Furthermore, capsaicin potently suppressed the growth of H69 human SCLC tumors in vivo as ascertained by CAM assays and nude mice models. The second part of our study attempted to provide insight into molecular mechanisms underlying the anti-proliferative activity of capsaicin. We found that the anti-proliferative activity of capsaicin is correlated with a decrease in the expression of E2F-responsive proliferative genes like cyclin E, thymidylate synthase, cdc25A and cdc6, both at mRNA and protein levels.

Capsaicin-induced cell death in a human gastric adenocarcinoma cell line
Capsaicin, a pungent ingredient found in red pepper, has long been used in spices, food additives, and drugs. Cell death induced by the binding of capsaicin was examined in a human gastric adenocarcinoma cell line (AGS cells).
...Recently, a series of studies have demonstrated that capsaicin inhibits mutagenicity and DNA binding of some chemical carcinogens, possibly by suppressing their metabolic activation[16-18]. With cells in culture, capsaicin-inhibited proliferation of HeLa, ovarian carcinoma, and mammary adenocarcinoma by decreasing NADH oxidase activity[19]. Capsaicin can also alter the expression of tumor forming-related genes by mediating the overexpression of p53 and/or c-myc genes in a Korean stomach cancer cell line[20]. Capsaicin was found to induce apoptosis in T cells by increasing the reactive oxygen species and by a subsequent mitochondrial ransmembrane potential[21]. In this report, we examined the underlying mechanism by which capsaicin induces apoptotic cell death in a human gastric adenocarcinoma cell line (AGS).
Capsaicin-induced apoptosis and reduced release of reactive oxygen species in MBT-2 Murine Bladder Tumor cells
Capsaicin, the major pungent ingredient in genusCapsicum, has recently been tried as an intravesical drug for overactive bladder and it has also been shown to induce apoptotic cell death in many cancer cells. In this study, we investigated the apoptosis-inducing effect and alterations in the cellular redox state of capsaicin in MBT-2 murine bladder tumor cells. Capsaicin induced apoptotic MBT-2 cell death in a time- and dose-dependent manner. The capsaicin-induced apoptosis was blocked by the pretreatment with Z-VAD-fmk, a broad-range caspase inhibitor, or AcDEVD-CHO, a caspase-3 inhibitor.
Capsaicin-induced apoptosis in human breast cancer MCF-7 cells through caspase-independent pathway
Our results suggest that capsaicin induces cellular apoptosis through a caspase-independent pathway in MCF-7 cells, and that reactive oxygen species and intracellular calcium ion fluctuation has a minimal role in the process.
Capsaicin Shows Promise In Inhibiting Growth Of Pancreatic Cancer
In our study, we discovered that capsaicin fed orally to mice with human pancreatic tumors was an extremely effective inhibitor of the cancer process, inducing apoptosis in cancer cells,” said Sanjay K. Srivastava, Ph.D., lead investigator and assistant professor, department of pharmacology, University of Pittsburgh School of Medicine. “Capsaicin triggered the cancerous cells to die off and significantly reduced the size of the tumors.”
TRPV6 mediates capsaicin-induced apoptosis in gastric cancer cells
In this study, both gastric cancer and normal epithelial cells were treated with capsaicin and examined for apoptosis by Annexin V binding. Our results showed that capsaicin induces apoptosis in both cells, although cancer cells are more susceptible. This susceptibility is dependent on the availability of TRPV6, a calcium-selective channel protein, as overexpression of TRPV6 in normal cells increased capsaicin-induced apoptosis and knockdown of TRPV6 in cancer cells suppressed this action. Our results further demonstrated that capsaicin increases mitochondrial permeability through activation of Bax and p53 in a JNK-dependent manner.

