This encyclopedic reference currently contains over 90 compounds and substances with cancer fighting properties that most people don’t know about, and the scholarly studies behind them. With this vast array of mostly natural substances you can apply these complimentary alternative treatments to boost your odds of beating cancer, and you can definitely increase your odds of never getting cancer.
DISCLAIMER: I’m not suggesting people don’t follow their doctors orders. I explain this better at the end of the presentation. There isn’t likely any sure single silver bullet to curing existing cancer, while in the right combination in your diet you shouldn’t ever have to worry about getting it.
By Ignorance Isn’t Bliss
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.”
*Acrylamide is a chemical used primarily for industrial purposes.
*Acrylamide has been found in certain foods, with especially high levels in potato chips, French fries, and other food products produced by high-temperature cooking.
*Food and cigarette smoke are the major sources of exposure to acrylamide.
*Acrylamide is considered to be a mutagen and a probable human carcinogen, based mainly on studies in laboratory animals.
*Scientists do not yet know with any certainty whether the levels of acrylamide typically found in some foods pose a health risk for humans.
How does cooking produce acrylamide?
Asparagine is an amino acid (a building block of proteins) that is found in many vegetables, with higher concentrations in some varieties of potatoes. When heated to high temperatures in the presence of certain sugars, asparagine can form acrylamide. High-temperature cooking methods, such as frying, baking, or broiling, have been found to produce acrylamide (3), while boiling and microwaving appear less likely to do so. Longer cooking times can also increase acrylamide production when the cooking temperature is above 120 degrees Celsius (4, 5).
Sources: Aloe Vera Plant, Aloe Vera Juice (inexpensive at Hispanic Markets).
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.
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 chemopreventment of oral cancer.
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 ?M and 83–92% maximal inhibition at 5–10 ?M. The proliferation of several other nonmammary tumoral cell lines was not affected by 10 ?M 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.
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.
Foods: Parsley, Celery, Coriander, Licorice, Majoram, Oregano, Rosemary, Tarragon, Citrus, Tea and Wheat.
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.
Apigenin induces apoptosis…in 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-overexpressing breast cancer cells but was much less effective for those cells expressing basal levels of HER2/neu.
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.
Induction of cell cycle arrest and apoptosis by apigenin in human prostate carcinoma cells
Apigenin, a common dietary flavonoid abundantly present in fruits and vegetables, may have the potential for prevention and therapy for prostate cancer. Here, we report for the first time that apigenin inhibits the growth of androgen-responsive human prostate carcinoma LNCaP cells and provide molecular understanding of this effect.
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 60?M 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.
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.
Apoptosis (aka Programmed Cell Death) is the internal mechanism of basically all biological cells to self-destruct when ‘malfunctioning’. With cancer cells mutate and overcome this design, making them in a sense immortal. So for about as long as cancer has been understood the holy grail in cancer research has been in discovering how to reinstitute apoptosis in cancer cells safely.
The thing is this holy grail has been found in numerous forms, yet the understanding of the general public is that it hasn’t and can only be solved with damaging radiation and chemotherapy. You might ask yourself why that is, and why haven’t known safe apoptosis inducers been aggressively pursued? Perhaps preventing terrorist attacks on national monuments are more important than the 550,000 individuals who die every year from cancer?
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.
Source: 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 receptor-dependent cytotoxicity of artemisinin–transferrin conjugates on prostate cancer cells and induction of apoptosis
Artemisinin, a natural product isolated from Artemisia annua, contains an endoperoxide group that can be activated by intracellular iron to generate toxic radical species. Cancer cells over-express transferrin receptors (TfR) for iron uptake while most normal cells express nearly undetectable levels of TfR. We prepared a series of artemisinin-tagged transferrins (ART-Tf) where different numbers of artemisinin units are attached to the N-glycoside chains of transferrin (Tf). The Tf bearing approximately 16 artemisinins retains the functionality of both Tf and artemisinin. Reduction of TfRs by TfR siRNA transfection significantly impaired the ability of ART-Tf, but not dihydroartemisinin, to kill cells. We also demonstrate that the ART-Tf conjugate kills the prostate carcinoma cell line DU 145 by the mitochondrial pathway of apoptosis.
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.
Source: Ginger Root
Antitumor effect of ?-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 ?M (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 ?-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 ?_elemene on Breast Cancer Tissue Inhibition and Cell Apoptosis and Proliferation
The effect of local arterial infusion of ?_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 by this presentation.
ß-Glucan…Uses Antibodies to Target Tumors for Cytotoxic Recognition by Leukocyte Complement Receptor Type 3 (CD11b/CD18)
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.
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.
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 ?-Glucan on Androgen-Independent Prostatic Cancer Cells
This study demonstrates a sensitized cytotoxic effect of BCNU with ?-glucan in PC-3 cells, which was associated with a drastic (~80%) inactivation of Gly-I. Therefore, the BCNU/?-glucan combination may help to improve current treatment efficacy by targeting Gly-I, which appears to be critically involved in prostate cancer viability.
