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• Bcl-2 mutation

• BRCA1*
• CA 125*
• CA 15-3*
• CA 27.29*
• CA 72-4
• Carbonic Anhydrase (CA) - 9
• Cathepsin-D
• Cathepsin-G
• CAV-1
• CD-24
• CD-44-4
• Ceruloplasmin*
• CK17
• CK19*
• CK5
• CK7
• Copper (serum)
• COX -2
• CTCs*
• DNA index*
• E-cadherin
• EGFR
• Estrogen Receptor
• HER2/neu
• Homocysteine
• HSP
• IL-8
• Ki-67
• MEK/ERK
• MIB1
• Mitotic Index*
• mTOR
• NFκB
• nm23 mutation
• p 53 mutation
• p21 mutation
• p27 mutation
• p63 mutation
• PAR-1
• PARP (poly ADP-ribose polymerase)
• P-cadherin
• PDGF
• Progesterone Receptor
• Prolactin
• PTEN mutation
• SPARC
• S-Phase expression
• VEGF

• Survivin
• TGF-β1
• Topoisomerase II
• T-PA

Note: Cancer targets highlighted in PURPLE are described in detail below. For a more detailed discussion of tissue pathology and blood marker testing please see our article on Understanding Breast Cancer.

Actions of Cancer Preventive Botanicals & Nutrients on Selected Cancer Targets

VEGF – vascular endothelial growth factor - is one of the most powerful stimulants of tumor angiogenesis. VEGF mRNA expression is upregulated by a wide array of oncogenes (including H-ras and K-ras, V-raf, src, PTEN, p53, Wnt, and c-jun, among others) and growth factors (including EGF, TGF-α, TGF-β, insulin-like growth factor-1, and PDGF). (Houck et al 1992) (Sima et al 1995) (Shweiki et al 1992) (Toi et al 2001) (Kerbal & Niklinska et al 2001) (Folkman 2002)  

Natural Compounds that Inhibit VEGF:

Artemisia annua (Chen et al 2004)

Camellia sinensis (green tea extract) (Lin et al 2008)

Curcuma longa (turmeric) (Schaaf et al 2010)

Ginkgo biloba (Zhang et al 2002)

Magnolia seed cones – 90% honokiol (Wen et al 2009) (Ahn et al 2006)

Ocimum spp. (Basil) Ursolic acid (Yan et al 2010)

Polygonum cuspidatum (Japanese knotweed) (Wang et al 2004) (Cao et al 2005) – 20% resveratrol

Pterostilbene – (Pan et al 2009)

Scutellaria baicalensis (Yoon et al 2009)

Silybum marianum (milk thistle) (Gallo et al 2003)

Taxus breviflora (Pacific yew) – taxol and other related taxins

Viscum album (Mistletoe) (Park et al 2001)

Vitus vinifera (grape seed extract) (Bai et al 2003)

 p53 – the Guardian of the Genome.

The highest frequency of p53 mutations reported in human cancers are lung, 56%; colon, 50%; esophagus,45%; ovary, pancreas and skin, 44%; stomach, 41%; head and neck, 37%; bladder, 34%; prostate, 30% and breast, endometrium and mesothelioma, 22%.

Natural Compounds that Normalize p53

6-Gingerol (Park et al 2006)

Coriolus versicolor (Ho et al 2005)

Curcumin (Boik 2001 p.55)

EGCG (Lee et al 2010)

Tocotrienols (Agarwal et al 2004) and Vit E succinate

OPCs

Oridonin (Rabdosia) (Cui et al 2007)

Paw paw seed

Quercetin (Beniston et al 2001)(Shi et al 2003)

Resveratrol (She et al 2001)(Pearce et al 2007)(Tang et al 2006)

Rhemannia glutinosa (Chao et al 2006)

Withanone (Ashwagandha extract) (Widodo et al 2008)

Note: Diets rich in refined sugars and starches, as well as rich in red meat promote p53 mutation. (Slattery et al 2002)

Bcl-2 – is an NF-κB regulated gene that functions by blocking the apoptosis pathway, thus immortalizing cancer cells. It has been suggested that Bcl-2 over expression results in the up regulation of VEGF expression with increased neoangiogenesis in human cancer xenografts.