Capsaicin Mediates Cell Death in Bladder Cancer T24 Cells Through Reactive Oxygen Species Production and Mitochondrial Depolarization
RESULTS: CAP decreased the viability of T24 cells in a dose-dependent manner without marked apoptosis. CAP induced ROS production and mitochondrial membrane depolarization, thereby inducing cell death, not apoptosis, in T24 cells at a concentration of 100 microM or higher. Furthermore, these effects of CAP could be reversed by capsazepine, the antagonist of transient receptor potential vanilloid type 1 channel. In vivo experiment showed that CAP significantly slowed the growth of T24 bladder cancer xenografts as measured by size (661.80 +/- 62.03 vs 567.02 +/- 43.94 mm(3); P

Chillies could help beat cancer as research finds capsaicin destroys diseased cells

Scientists say breast, colon, bone and pancreatic cancer cells could be caused to self destruct by the spicy ingredient


Food: Cinnamon 

Can Cinnamon be the Silver Bullet for Cancer?
Surprisingly, one of the potential agents for this role, cinnamon, is readily available at your local Café. Two of the main ingredients of cinnamon, cinnamaldehyde and procyanidins, have been previously shown to have health-beneficial activities, such as antioxidant, antimicrobial, anti-inflammatory, and anti-diabetic activity. Moreover, an extract from cinnamon (CE) was recently shown to have antitumor and anti-angiogenesis activity as well.

In a recent article published in Molecular Carcinogenesis, scientists from the US have showed that treatment with CE results in reduced migration of invasive breast and ovarian cancer cells, accompanied by reduced protein expression levels of both VEGF and HIF-1. In addition, a significant suppression of blood-vessel formation (see Figure below) and tumor growth was shown after CE treatment in a human ovarian tumor mouse model, which is the most deadly malignancy in women.
Cinnamon Compound Curtails Cancer
The second leading cause of cancer deaths in the US, colorectal cancer is a progressive disease generally with poor prognosis. Consequently, scientists are exploring approaches that may prevent the disease. Previously, Georg Wondrak, from the University of Arizona (Arizona, USA) identified the ground bark of Cinnamomum aromaticum (cassia cinnamon) and Cinnamomum verum (Ceylon cinnamon), as rich dietary sources of cinnamaldehyde – an inducer of Nrf2 (nuclear factor-E2-related factor 2), a master regulator of the cellular antioxidant defense that represents a promising molecular target for colorectal cancer chemoprevention.
Cinnamaldehyde induces apoptosis by ROS-mediated mitochondrial permeability transition in human promyelocytic leukemia HL-60 cells
Cinnamaldehyde is an active compound isolated from the stem bark of Cinnamomum cassia, a traditional oriental medicinal herb, which has been shown to inhibit tumor cell proliferation. In this study, we investigated the effects of cinnamaldehyde on the cytotoxicity, induction of apoptosis and the putative pathways of its actions in human promyelocytic leukemia cells. ...Taken together, our data indicate that cinnamaldehyde induces the ROS-mediated mitochondrial permeability transition and resultant cytochrome c release. This is the first report on the mechanism of the anticancer effect of cinnamaldehyde.
More Cinnamon, Less Cancer
It has been know for a few years that several types of spices contain large amounts of cancer-fighting compounds that could help in the prevention of the disease. In addition to the well-known health properties of tumeric and ginger, a recent study has suggested that cinnamon could be equally useful in reducing tumour growth by blocking the formation of new vessels using a process called angiogenesis.
Cinnamon extract induces tumor cell death through inhibition of NFκB and AP1
Cinnamon extract strongly inhibited tumor cell proliferation in vitro and induced active cell death of tumor cells by up-regulating pro-apoptotic molecules while inhibiting NFκB and AP1 activity and their target genes such as Bcl-2, BcL-xL and survivin. Oral administration of cinnamon extract in melanoma transplantation model significantly inhibited tumor growth with the same mechanism of action observed in vitro.


Food: Lemon Grass
Sources: Asian grocery's (lemon grass), Health food stores (extracts).

Fresh lemon grass fields in Israel become Mecca for cancer patients

A drink with as little as one gram of lemon grass contains enough citral to prompt cancer cells to commit suicide in the test tube. Israeli researchers find way to make cancer cells self-destruct - Ben Gurion University

Lemongrass Fights More than a Dozen Different Types of Cancers

A 2009 study published in the journal Chemico-Biological Interactions revealed that lemongrass essential oil is effective in targeting at least 12 different human cancer cell lines. Animal trials show that direct injection of lemongrass essential oil inhibits cancer tumors in a dose-dependent way, meaning the higher the dose of the oil, the better the outcome.