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.
?-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;
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 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 <1 year of age with disseminated disease. Stage 4s disease regresses with no chemotherapy in 50% of the patients. The mechanism by which this occurs is not understood but may be programmed cell death or apoptosis. Betulinic acid (BA) has been reported to induce apoptosis in human melanoma with in vitro and in vivo model systems.
Betulinic acid induces apoptosis in skin cancer cells
Betulinic acid (BA), a pentacyclic triterpene of plant origin, induces cell death in melanoma cells and other malignant cells of neuroectodermal origin. Little is known about additional biological effects in normal target cells. We show, in this study, that BA induces differentiation as well as cell death in normal human keratinocytes (NHK).
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.
In vivo and in vitro anti-inflammatory and anti-nociceptive effects of the methanol extract of Inonotus obliquus
The mushroom Inonotus obliquus (Fr.) Pilát (Hymenochaetaceae), has been traditionally used for the treatment of gastrointestinal cancer, cardiovascular disease and diabetes in Russia, Poland and most of Baltic countries. This study was designed to investigate the anti-inflammatory and anti-nociceptive effects of the methanol extract from Inonotus obliquus (MEIO) in vivo and in vitro. MEIO (100 or 200 mg/(kg day), p.o.) reduced acute paw edema induced by carrageenin in rats, and showed analgesic activity, as determined by an acetic acid-induced abdominal constriction test and a hot plate test in mice.
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 ?g/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 ?g/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.
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.
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.
This is formed naturally during the digestion of dietary fibers. Not enough BA and you’re prone to colon cancer. If you get colon cancer you it’s time to go into fiber overdrive.
Sources: Sweetpotato Leaves, Propolis, Apples, White Grapes, White Wine, Olives, Olive Oil, Spinach, Cabbage, Turnips, Radish, Cauliflower, Bok Choy, Arugula, Kale, Asparagus, and Coffee.
Caffeic Acid isn’t related to Caffeine.
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 NF?B and Activation of Fas in Human Breast Cancer MCF-7 Cells
Our findings demonstrate that NF?B inhibition is sufficient to induce apoptosis and that Fas activation plays a role in NF?B 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. 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. Capsaicin was found to induce apoptosis in T cells by increasing the reactive oxygen species and by a subsequent mitochondrial ransmembrane potential. 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.
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 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.”
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 <.01).
CONCLUSIONS: CAP mediates cell death in T24 cells through calcium entry-dependent ROS production and mitochondrial depolarization, and it may have a role in the management of bladder cancer.
Foods: Carrots, Sweet Potato, Kale, Apricots, Mangos, Squash, Spinach, Kale, Collard Greens, Salmon, Shellfish, Egg Yolks, Hot Peppers, Brown Algae.
Carotenoids Affect Proliferation of Human Prostate Cancer Cells
We investigated whether various carotenoids present in foodstuffs were potentially involved in cancer-preventing action on human prostate cancer. The effects of 15 kinds of carotenoids on the viability of three lines of human prostate cancer cells, PC-3, DU 145 and LNCaP, were evaluated. When the prostate cancer cells were cultured in a carotenoid-supplemented medium for 72 h at 20 µmol/L, 5,6-monoepoxy carotenoids, namely, neoxanthin from spinach and fucoxanthin from brown algae, significantly reduced cell viability to 10.9 and 14.9% for PC-3, 15.0 and 5.0% for DU 145, and nearly zero and 9.8% for LNCaP, respectively.
Serum carotenoids and mortality from lung cancer
Higher serum levels of carotenoids such as – and ?-carotenes may play a role in preventing death from lung cancer
Human Breast Cancer Cells Treated with Carotenoids or Retinoids
These results demonstrate that ER status is an important, although not essential factor for breast cancer cell response to carotenoid and retinoid treatments, and the mode of action of all-t-RA in MCF-7 and Hs578T cells is not through the induction of RAR. Other mechanistic pathways that are either followed by or concomitant with growth inhibition are possible.
Carotenoids, antioxidants and ovarian cancer risk in pre- and postmenopausal women
From a population-based study of 549 cases of ovarian cancer and 516 controls, we estimated the consumption of the antioxidant vitamins A, C, D and E and various carotenoids, including alpha- and beta-carotene and lycopene, using a validated dietary questionnaire. Multivariate logistic regression was used to calculate the exposure odds ratios adjusted for established ovarian cancer risk factors. Intakes of carotene, especially alpha-carotene, from food and supplements were significantly and inversely associated with risk for ovarian cancer, predominantly in postmenopausal women. Intake of lycopene was significantly and inversely associated with risk for ovarian cancer, predominantly in premenopausal women. Food items most strongly related to decreased risk for ovarian cancer were raw carrots and tomato sauce. Consumption of fruits, vegetables and food items high in carotene and lycopene may reduce the risk of ovarian cancer.
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