Expression of the Bcl-2 protein confers resistance to chemotherapy-mediated apoptotic signals in patients with breast cancer. (Rom et al 2009)

Natural Compounds that Reduce Bcl-2

Andrographolide (Zhou et al 2006) – Andrographis

Baicalin and baicalein (Chen et al 2000) - Scutellaria baicalensis

Beta-lapachone – Lapacho (Woo et al 2005)

Carnosol – Rosemary (Dorrie et al 2001)

Casticin – Yarrow (Achillea millefolium) (Khadidja et al 2006)

Chelidonium alkaloids – Chelidonine (Habermehl et al 2006)

Curcumin (Bharti et al 2003) (Schaaf et al 2010)

DIM – (Hong et al 2002)

Echinocystic acid (EA) (Tong et al 2004) – Panax ginseng

EGCG (Lee et al 2010) and Theophylline - Green tea (Leone et al 2003)(Byrd et al 2000)

EPA – from fish oil (Chiu and Wan 1999)

Gingerol – Ginger (Wang et al 2003)

Hibiscus protocatechuic acid (PCA) (Tseng et al 2000)

Mistletoe – (Choi et al 2004)

OPCs – grape seed extract – (Bagchi et al 2000)

Parthenolide – feverfew (Zhang et al 2004)

Resveratrol – (Aziz et al 2006)  

NF-kappaB - is an important transcription factor that is up-regulated in practically all cancers.  It up regulates inflammation, angiogenesis, metastasis and tumor promotion.  It is hyperactive in many cancers raising the resistance of cancer cells to chemotherapy drugs and chemo radiation.

Natural Compounds that Inhibit or Down-Regulate NF-kappaB:

Chinese skullcap (Piao et al 2008) (Peng et al 2008)

Curcumin – (Rafiee et al 2010) (Kamat et al 2009)

DIM (Banerjee et al 2009)(Rahman et al 2007) and I-3-C (Rahman et al 2006) (Takada et al 2005)

Green Tea Polyphenols EGCG (Lee et al 2009) (SBabu et al 2009) (Siddiqui et al 2008)

Magnolol (Ahn et al 2006)

N-acetyl cysteine (NAC) (Sailai et al 2010)

Panax ginseng (Jou et al 2009) and panax notoginseng (Son et al 2009)

Parthenolide (Nehra et al 2010) (Riggins et al 2005)

Pterostilbene (Pan et al 2009) and quercetin (Granado-Serrano et al 2010)

Reishi powdered extract ((Jiang et al 2008) (Ho et al 2007)

Resveratrol (Singh et al 2010) (Park et al 2009) (Benitez et al 2009)

Silymarin (Momeny et al 2010)

Sulforaphane (PEITC) (Xu et al 2005) (Brunelli et al 2010)

Ursolic acid (Manu & Kuttan 2008) – in Holy Basil

COX-2 is up-regulated in practically all cancers.  It is induced by phorbol esters, cytokines and growth factors, including TGF-beta-1 and bFGF.  COX-2 is a potent inducer of angiogenesis by inducing angiogenic factors. Most common cancers with altered (amplified) COX-2 expression include: prostate, colon, breast, cervical brain, gastric, pancreatic, lung, head and neck, kidney and bladder.

     Breast cancers that demonstrate elevated COX-2 expression were more predictive of poor survival in patients with estrogen receptor (ER)-positive tumors than in those with ER-negative tumors, according to a 2002 report by Finnish researchers. Similarly elevated expression was of greater prognostic value in patients with no abnormalities of the p53 gene and the HER-2 gene.

      Breast cancer is associated with inflammatory processes based on an up-regulation of cyclooxygenase-2 (COX-2) expression, the prostaglandin E2 (PGE2) synthesizing enzyme. (Thill et al 2009)

Natural Compounds that Inhibit or Down-Regulate COX-2:

EPA and DHA in n-3 fatty acids from fish oils (Lee et al 2009) (Lim et al 2009)

Baicalein, from Chinese skullcap (Chiu et al 2010)

Curcumin (Lin et al 2010) (Moon et al 2010) (Leite et al 2009)

Resveratrol (Kang et al 2009)

Panax notoginseng (Son et al 2009)

Parthenolide (Weng et al 2009)

Pterostilbene (Pan et al 2008)

Quercetin (Lee et al 2010) (Turner et al 2009) (Warren et al 2009)

Salicin (Corydalis 30%) Willow bark extract (WBE)

WBE inhibits the cell growth and promote apoptosis in human colon and lung cancer both through COX-selectivity and nonCOX-2. Other synergistic compound WBE include other salicyl alcohol derivates, flavonoids, proanthocyanidins.