When administered at a dosage of 200 milligrams per kilogram (mg/kg) concentration, lemongrass essential oil was shown to inhibit both ascitic (in the fluid of the abdominal cavity) and solid tumors of Ehrlich Ascites (a type of tumor cell line) by 97.34 percent and 57.83 percent, respectively. For Sarcoma-180 tumor cells, the same dosage resulted in ascitic and solid tumor inhibition of 94.07 percent and 36.97 percent, respectively.

An essential oil and its major constituent isointermedeol induce apoptosis by increased expression of mitochondrial cytochrome c and apical death receptors in human leukaemia HL-60 cells.
An essential oil from a lemon grass variety of Cymbopogon flexuosus (CFO) and its major chemical constituent sesquiterpene isointermedeol (ISO) were investigated for their ability to induce apoptosis in human leukaemia HL-60 cells because dysregulation of apoptosis is the hallmark of cancer cells. ...The easy and abundant availability of the oil combined with its suggested mechanism of cytotoxicity make CFO highly useful in the development of anti-cancer therapeutics.
Citral is a New Inducer of Caspase-3 in Tumor Cell Lines

Citral, 3,7-dimethyl-2,6-octadien-1-al, a key component of the lemon-scented essential oils extracted from several herbal plants such as lemon grass (Cymbopogon citratus), melissa (Melissa officinalis), verbena (Verbena officinalis) is used as a food additive and as a fragrance in cosmetics. In this study, we investigated the anti-cancer potential of citral and its mode of action. Concentrations of 44.5 μM, comparable to the concentration of citral in a cup of tea prepared from 1 g of lemon grass, induced apoptosis in several hematopoietic cancer cell lines. Apoptosis was accompanied by DNA fragmentation and caspase-3 catalytic activity induction. Citral activity (22.25 μM) was compared to a reference compound like staurosporine (0.7 μM), in respect to DNA fragmentation and caspase-3 enzymatic activity. The apoptotic effect of citral depended on the α,β-unsaturated aldehyde group.

Citral inhibits cell proliferation and induces apoptosis and cell cycle arrest in MCF-7 cells.
In this study, we investigated the effect of citral (3,7-dimethyl-2,6-octadienal), a key component of essential oils extracted from several herbal plants, on the proliferation rate, cell cycle distribution, and apoptosis of the human breast cancer cell line MCF-7. The effects of this compound were also tested on cyclo-oxygenase activity. Citral treatment caused inhibition of MCF-7 cell growth (IC(50)-48 h: 18 x 10(-5)m), with a cycle arrest in G(2)/M phase and apoptosis induction. Moreover, we observed a decrease in prostaglandin E(2) synthesis 48 h after citral treatment. These findings suggest that citral has a potential chemopreventive effect.

Cod Liver Oil

Women and Lung Cancer - Could Cod Liver Oil Improve Survival
My Scandinavian, cod-liver-oil-serving grandma was right again – based on the results of a new Norwegian study. Women who used cod liver oil daily for a year prior to their diagnosis of lung cancer, had a 44% lower chance of dying. Though my grandmother would have turned 100 last week, support for her advice will be published next month in the International Journal of Cancer. Researchers looked at questionnaires completed by over 68,000 women between 1996 and 1999. They then analyzed 2,242 women who developed cancer following the questionnaire and up to the year 2007. Women who used cod liver oil daily, had a 23% lower chance of dying from solid tumors in general (breast, colorectal, and lung cancers), and a 44% reduced risk of dying from lung cancer.

Coenzyme Q10

Foods: Fish, chicken, peanuts, seasame seeds, pistachios, olive oil, soy beans, grapeseed, parsley, perilla, broccoli (and relatives).

