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Friday, September 9, 2016

Phytochemicals for Treatment of Myeloma (Multiple Myenoma)

Kyle J. Norton(Scholar, Master of Nutrients), all right reserved.
Health article writer and researcher; Over 10.000 articles and research papers have been written and published on line, including world wide health, ezine articles, article base, healthblogs, selfgrowth, best before it's news, the karate GB daily, etc.,.
Named TOP 50 MEDICAL ESSAYS FOR ARTISTS & AUTHORS TO READ by Disilgold.com Named 50 of the best health Tweeters Canada - Huffington Post
Nominated for shorty award over last 4 years
Some articles have been used as references in medical research, such as international journal Pharma and Bio science, ISSN 0975-6299.


Phytochemials are defined as a group of chemical compound found naturally in plants, including fruits, vegetables, beans, grains, etc. Many studies have proven that they can because of certain phytochemicals, but for what ever reason, there are either no clinical trials follow through or the studies can not make to stage of clinical trials. Do not expect the pharmateutical or foods industrial companies to pay for the researches, as the discovery of the phytochemicals to cure cancers can only dampen the profits of both industries as phytochemicals can not be patented.

Cancer is a class of diseases in which a group of cells growing and multiplying disordered and uncontrollable way in our body, have become progressively worse and damaged other healthy tissues, sometimes spreads to other organs in the body via lymph or blood and results may be in death.
Food intake can help to prevent and treat cancers.


             Myeloma (Multiple Myenoma)

Multiple myeloma (Myeloma) is a type of cancer originated from plasma cells in the bone marrow. It is a type of white blood cell normally responsible for the production of antibodies to protect our body against infection with some characteristics.

Types of food to prevent and treat Multiple myeloma (Myeloma)
1. Turmeric
In the study of Curcumin (diferuloylmethane) down-regulates the constitutive activation of nuclear factor-kappa B and IkappaBalpha kinase in human multiple myeloma cells, leading to suppression of proliferation and induction of apoptosis, scientists at the The University of Texas MD Anderson Cancer Center, showed that Curcumin suppressed the constitutive IkappaBalpha phosphorylation through the inhibition of IKK activity. Curcumin also down-regulated the expression of NF-kappaB-regulated gene products, including IkappaBalpha, Bcl-2, Bcl-x(L), cyclin D1, and interleukin-6. This led to the suppression of proliferation and arrest of cells at the G(1)/S phase of the cell cycle. Suppression of NF-kappaB complex by IKKgamma/NF-kappaB essential modulator-binding domain peptide also suppressed the proliferation of MM cells. Curcumin also activated caspase-7 and caspase-9 and induced polyadenosine-5'-diphosphate-ribose polymerase (PARP) cleavage. Curcumin-induced down-regulation of NF-kappaB, a factor that has been implicated in chemoresistance, also induced chemosensitivity to vincristine and melphalan(1).

2. Green tea
(-)-epigallocatechin-3-gallate extracted from green tea have exerted the inhibitory effect against multiple myeloma cells. Dr. Shammas MA and the research team at Veterans Administration Boston Health Care System, and Dana Farber Cancer Institute/Harvard Medical School, showed that EGCG interacts with the 67-kDa laminin receptor 1 (LR1), which is significantly elevated in myeloma cell lines and patient samples relative to normal PBMCs. RNAi-mediated inhibition of LR1 resulted in abrogation of EGCG-induced apoptosis in myeloma cells, indicating that LR1 plays an important role in mediating EGCG activity in MM while sparing PBMCs. Evaluation of changes in gene expression profile indicates that EGCG treatment activates distinct pathways of growth arrest and apoptosis in MM cells by inducing the expression of death-associated protein kinase 2, the initiators and mediators of death receptor-dependent apoptosis (Fas ligand, Fas, and caspase 4), p53-like proteins (p73, p63), positive regulators of apoptosis and NF-kappaB activation (CARD10, CARD14), and cyclin-dependent kinase inhibitors (p16 and p18)(2).

3. Skins and seed of grape and wine
In the study to investigate the effect of Resveratrol trans-3, 4', 5,-trihydroxystilbene, insuppressing the multiple myeloma (MM), found thatResveratrol activated IRE1α as evidenced by XBP1 messenger RNA splicing and phosphorylation of both IRE1α and its downstream kinase c-Jun N-terminal kinase in MM cells. These responses were associated with resveratrol-induced cytotoxicity of MM cells. Resveratrol selectively suppressed the transcriptional activity of XBP1s while it stimulated gene expression of the molecules that are regulated by the non-IRE1/XBP1 axis of the ER stress response. Luciferase assays indicated that resveratrol suppressed the transcriptional activity of XBP1s through sirtuin 1, a downstream molecular target of resveratrol. Chromatin immunoprecipitation studies revealed that resveratrol decreased the DNA binding capacity of XBP1 and increased the enrichment of sirtuin 1 at the XBP1 binding region in the XBP1 promoter(3).

4. Carrot
Retinoic acid found of a measure amount in carrot has a potential in prevent and treat Myeloma (Multiple Myenoma). Study showed that The inhibitory effect of cRA was significantly superior to tRA (P = 0.0129) and IFN-alpha, similar to IFN-gamma and DEX. The combinations of cRA + IFN alpha, tRA + IFN-gamma, tRA + DEX did not show any synergistic effect on myeloma proliferation. In contrast, the combination cRA + DEX (0.29 +/- 0.04, M +/- SEM) markedly increased the effect of both cRA and DEX used as single agents. Ig synthesis was not significantly affected by CRA, tRA, IFN-gamma and the combination tRA + IFN-gamma. As expected, only IFN-alpha (P = 0.002) and DEX (P < 0.001) inhibited Ig production(4).

5. Etc.

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Sources
(1) http://www.ncbi.nlm.nih.gov/pubmed/12393461
(2) http://www.ncbi.nlm.nih.gov/pubmed/16809610
(3) http://www.ncbi.nlm.nih.gov/pubmed/21723843
(40 http://www.ncbi.nlm.nih.gov/pubmed/7734354

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