      Natural COX inhibitory curcuminoid components of curcumin are active in the regulation of COX-2, EGFR, VEGF, PI3K/Akt, MEK/ERK, p53, c-Myc, NF-kappaB, Bcl-2, e-cadherin, and apoptotic pathways all known to be critically involved in breast carcinomas in general and in triple negative disease in particular, as well as HER2 (ErbB2), and some of which are also regulated by the activity of the EGCG (epigallocatechin-3 gallate) component of green tea. (Kaniklidis 2007)

Several foods and common culinary herbs contain particular compounds that reduce inflammation, in part, by acting as COX-2 inhibitors. These include:

Grapes (leaf and skin)

Curcumin longo (turmeric)

Ocimun sanctum (basil)

Fish

Flax

Oregano

Rosmarinus (rosemary)        

Licorice root (glycyrrhizin glabra)

PDGF - Expression of PDGF, and activation of its receptor (PDGFR), a tyrosine kinase, is associated with the growth of metastasis in several forms of cancer including kidney, breast, prostate, sarcomas, cervical and in head and neck cancer. Inhibition of PDGF has shown to suppress metastatic cancer.

Natural Compounds that Suppress PDGF

Curcumin causes an interruption of the PDGF and EGF signaling pathways by stimulating gene expression of PPARγ.

Curcumin, also decreases the proportion of S phase cells after PDGF stimulation 

Baicalein, in Chinese skullcap, one of the most powerful anti-cancer agents induces apoptosis of cancer cells.  One known mechanism is by down-regulating 12-LOX – reducing PDGF.

EGCG, from GTE, inhibits PDGF-induced VEGF expression via blocking PDGF receptor and Erk-1/2.

EGFR

·     There are now several trials exploring the potential of EGFR inhibitors in triple negative disease in the metastatic breast cancer setting and evaluating a combination of EGFR-inhibitors + platinum agent.

·     Several selected targeted agents are being investigated in combination with endocrine therapy for patients with breast cancer in an attempt to overcome or prevent endocrine resistance. The role of type I growth factor receptors epidermal growth factor receptor (EGFR) and HER2 in cross-talk with estrogen receptor (ER) signaling has been confirmed in preclinical studies in which various inhibitors have yielded additive or synergistic effects when combined with endocrine agents. (Johnston 2009)

Natural compounds shown to block EGF receptor activation and its downstream effectors include:

o       Resveratrol

o       Vitamin D-3

o       Licorice

o       Quercetin (inhibits both EGF and HER2-neu expression)

o       Cysteine (un-denatured whey protein concentrate)

o       Selenium

o       Curcumin

o       I-3-C/DIM

mTOR

·        Both caloric restriction and glucose / insulin control may play specific beneficial functions in triple negative disease via the newfound contribution of mTOR inhibition, and add another item of defense to the growing arsenal deployable against triple negative breast carcinoma.

·    mTOR - The natural agent curcumin's anticancer activity appears to operate primarily by blocking mTOR-mediated signaling pathways in the tumor cells, also inducing apoptosis and inhibiting the basal or type I insulin-like growth factor-induced motility of the cells, also inhibiting at high concentrations the phosphorylation of Akt in tumor cells.

·    mTOR - Honokiol, a natural dietary product isolated from an extract of seed cones from Magnolia grandiflora, can decrease PI3K/mTOR pathway-mediated immunoresistance of glioma, breast and prostate cancer cell lines, without affecting critical proinflammatory T cell functions. (Crane et al 2009)

PTEN

·    When PTEN mutates it is the likely driver that activates NF-κB.  Mutations or deletions of the PTEN gene are increasingly being reported in human malignancies, including breast cancer.

·     The inactivation of PTEN – phosphatase and tensin homologue – an important tumor suppressing gene -- was found in about one third of all breast cancers.  The reduced expression of PTEN protein correlated with lymph node metastases and a worse prognosis in the patients with breast cancer.

Known activators of PTEN and/or inhibitors of PTEN mutation include:

o       Honokiol, from Magnolia grandifloria/officinalis

o       Quercetin

o       Resveratrol

o       Sulforaphane

o       Isoflavones (red clover)

·         DIM (3,3'-Diindolylmethane) is a known anti-tumor agent against breast and other cancers; however, its exact mechanism of action remains unclear.  B-DIM (a clinically active DIM) can directly inhibit VEGF and MMP-9 leading to the inhibition of cell growth and migration of breast cancer cells. (Ahmad et al 2009)

·        Flaxseeds have potent antiestrogenic effects on estrogen receptor positive breast cancer, and recently were found to down-regulate cancer-induced VEGF.

·        Raising Vitamin D levels may prevent up to half of all breast and two thirds of colorectal cancer cases in the US.  The investigators recommend a daily intake of 2000 IU of Vit. D3 and when possible moderate sun exposure.

·        A diet rich in fruits and vegetables protects a woman from the BRCA gene becoming activated.

·        Astragalus suppressed Basal-like breast cancer: down-regulating EGF and p53.

·        Curcumin and genistein inhibit EGF.

·        Olive oil has been shown to suppress Her-2/neu in Her-2/neu positive breast cancer.