How does CoQ10 work against cancer?
Co-Q10 is present in most "eukaryotic" cells (muscle tissues and more). It's produced naturally in the body, which uses it for cell growth and to protect cells from damage that could lead to cancer. In animals it's most concentrated in the heart. Co-Q10 both boosts the immune system, and has been shown to induce apoptosis.
A Gentle Cancer Killer
In laboratory and animal studies, the UM researchers found that by delivering CoQ10 to cancer cells and tissues, the molecule induced apoptosis, which is the normal programmed cell death that goes awry in the disease process.
Coenzyme Q10 (PDQ®)–Patient Version
Low blood levels of coenzyme Q10 have been found in patients with myeloma, lymphoma, and cancers of the breast, lung, prostate, pancreas, colon, kidney, and head and neck. Studies suggest that coenzyme Q10 may help the immune system work better. Partly because of this, coenzyme Q10 is used as adjuvant therapy for cancer. Adjuvant therapy is treatment given following the primary treatment to increase the chances of a cure.
Clinical trials have shown that coenzyme Q10 helps protect the heart from the damaging side effects of doxorubicin, a drug used to treat cancer.

Normalizattion of BCL-2 family members in breast cancer by Coenzyme Q10
Because of their integral role in intrinsic apoptosis any imbalance can lead to a variety of diseases; under expression can lead to degenerative diseases while over expression can lead to cancer and autoimmune disease. Due to their life or death role in the cell, Bcl-2 family members are currently the targets of many therapies in various disease states. Bcl-2 itself is over expressed in most tumors and all anti-apoptotic Bcl-2 family members are considered to have oncogenic potential. Conversely, the pro-apoptotic members are considered to be tumor suppressors and many mimetics are foci for cancer research. ...Both pro- and anti-apoptotic protein levels were measured in the two breast cancer cell lines after Q10 exposure. Protein levels were measured at 4,8,12, and 24 hours respectively in order to capture evidence of Q10's normalizing influence on disrupted apoptotic function. In the MCF-7 cell line Bcl-2 levels were seen to significantly drop after only 4 hours of Q10 exposure.


Food: Cumin Seeds.

Primary ingredient in Chili Powder.

Cumin: natures potent cancer combatant
This herb has been seen to effectively decrease the incidence of chemically induced tumors of the stomach, colon, and cervix. Its significant antioxidant activity and the ability to modulate the metabolism of carcinogens (toxins) explain its cancer-preventive prowess. Cumin seeds are known to induce the activity of glutathione-S-transferase, a protective enzyme that helps eliminate cancer-causing substances. Cumin offers a significant level of caffeic, chlorogenic, ferulic, and other phenolic acids that have anti-inflammatory potential.


Foods: Tumeric roots / powder, curry powder, yellow mustard.
Sources: Health food stores (extracts), large farmers markets (roots), Indian grocery stores (tumeric powder in bulk).

Induction of apoptosis in human lung cancer cells by curcumin
This study investigated the cellular and molecular changes induced by curcumin leading to the induction of apoptosis in human lung cancer cell lines—A549 and H1299. A549 is p53 proficient and H1299 is p53 null mutant. The lung cancer cells were treated with curcumin (0–160 μM) for 12–72 h. Curcumin inhibited the growth of both the cell lines in a concentration dependent manner. Growth inhibition of H1299 cell lines was both time and concentration dependent. Curcumin induced apoptosis in both the lung cancer cell lines. A decrease in expression of p53, bcl-2, and bcl-XL was observed after 12 h exposure of 40 μM curcumin. Bak and Caspase genes remained unchanged up to 60 μM curcumin but showed decrease in expression levels at 80–160 μM. The data also suggest a p53 independent induction of apoptosis in lung cancer cells.

Curcumin induces apoptosis in immortalized NIH 3T3 and malignant cancer cell lines
Curcumin, which is a widely used dietary pigment and spice, has been demonstrated to be an effective inhibitor of tumor promotion in mouse skin carcinogenesis. We report that curcumin induces cell shrinkage, chromatin condensation, and DNA fragmentation, characteristics of apoptosis, in immortalized mouse embryo fibroblast NIH 3T3 erb B2 oncogene-transformed NIH 3T3, mouse sarcoma S180, human colon cancer cell HT-29, human kidney cancer cell 293, and human hepatocellular carcinoma Hep G2 cells

