Cancer

Pine Bark, Pycnogenol, havupuu-uutejuoma
Pine bark extract boost blood flow and heart health



Sodium Dichloroacetate, DCA
puredca.com
Tumors may be non-malignant or malignant, spreading tumors associated with cancer. Cancers frequently mutate and evolve up to 10 changes in their cancer cell DNA as they develop, though they may begin with a single nucleotide polymorphism (SNP). Cancer never occurs in non-mitotic cells, but only in mitotic, dividing cells. Cancerous tumors develop clonally from a single cell, as indicated by an analysis of X-inactivation of the X1 or X2 alleles of female tumor cells. X-inactivation is found in either X1 or X2 alleles in a group of normal cells, but is always entirely X1 or entirely X2 in associated cancer tumor cells, indicating a tumor cell clonal origin from a single cell.

Cancer tumor cells, unlike normal cells in the body, are not subject to density-dependent inhibition of cellular proliferation, and so grow to high cellular densities without arriving at the quiescent G0 state of the cell cycle. Some tumor cells may produce their own growth factors, producing autocrine growth stimulation. These cells typically lack cell surface adhesion molecules, a factor promoting metastasis of cancer tumor cells.

Cancer tumor cells typically emit proteases such as collagenase allowing them to penetrate the extracellular matrix, and produce factors supporting angiogenesis (capillary growth) required for tumor enlargement beyond about a million cells.

Angiogenesis inhibitors
Internal DNA damage due to the original mutation may prevent cancer cell apoptosis, so that cancer cells often survive in the abscence of growth factors required by their normal counterparts. Cancer cells often also activate hTERT to allow continued cell division. Thus drugs inhibiting hTERT transcription with telomerase inhibitors, drugs promoting inhibition of angiogenesis, and drugs promoting apoptosis (often via telomerase inhibitors) provide targeted approaches to cancer treatment. Colon cancer is usually a consequence of eating meat fat, which results in secondary bile products produced by bacteria that generate carcinogens. Nearly 90% of cancers are epithelial cell carcinomas, while leukemias and lymphomas account for 7% of cancers and sarcomas and brain cancers are rare.

Cancer incidence rises steeply as a function of age, rising in nearly exponential form from t0=25. However, cancer is often associated with a substantial delayed-onset time in regard to exposure to carcinogens. The time delay between carcinogen exposure to the onset of cancer may be on the order of a decade or two

Telomerase inhibitors are often employed to cure cancer. Treatment of tumors is more effective when a telomerase inhibitor is given with angiogenesis inhibitors. This technique fails when the cancer uses the ALT mechanism to continue cell division. Most cancers (85%-90%) do not use the ALT mechanism. Those that do especially include specific subtypes of soft tissue sarcomas where ALT occurs most often in tumors with complex karyotypes, astrocytic brain tumors and osteosarcomas. Monoclonal antibodies may be useful in treating cancers not treatable with telomerase inhibitors. About 90% of human cancers are carcinomas or adenocarcinomas in epithelial tissue. More than 50% of human cancers contain inactivating mutations of the p53 gene.
Mutant p53 enhances nuclear factor kappaB activation by tumor necrosis factor alpha in cancer cells, Cancer Research 76:2396-2401.

NF-kB activates genes associated with inflammation, proliferation, angiogenesis, metastasis, and resistance to apoptosis that can be dampened with NF-kB inhibitors. In cases involving p53 mutation cell division may continue past the M1 senescence checkpoint at a telomere length of about 4000 bp until telomeres are so short that they fuse at the critical length. (See p38, telomere fusion, and cancer.) Then fused chromosomes lead to fusion-bridge breakage, non-reciprocal translocations from fusion-bridge breakage and aneuploidy supportive of tumor initiation. Adeno-associated virus AAV2 may be used to transfect skeletal muscles, neurons, vascular smooth muscle cells and hepatocytes, and apparently kills cancer cells without harming healthy ones

Copper from beef seems to help cancer spread, so that it is useful to avoid beef and chelate copper with resveratrol, quercetin, R alpha lipoic acid, curcumin, or carnosine.

Modified Citrus Pectin
inhibits cancer metastasis, as does regular citrus pectin to a lesser degree.

Vitamin D
Women deficient in vitamin D have a 253% increased risk of colon cancer, and women with the lowest level of vitamin D had a 222% increased risk of breast cancer. Men with higher levels of vitamin D have a 52% reduced incidence of prostate cancer. "In September 2006, a long-term study concluded that taking vitamin D can substantially cut the risk of pancreatic cancer (as well as other cancers) by up to 50%."  

Vitamin K2 
reduces prostate cancer risk.

Soy
Populations with diets rich in phytoestrogens (as in soy products, which contain the phytoestrogens genistein and daidzein) have a lower risk of hormonally-induced cancers.

Aloe Arborescens
-3-4 large aloe arborescens leaves 
-1.1 lbs. of pure honey  
-2-3 Tablespoons of grappa, whisky, cognac (pure alcohol, wine, beer and liqueurs cannot be used).  (This ingredient is considered a distillate responsible for accelerating the cleansing process and dissolving ingredients in the aloe that our bodies are unable to fully absorb.)
-If using as a cancer or AIDS cure, take 2 tablespoonfuls 3 times a day for 10 days, discontinue use for 10 days, and then resume for another 10 days.  Follow this program until all signs of cancer are gone.
-If using as a preventative measure, take 2 tablespoonfuls 3 times a day for 10 days once per year.
-Store in a dark jar in your refrigerator and enjoy!