·        Chaste tree (Vitex agnus-castus) berry has been shown to reduce prolactin levels in a study of women with hyperprolactinemia. Laboratory Tests and Diagnostic Procedures, p. 907 (2008)

·        Curcumin and EGCG can interfere with the expression of VEGF by processes other than hypoxia, such as transforming growth factor (TGF)-β release, COX-2 over-expression, hydrogen peroxide release from bone cells, constitutive and aberrant EGFR and Src signaling, and most importantly, by aberrant NF-κB signaling in established cancers.

·        Folate and B6 – Higher levels of folate and B6 reduce the risk of developing breast cancer.

Cancer Preventive Botanicals with an Emphasis on Breast Cancer

·        Andrographis paniculata extract and andrographolide inhibit tumor specific angiogenesis by lowering the pro-angiogenic factors such as proinflammatory cytokine, nitric oxide and VEGF; and elevating the anti-angiogenic factors such as IL-2 and TIMP-1.

·        Andrographolide -- significantly decreased the number of surviving hepatoma-derived Hep3B cells in the MTT assay and induced cell apoptosis by inducing activation of MAPKs including p38 kinase, JNK and ERK ½.

·        Artemisinin - killed virtually all human breast cancer cells exposed to it within 16 hours.

·        Artemisinin – reacts with iron within the cancer cell causing a generation of free radicals to damage the cancer cell and induce death to the cell.  Since cancer cells uptake relatively larger amounts of iron than normal cells, they are more susceptible to the toxic effect of artemisinin.  Artemisinin is more toxic to cancer cells than to normal cells.

·        Artemisinin and quercetagetin 6,7,3’,4’-tetramethyl ether showed significant cytotoxicity against p-388, A-549, HT-29, MCF-7 and KB tumor cells.

·        Astragalus – increases interferon production, IL-2 production, NK cell enhancement; makes T-cells and NK cells more aggressive. It improves Th1 cytokine, while reduces Th2, mild anti-tumor activity.  It is anti-viral, chemo and radiation protective; detoxifier, liver and heart protective, and reduces free radical damage.

·        Atractylodes  - The aqueous extract of Atractylodes japonica suppressed PGE(2) synthesis by inhibition of COX-2.

·        Atractylodes improves the production of IL-2 and restores immunity in people with cancer who have had immune suppressing therapies like chemotherapy.

·        Burdock seed (Articum lappa)- The hepatoprotective mechanism of A. lappa could be attributed, at least in part, to its antioxidative activity, which decreases the oxidative stress of hepatocytes, or to other unknown protective mechanisms.

·        Calcium-D-glucarate - Oral administration of large doses of Calcium-D-glucarate have been shown to lower serum estrogen levels in animals by 23% and breast cancer by 70%.

·        Calcium-D-glucarate enhances glucoronidation and subsequent excretion of carcinogens and other cancer-promoting agents.

·        Cat’s Claw bark (Uncaria tomentosa) -In addition to the antimutagenic activity, U. tomentosa extracts and fractions exert a direct antiproliferative activity on MCF7 breast cancer.

·        Cordyceps – Studies on Cordyceps mushroom extract show that the main activities are oxygen-free radical scavenging, anticancer, anti-senescence (inhibits aging of the brain), endocrine-modulating, hypolipidemic and anti-atherosclerotic.

·        Coriolus hirsutus/versicolor – Coriolus versicolor extract (CVE) significantly extended survival at five years or beyond in cancers of the stomach, colon-rectum, esophagus, nasopharynx and lung (non-small cell types), and in HLA B40-positive breast cancer subset.

·        Curcumin - In addition, curcumin exerts strong anti-invasive effects in vitro that are not estrogen dependent in the ER-negative MDA-MB-231 breast cancer cells.  These anti-invasive effects appear to be mediated through the downregulation of MMP-2 (matrix metalloproteinase) and the upregulation of TIMP-1 (tissue inhibitor of metalloproteinase), 2 common effector molecules that have been implicated in regulating tumor cell invasion. This study also demonstrates that curcumin inhibits the transcript levels of 2 major angiogenesis factors VEGF (vascular endothelial growth factor) and b-FGF (basic fibroblast growth factor) mainly in ER-negative MDA-MB-231. (Shao et al 2002)

·         Curcumin - The inhibition of cell growth and induction of apoptosis by curcumin in MCF-7 breast cancer cells might be mediated, at least partially, by its ability to down-regulate the insulin-like growth factor-1 (IGF-1) axis. (Yangqui et al 2007)

·        Curcumin inhibits cell proliferation of MDMA-MB-231 and BT-483 breast cancer cells mediated by down-regulation of NFκB, cyclin D and MMP-1 transcription.  (Liu et al 2009)

·        Curcumin treatment caused a reduction in the expression of Ki67, PCNA, and p53 mRNAs in breast cancer cells.  The results suggest that apoptosis is involved in the curcumin-induced inhibition of tumor cell growth, and genes associated with cell proliferation and apoptosis may be playing a role in the chemopreventive action of curcumin. (Ramchandran 1999)

·        CVE boosted immune cell production, ameliorated chemotherapy symptoms, and enhanced tumor infiltration by dendritic and cytotoxic T-cells.  Their extremely high tolerability, proven benefits to survival and quality of life, and compatibility with chemotherapy and radiation therapy makes them well suited for cancer management regimens.