Curcumin induces apoptosis in human breast cancer cells
The aim of this study was to determine the mechanisms of curcumin-induced human breast cancer cell apoptosis. From quantitative image analysis data showing an increase in the percentage of cells with a sub-G0/G1 DNA content, we demonstrated curcumin-induced apoptosis in the breast cancer cell line MCF-7, in which expression of wild-type p53 could be induced. Apoptosis was accompanied by an increase in p53 level as well as its DNA-binding activity followed by Bax expression at the protein level. Further experiments using p53-null MDAH041 cell as well as low and high p53-expressing TR9-7 cell, in which p53 expression is under tight control of tetracycline, established that curcumin induced apoptosis in tumor cells via a p53-dependent pathway in which Bax is the downstream effector of p53. This property of curcumin suggests that this molecule could have a possible therapeutic potential in breast cancer patients.
Chemopreventive Effect of Curcumin, a Naturally Occurring Anti-Inflammatory Agent, during the Promotion/Progression Stages of Colon Cancer
The inhibition of adenocarcinomas of the colon was, in fact, dose dependent. Administration of curcumin to the rats during the initiation and postinitiation stages and throughout the promotion/progression stage increased apoptosis in the colon tumors as compared to colon tumors in the groups receiving AOM and the control diet. Thus, chemopreventive activity of curcumin is observed when it is administered prior to, during, and after carcinogen treatment as well as when it is given only during the promotion/progression phase (starting late in premalignant stage) of colon carcinogenesis.

Antiproliferation and apoptosis induced by curcumin in human ovarian cancer cells

Curcumin, an active ingredient from the rhizome of the plant, Curcuma longa, has antioxidant, anti-inflammatory and anti-cancer activities. It has recently been demonstrated that the chemopreventive activities of curcumin might be due to its ability to inhibit cell growth and induce apoptosis. In the present study, we have investigated the effects of curcumin on growth and apoptosis in the human ovarian cancer cell line Ho-8910 by MTT assay, fluorescence microscopy, flow cytometry and Western blotting. Our data revealed that curcumin could significantly inhibit the growth and induce apoptosis in Ho-8910 cells. A decrease in expression of Bcl-2, Bcl-X(L) and pro-caspase-3 was observed after exposure to 40 microM curcumin, while the levels of p53 and Bax were increased in the curcumin-treated cells. These activities may contribute to the anticarcinogenic action of curcumin.
Curcumin, an antioxidant and anti-tumor promoter, induces apoptosis in human leukemia cells

Curcumin, widely used as a spice and coloring agent in food, possesses potent antioxidant, anti-inflammatory and anti-tumor promoting activities. In the present study, curcumin was found to induce apoptotic cell death in promyelocytic leukemia HL-60 cells at concentrations as low as 3.5 micrograms/ml.
Notch-1 down-regulation by curcumin is associated with the inhibition of cell growth and the induction of apoptosis in pancreatic cancer cells
Curcumin inhibited cell growth and induced apoptosis in pancreatic cancer cells. Notch-1, Hes-1, and Bcl-XL expression levels concomitantly were down-regulated by curcumin treatment. These results correlated with the inactivation of NF-κB activity and increased apoptosis induced by curcumin. The down-regulation of Notch-1 by small-interfering RNA prior to curcumin treatment resulted in enhanced cell growth inhibition and apoptosis.


Natural Cancer Bullets A - Z


Foods: Soybeans, Kwao Krua & Kudzu.


Biphasic effect of daidzein on cell growth of human colon cancer cells
LoVo cells were treated with 0.1, 1, 5, 10, 50 and 100 microM daidzein for 2, 3, 4 or 5 d. The results indicated that daidzein stimulated the growth of LoVo cells at 0.1 and 1 microM whereas at higher concentrations (10, 50 and 100 microM) cell growth was inhibited in a dose-dependent manner. Treatment of daidzein at 10, 50 and 100 microM resulted in cell cycle arrest at G0/G1 phase, DNA fragmentation and increases in caspase-3 activity. There were no changes in alkaline phosphatase activity (ALP), an indicator of cell differentiation, upon treatment with daidzein when compared to controls. These results indicate that daidzein has a biphasic effect on LoVo cell growth and its tumor suppressive effect is by means of cell cycle arrest and apoptosis but not through cell differentiation.