·        Diindylmethane (DIM) - can induce apoptosis in breast cancer cells independent of estrogen receptor status by a process that is mediated by the modulated expression of the Bax/Bcl-2 family of apoptotic regulatory factors and NF-κB pathways. (Rahman et al 2004) (Hong et al 2002)

·        DIM induces Phase I and II enzymes involved in carcinogen metabolism.  They shift metabolism to the 2-hydorxylation excretory pathway of estradiol and the 16-α-hydroxylation pathway, which contains 17-Keto-metabolites that are more strongly estrogenic and which stimulate proliferation of the terminal ductotubular acinar epithelium.

·        DIM synergizes with chemotherapeutic agents by inhibiting multi-drug resistance through downregulation of P-glycoprotein (P-gp), and is a potent chemopreventive agent for hormonal-dependent cancers such as breast, prostate and cervical cancer. (Aggarwal and Ichikawa, 2005)

·        DIM synergizes with chemotherapeutic agents by inhibiting multi-drug resistance through down regulation of P-glycoprotein (P-gp) and is a potent chemopreventive agent for hormonal-dependent cancers such as breast, prostate and cervical cancer. (Aggarwal and Ichikawa 2005)

·        DIM* & I-3-C – both exhibit antitumor effects through multiple mechanisms, including gene behavior modification, growth-factor suppression, and the inhibition of NF-κB activation. - DIM (Diindylmethane) is the bioactive form of Indole-3-carbinal (I-3-C), which is a compound found in cruciferous vegetables.  DIM promotes healthier estrogen metabolism by preventing the receptor binding of “stronger” more stimulating estrogens.

·        Dong Quai – the coumarins activate white blood cells, making them capable of destroying tumor cells.  It also contains B12 and is therefore useful in the treatment of anemia caused by chemotherapy. 

·        Echinacea – promotes T-cell activation, interferon production, natural killer cell activity, antibody binding, lymphatic function and macrophage phagocytosis.

·        Echinacea has been shown to possess antitumor activity in several studies.

·        Echinacea inhibits hyaluronidase, thereby increasing wound healing and indirectly inhibiting cancer growth. This occurs through the activation of hyaluronic acid.

·        Feverfew -- also inhibits multi-drug resistance, chemo (Taxane)-enhancer Parthenolide has multifaceted anti-tumor effects against MM by altering the microenvironment (anti-inflammatory).

·        Feverfew -- has potent anti-inflammatory/anti-cancer actions including the inhibition of platelet phospholipase A2, down-regulation of TNF-α, PG2, Bcl-2 and NF-κB (suppressing STAT 3)

·         Ginkgo suppresses breast cancer: Terpenoid constituents, ginkgolikde B, inhibited the proliferation of a highly aggressive human breast cancer. (Anticancer Res. 2006 Jan-Feb;26(IA):9-22)

·        Glycyrrhizic acid, present in licorice, inhibits lipoxygenase and cyclooxygenase, inhibits protein kinase C and down regulates the epidermal growth factor receptor (EGF).

·        Gotu kola can also stimulate the production of tissue plasminogen activator (tPA), which is associated with the ability to break down fibrin.  Fibrin formation and platelet aggregation are important steps to tumor formation.

·        Green Tea extract (GTE) – demonstrates profound cancer-suppressing effects including inhibition of various tumor promoting growth factors such as: VEGF, Protein kinase C, tissue-type plasminogen activator (t-PA), PG2, matrix metalloproteinase, and NFκB.

·        GTE -- also modulates androgen and other hormones, enhances the effectiveness of certain chemotherapeutic drugs, is anti-inflammatory, via the COX and LOX pathways, possesses lipolytic activity, reduces lipids and lipoproteins, inhibits muscle wasting and is antiviral.

·        Honokiol - Here we show that Honokiol, a natural dietary product isolated from an extract of seed cones from Magnolia grandiflora, can decrease PI3K/mTOR pathway-mediated immunoresistance of glioma, breast and prostate cancer cell lines, without affecting critical proinflammatory T cell functions. (Crane et al 2009)

·        Honokiol inhibits in vitro and in vivo growth of breast cancer through induction of apoptosis and cell cycle arrest.  (Wolf et al, 2007)

·        I-3-C (indole-3-carbinol) – which converts into DIM, induced marked reduction of EGFR in human breast cancer cell lines prior to cell death. (Moiseeva, Heukers & Manson 2006)

·        ITC also can induce apoptosis, alter steroid hormone metabolism, regulate estrogen receptor response, stabilize cellular proliferation and offer protection from chemotherapy.

·        ITC inhibits activator protein 1 (AP-1) and MAPK signaling pathways.

·        Licorice polyphenols induce apoptosis in cancer cells.

·        Licorice’s anti-inflammatory mechanism is believed to be due to its protective effect on the hepatic cellular membranes, which may explain its ability to lower the serum transaminase levels in patients with chronic HCV.

·        Magnolol and honokiol – have been shown to suppress COX-2, induce apoptosis in cancer cells, and inhibit metastasis. 

·        May Apple (Podophyllum peltatum) – contains a group of resinous components found in the alcohol extract referred to as podophyllotoxins, which possess antitumor activity in both animal and human studies.

·        Milk Thistle (Silybum marianum) Silymarin – exerts exceptional anticarcinogenic effects against breast cancer through an apparent down-regulatory effect on certain breast cancer promoting enzymes, namely cyclin-dependent kinases (CDKs) in the G1 phase of the cell cycle.

·        Milk thistle is a liver protectant that stabilizes and strengthens the structure of the cell membrane.  It is a great free radical scavenger and it protects the liver and kidneys against damage caused by drugs, heavy metals and chemotherapy.

·        Mistletoe - A German study showed that mistletoe-treated patients survived for a mean of 4.23 yeas after inclusion in the study versus 3.05 years for the control group.  A second part of the study done among 17 pairs of patients with breast cancer with axillary metastases showed a mean survival time increase from 2.41 years in the control group to 4.79 years in the mistletoe-treated group.

·         N-acetylcysteine (NAC) – enhances apoptosis through inhibition of NF-κB. (Biol Chem 2004)

·        Omega-3 fatty acids - Diets high in omega3 fatty acids exert suppressive effects on cancer growth and are associated with impaired angiogenesis.  Both EPA and DHA have shown to inhibit metastasis of several cancer cell lines including breast, prostate and colon cancer.  For example, one study found that total n-6 poly-unsaturated fatty acids may be contributing to the high risk of breast cancer in the United States and that specific long chain n-3 poly-unsaturated fatty acids derived from fish oils may have a protective effect. (Bagga et al 2002)

·        Pacific Yew – (Taxus brevifolia) – The yew tree contains a group of unique alkaloids referred to as taxanes that have been shown to exhibit significant antineoplastic actions.  Taxanes represent the most important class of antitumor agents introduced in cancer therapy in the last decade.  The first member of the family isolated from the yew tree was paclitaxel (taxol).  Paclitaxel and docetaxel are two of the most effective chemotherapeutic drugs used today.  They are used to treat many types of cancers including ovarian, breast and non-small cell lung cancer.

·        Panax ginseng – extract showed inhibition of the p38 MAPK pathway and NF-κB in vitro, and inhibition of proinflammatory cytokines in vivo.

·        Panax ginseng extract -- and its chemical constituents have been tested for their inhibiting effect on putative carcinogenesis mechanisms (e.g. cell proliferation and apoptosis, immune-surveillance, angiogenesis); in most experiments inhibitory effects were found.

·        Panax ginseng extract-- has been shown to enhance the overall activity of the immune system including antibody response, Natural Killer (NK) cell activity, interferon production and the proliferative and phagocytotic ability of the immune system.

·        Paw Paw – (Asimina triloba, Annonaceae) – Annonaceous acetogenins are a group of potential anti-neoplastic agents, which have been isolated from Paw paw seeds, bark and twigs, as well as other annonaceae plants.  They act selectively to inhibit cancer cellular energy (ATP).

·        Paw Paw - Two new bioactive mono-tetrahydrofuran (THF) gamma-lactone acetogenins, asitrilobins C (1) and D (2), were isolated from the seeds of paw paw.  Compounds 1 and 2 showed selective cytotoxicity comparable with adriamycin for the breast carcinoma (MCF-7) and the colon adencarcinoma (HT-29) cell lines.