Wednesday, April 12, 2017

Second Opinion from Doctor Results in Different Diagnosis 88% of Time

Science Daily clearly takes point of view of the Medical Industrial Complex (MIC)--profit before patients--that the value of second opinions are demonstrated in a study, whereas I see this from the highly skeptical-of-the-deeply-rooted-MIC point of view that it can't be trusted 88% of the time. We don't know whether the first or second opinion is right or wrong. What about a third opinion? Would that opinion disagree with the first and the second?
Many patients come to Mayo Clinic for a second opinion or diagnosis confirmation before treatment for a complex condition. In a new study, Mayo Clinic reports that as many as 88 percent of those patients go home with a new or refined diagnosis — changing their care plan and potentially their lives. Conversely, only 12 percent receive confirmation that the original diagnosis was complete and correct.
We take it for granted that the Mayo Clinic is right because, well, they're the Mayo Clinic, the poster child for the MIC, this vast networked system that we've been indoctrinated to believe in since birth.
It's not that the MIC is all bad, or hasn't saved many lives and improved the quality of many others.  It's the fact that the opposite is also true, it has destroyed and ruined lives, possibly in equal measure   and we're made to believe there are no other viable options. 
We are not saying that there are no useful or helpful things within the MIC. It has saved many of our lives or the lives of people we love. We are not anti healthcare or science, but are rather exposing the reality that many of us are dependent on the MIC while we are simultaneously trying to change it and ultimately build alternatives to it. Many of us don’t want to have to turn to the MIC, yet have few other viable options. And still many of us are fighting for access to current (or better) services within the MIC. There are no easy answers and the contradictions we are living in are often painful and unjust. Similar to our work to resist and challenge capitalism or to create alternatives to the police and prisons, resisting and challenging the MIC is rife with complexity and there is so much we need that we don’t have yet.

We are asking, why we have so few options when it comes to our healthcare needs? And why insurance and pharmaceutical companies get to call the shots on the kind of care we receive—or don’t? Why don’t we talk more about the ways that forced medicalization has become part of our prison system? Or how non-western and alternative healing practices are often no less ableist than western medical practices? We are asking, what could “health,” “wellness,” “care,” “accessibility” and “sustainability” look like in practice, outside of theory? We are revealing where and how the MIC is already in our lives in ways we might not have thought of before. We are urging us all to connect the MIC to our political work, because healing, wellness, care, “health” and disability are part of whatever liberatory work we are engaged in.


Medical Industrial Complex Visual
The Medical Industrial Complex is an enormous system with tentacles that reach beyond simply doctors, nurses, clinics, and hospitals. It is a system about profit, first and foremost, rather than “health,” well being and care. Its roots run deep and its history and present are connected to everything including eugenics, capitalism, colonization, slavery, immigration, war, prisons, and reproductive oppression. It is not just a major piece of the history of ableism, but all systems of oppression.


Tuesday, March 21, 2017

Is Mainstream Science a Religion?

Why Mainstream Science is a Religion

Mainstream science, despite all its claims of objectivity, and despite the fact it attempts to lay claim to the truth, is itself a religion. Science places itself on a pedestal and assures everyone it has dispassionately arrived at its conclusions. Meanwhile, however, it is full of assumptions, denials and limitations, and makes the serious mistake of presenting its theories as facts. The errors of mainstream science are gladly seized upon by technocrats, eager to use science and technology to further their own ambitions of control, and include forcing the vaccine, GMO, surveillance, man made global warming, geoengineering, SMART and micro-chipping agendas onto an unsuspecting public. The planned New World Order has a massive technocratic aspect. Materialism, the driving force behind mainstream science, has been shown again and again to lack the capacity to explain the world around us, especially in relation to idealism or other theories that account for the energetic nature of reality. Yet, despite this, we remain collectively bedazzled by materialism, because science is a religion that has induced a certain faith in us. Up until recently, it has still been difficult for society at large to accept the fact that the unseen energetic realms are more powerful and more primal than the material realms we can see and touch … but that is starting to change.

This is certainly not the first time we have struggled with the debate of whether the world can best be described by materialism. The ancient Greek philosophers and scientists thought long and hard about the issue. Materialism vs. idealism is really the philosophical battle between the ideas that matter exists independently (and that consciousness doesn’t exist or is secondary), as opposed to the idea that consciousness, thought and energy are primary (and that matter is secondary). Democritus championed the first viewpoint (and his ideas were taken further by Aristotle), whereas Plato proposed the second with his famous theory of the World of Forms or World of Ideas. According to Plato, our materialist reality is an inferior copy of a more perfect world. This is exactly in alignment with what various cultures, shamans, religions and spiritual traditions have been saying about the preeminence of energy and mind over matter.