·         Pomegranate juice extract  - The flavonoids-rich polyphenols fractions from the pomegranate fruit exert anti-proliferative, anti-invasive, anti-eicosanoid and pro-apoptotic actions in breast and prostate cancer cells and anti-angiogenic activities. Pomegranate juice extract has shown to inhibit breast cancer, lung and prostate cancer. (Breast Cancer Research & Treatment 71(3):203-17, 2002 Feb)

·        Rabdosia (Rabdosia rubescens Hora) – contains oridonin which effectively inhibited the proliferation of a wide variety of cancer cells including those from prostate (LNCaP, DU145, PC3), breast (MCF-7, MDA-MB231), non-small cell lung (NSCL) (NCI-H520, NCI-H460, NCI-H1299) cancers, acute promyelocytic leukemia (NB4) and glioblastoma multiforme (U118, U138).

·        Reishi mushroom powdered extract (RPE) -- inhibited active NF-κB, demonstrating strong inhibition of cancer cell migration.

·        Reishi mushroom powdered extract (RPE) -- suppressed cell adhesion and cell migration of highly invasive breast and prostate cancer cells, suggesting its potency to reduce tumor invasiveness. 

·        Resveratrol – IGF-II is a potent mitogen and inhibitor of apoptosis in breast cancer. Resveratrol regulates insulin-like growth factor-II (IGF-II) in breast cancer cells.  (Vyas, Asmerom and DeLeon, 2005)

·        Rhaponticum (Luzea carthamoides) - Rhaponticum extract increases the resistance of hepatocytes to toxins and possesses the capacity for blocking processes of free-radical oxidation.

·        Rhodiola rosea extract -- has been shown to enhance the antitumor effects of the chemotherapeutic drug cyclophosphamide (Cytoxin), while at the same time assisting in the regenerative process of the immune system.

·        Rhodiola rosea extract -- has been shown to enhance the antitumor effects of the chemotherapeutic drug cyclophosphamide (Cytoxin), while at the same time assisting in the regenerative process of the immune system.

·        Rhodiola rosea extract -- has shown to shorten the recovery time on suppressed while blood cells following chemotherapy or radiation treatment.

·        Rhodiola rosea extract -- has shown to shorten the recovery time on suppressed white blood cells following chemotherapy or radiation treatment.

·        Rhodiola rosea extract - In animal experiments, adding Rhodiola rosea extract to a protocol with Adriamycin resulted in an improved inhibition of tumor dissemination (compared to Adriamycin alone) and the combined protocol prevented liver toxicity.

·        Rhodiola rosea extract - In animal experiments, adding Rhodiola rosea extract to a protocol with Adriamycin resulted in an improved inhibition of tumor dissemination (compared to Adriamycin alone) and the combined protocol prevented liver toxicity.

·        Silymarin has also demonstrated a synergistic effect when combined with cisplatin and doxorubin in treatment of ovarian cancer.

·        Silymarin has been shown to provide substantial protection against different stages of UBV-induced carcinogenesis.  Silymarin’s action can be accounted for by the inhibition of NF-κB activation normally induced UV damage, which in turn leads to the inhibition of COX-2, pro-inflammatory cytokines, and the suppression of oncogene expression.

·        Silymarin possesses exceptionally high protective effects against tumor promotion, primarily targeted against stage I tumors.

·        Silymarin protects kidneys and liver from cisplatin induced toxicity without interfering with the cytotoxic effects of the drug against cancer cells.

·        Sulforaphane - One study showed that sulforaphane can block late stages of the cancer process by disrupting components of the cell called microtubules, and may help to block the growth of breast cancer cell growth.

·        Sulforaphane blocked the formation of mammary tumors in rats treated with a potent carcinogen

·        Sulforaphane induces p21 expression an important gene-protein involved in maintaining and regulating cell behavior.  High levels of p21 are associated with cancer protection while the lost expression of p21 is associated with cancer progression.

·        Sulforaphane inhibits human mcf-7 mammary cancer cell mitotic progression and tubulin polymerization.

·        Sulforaphane is an isothiocyanate (ITC) found in organic broccoli sprouts. - The ITC sulforaphane induces p53-independent apoptosis and modulates Bcl-2 family protein expression.

·        Ukrain (NSC-631570) is a semisynthetic derivative of the Chelidonium majus L. alkaloid chelidonine and the alkylans thiotepa.  The potent proapoptotic effects of Ukrain are not due to the suggested “Ukrain-molecule” but to the cytotoxic efficacy of Chelidonium majus L. alkaloids including chelidonine.