Even many distinguished mainstream Western scientists over the last 100+ years have grasped the point that matter is not solid. Here are the very best and brightest of them alluding to the fact that energy is preeminent to matter:

“All matter originates and exists only by virtue of a force which brings the particle of an atom to vibration and holds this most minute solar system of the atom together. We must assume behind this force the existence of a conscious and intelligent mind. This mind is the matrix of all matter.” – Max Planck
“If you want to find the secrets of the universe, think in terms of energy, frequency and vibration.” – Nikola Tesla
“The day science begins to study non-physical phenomena, it will make more progress in one decade than in all the previous centuries of its existence.” – Nikola Tesla
“The atoms or elementary particles themselves are not real; they form a world of potentialities or possibilities rather than one of things or facts.” – Werner Heisenberg
“We may therefore regard matter as being constituted by the regions of space in which the field is extremely intense … there is no place in this new kind of physics for the field and matter, for the field is the only reality.” – Albert Einstein
“The field is the sole governing agency of the particle.” – Albert Einstein
“Everything we call real is made of things that cannot be regarded as real.” – Niels Bohr
Plato also wrote that the entire universe can be explained mathematically by numbers. This exactly aligns itself with the idea that we live in a holographic universe – a kind of computer simulation with digital numbers at its foundation.

The Renaissance was heralded as a golden age for humanity, and in many ways it was, but it also further cemented the left-brain materialist view of the world, which can be found in the works of Copernicus, Galileo, Descartes and Newton. Copernicus and Galileo famously proposed heliocentrism over the existing geocentric model, but as the recent rise of the flat earth movement has shown, there is a copious amount of evidence to suggest that the heliocentric theory is far from being complete and foolproof. It was Descartes who famously claimed “I think, therefore I am” and gave birth to the falsehood that thinking, reason and logic is the base of our existence, when in fact being or consciousness is. There is no brain to think without a consciousness that animates it.

Newton, for all the great work he did for physics, came up with a set of abstract, mathematically-based, mechanical formulae which he called “the laws of nature”. Though he was to live several centuries after Newton, genius inventor and true scientist Nikola Tesla made a very telling comment regarding the tendency of mainstream science and scientists to get stuck in a rut with their abstract mathematical theories. This statement could most definitely be applied to Einstein, who despite his brilliance in proposing the theory of relativity, worked for 3+ decades afterwards and could never come up with a more complete theory. Tesla said:

“Today’s scientists have substituted mathematics for experiments, and they wander off through equation after equation, and eventually build a structure which has no relation to reality.”

Darwinian Eugenics and Evolution

Charles Darwin, for those of you who didn’t know, was part of an elite family who favored eugenics, and it is not surprising that his theory of evolution emphasized dog-eat-dog competitiveness, survival of the fittest and might is right – all habits and values of the psychopathic ruling class. Those who insist that the idea that “science is a religion” is false may be hard-pressed to explain why someone like Darwin chose to focus on those elements of Nature in this theory, instead of focusing on the incredible symbiosis and cooperation which are also widespread in Nature – and to a greater extent than competition.

Fast forward to today, and it seems science is a religion like never before. What’s happening at CERN with the Hadron Collider’s search for ever smaller and smaller particles seems like materialistic mainstream science desperately trying to justify itself and its outmoded theory, like a dog forever chasing its tail in vain. Recently in November 2014 Dr. Brian Whitworth published a paper which contrasted the materialistic and idealistic views, which he framed as physical realism and quantum realism. When he matched them to data, he found the quantum realism (simulation) model fit the observations and facts much better. He writes:

“The Higgs boson is the virtual particle created by an invisible field to explain another virtual particle created by another invisible field to explain an actual effect (neutron decay). Given dark energy and dark matter, it explains at best 4% of the mass of the universe, but the standard model needs it, so when after fifty years CERN found a million, million, million, millionth of a second signal in the possible range, physics was relieved. There is no evidence this “particle” has any effect on mass at all, but the standard model survives.