References

Books

1. Bagachi, Debasis & Harry G. Preuss, Phytopharmaceuticals in Cancer Chemoprevention, CRC Press, Boca Raton, 2005

2. Boik, John, Natural Compounds in Cancer Therapy, Oregon Medical Press, Princeton, MN, 2001

3. Boik, John, Cancer & Natural Medicine, A Textbook of Basic Science and Clinical Research, Oregon Medical Press, Princeton, MN, 1996

4. Chernecky, Cynthia C, and Barbara J. Berger, Laboratory Tests and Diagnostic Procedures, Saunders, St. Louis, 2008

5. Yance, Donald, Herbal Medicine, Healing & Cancer, Keats Publishing, Lincolnwood (Chicago) IL, 1999

Monographs

6. Yance, Donald, “A Novel Approach to Cancer Treatment”, Medicines from the Earth 2005, Official Proceedings, June 4^th to June 6^th, 2005, pages 189-213, Herbal Educational Services, Ashland, OR, 2005

7. Yance, Donald, “A Revolutionary Approach to Weight Management”,  Medicines from the Earth 2006, Official Proceedings, June 2 through June 5, 2006, pages 154-168, Herbal Educational Services, Ashland, OR, 2006

8. Yance, Donald, “Andrographis (Andrographis paniculata)” (Monograph) 2008
9. Yance, Donald, “Astragalus root (Astragalus membranasceus)” (Monograph) 2009

10. Yance, Donald, “Boswellia serrata (Indian Frankincense)” (Monograph) 2009
11. Yance, Donald, “Botanical Compounds for Cancer-Related Pain”,  Medicines from the Earth 2006, Official Proceedings, June 2 through June 5, 2006, pages 169-190, Herbal Educational Services, Ashland, OR, 2006

12. Yance, Donald, “Cancer and Inflammation”, Medicines from the Earth, Official Proceedings, May 29-June 1, 2009, pages 132-140, Herbal Educational Services, Ashland, OR, 2009

13. Yance, Donald, “Carnitine” (Monograph) 2009
14. Yance, Donald, “Cat’s claw (Uncaria tomentosa) Uno de gato” (Monograph) 2009

15. Yance, Donald, “Cholesterol, Statins and the Truth about Cardiovascular Health and Disease”, (Monograph)  2009

16. Yance, Donald, “Cholesterol, Statins, and the Truth about Cardiovascular Health”, Medicines from the Earth 2005, Official Proceedings, June 4^th to June 6^th, 2005, pages 165-188, Herbal Educational Services, Ashland, OR, 2005

17. Yance, Donald, “Copper Antagonists Inhibit Angiogenesis” (Monograph) 2009
18. Yance, Donald, “Donald Yance’s Eclectic Triphasic Medical System (ETMS): An Integrative Wholistic Approach to Treating and Preventing Cancer”, (Monograph) 2009

19. Yance, Donald, “EPA and DHA rich fish oil” (Monograph) 2009
20. Yance, Donald, “Feverfew” (Monograph) 2008
21. Yance, Donald, “Ginger” (Monograph) 2008
22. Yance, Donald, “Grape (Vitis vinifera) & Japanese Knotweed (Polygonum cuspidatum)” (Monograph) 2009

23. Yance, Donald, “Green Tea” (Monograph) 2008
24. Yance, Donald, “Hyper-coagulation and Cancer” (Monograph) 2009
25. Yance, Donald, “Insulin Resistance” (Monograph) 2004
26. Yance, Donald, “Korean ‘Asian’ Ginseng & American Ginseng” (Monograph) 2009

27. Yance, Donald, “L-Arginine” (Monograph) 2009
28. Yance, Donald, “Licorice” (Monograph) 2009
29. Yance, Donald, “Magnolia bark” (Monograph) 2009
30. Yance, Donald, “Milk Thistle” (Monograph) 2009
31. Yance, Donald, “Natural Compounds that modulate the Bcl-2 Protein” (Monograph) 2008

32. Yance, Donald, “Osteoporosis, Nutrition, and Botanical: Myths, Perceptions, Truths and Natural Solutions”, Medicines from the Earth, Official Proceedings, May 29-June 1, 2009, pages 141-149, Herbal Educational Services, Ashland, OR, 2009

33. Yance, Donald, “Prostate Cancer, A Revolutionary Wholistic Approach.  Applications for Botanical and Nutritional Medicine”, (Monograph) 2009

34. Yance, Donald, “Pterocarpus marsupium” (Monograph) 2009

35. Yance, Donald, “Quercetin” (Monograph) 2009
36. Yance, Donald, “Rhaponticum carthamoides”, Journal of the American Herbalists Guild, Fall/Winter 2004 (Vol. 5, No.2)

37. Yance, Donald, “Selenium” (Monograph) 2009
38. Yance, Donald, “Skullcap, Chinese” (Monograph) 2009
39. Yance, Donald, “Sulforaphane glucosinolate (SGC)” (Monograph) 2005
40. Yance, Donald, “The p53 suppressor gene” (Monograph) 2009
41. Yance, Donald, “Turmeric” (Monograph) 2009

Online

42. PubMed, http://www.ncbi.nlm.nih.gov/pubmed/

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