By piling fields upon fields, the standard model now has at least 48 point particles, 24 fitted properties, 5 overlapping invisible fields and 14 virtual particles that pop in and out of existence on demand, anywhere, anytime. And it isn’t finished yet, as each new effect needs a new field, e.g. inflation needs an inflaton field. If this approach, founded on physical realism, is preferred, it isn’t because of its simplicity, as it is hard to imagine anything more complicated! Chapter 4 suggests that while the fitted calculations work, their interpretation is a mythology on a scale not seen since Ptolemy’s epicycles.”

Materialism places so much stock in what we can apprehend with our 5 senses, especially sight, since it is the dominant sense for most people. Yet, of what we know exists in the full electromagnetic spectrum, we can only see a tiny range from approximately 700 nanometers (abbreviated nm) to 400 nm, between the infrared and ultraviolet rays. According to this short video clip, if the electromagnetic spectrum were a reel of film 2500 miles long (stretching from California to Alaska), then the band of visible light would be around 1 inch! According to my calculations, if these numbers are correct, that means that we only perceive 0.00000000631313% of what is really there. So why does mainstream science place so much faith in our 5-sense reality and disregard the unseen as fantasy or imagination, when we are so blind?

The fraudulent scientific research of Big Pharma is rife, and has been acknowledged as untrustable by medical journal editors, professors, doctors, government officials and former Big Pharma insiders.

Mainstream Science – Bogged Down by Fraud and Fakery

So far, I have discussed the reasons why mainstream science is ideologically or theoretically on the wrong track. I haven’t even begun to touch the ways in which science is horribly misguided and mistaken on a practical level. Sad to say, science has been totally corrupted by special interests who fund and determine the outcome of much of the research. They can pay for whatever “scientific result” they want for their agenda, not only because one’s very act of observation determines one’s reality, but also because they can slant, distort and omit data in line with their goals. Simply put, a scientist discovering the “wrong” result will be quickly rejected and defunded.

This fake and fraudulent science, which is not true science at all but rather corporate junk science which passes under the rubric of science, is all pervasive. See my articles The Massive Flaw with the Scientific Hierarchy of Evidence, The Top 10 Tricks Used by Corporate Junk Science and Most Scientific Research of Western Medicine Untrustable & Fraudulent, Say Insiders and Experts for a fuller discussion of this point. As Marcia Angell, former editor-in-chief of the esteemed New England Journal of Medicine (NEJM), had to say about the pervasive fraudulent scientific research:

It is simply no longer possible to believe much of the clinical research that is published, or to rely on the judgment of trusted physicians or authoritative medical guidelines … I take no pleasure in this conclusion, which I reached slowly and reluctantly over my two decades as an editor of The New England Journal of Medicine.”

Happily, there are many true scientists standing outside of the fakery and putting forth alternative evidence to consider (e.g. with the political manmade global warming agenda). The truth cannot be hidden forever.

Mainstream scientists will probably feel aghast to hear it, but the truth is that science is a religion with its own high priests – they just wear white coats rather than black gowns. It requires belief (faith) in its theories (doctrine) which can never ultimately be proven (Evolution, Relativity, Big Bang) because they are full of assumptions and contradictions. There is always at least one question that can never be answered, and constantly redefining terms, omitting numbers or inventing new factors becomes, at a certain point, like twisting facts to suit theories, rather than twisting theories to suit facts, as the fictional character Sherlock Holmes liked to say.

Terrence McKenna humorously put it like this:
Modern science is based on the principle: ‘Give us one free miracle, and we’ll explain the rest.’ The one free miracle is the appearance of all the mass and energy in the universe and all the laws that govern it in a single instant from nothing.”

Materialist science has tried to convince us that everything can be explained with solid atoms, but as various experiments have proven, only theories which account for consciousness, energy, non-locality and other phenomena make sense. Particles are probability distributions, not little hard things. Materialism falls short again and again in describing and predicting our world. We actually live in a holographic universe – a computer simulation which looks and feels real but which is composed of stuff which is not solid.

Mainstream materialistic science is a religion – and the time is long overdue to give up the faith.

Petitions by|Start a Petition »

  © Blogger templates The Professional Template by 2008

Back to TOP