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Thread: Woops! Study Accidentally Finds Chemotherapy Makes Cancer Far Worse

  1. #1
    Distinguished Community Member houghchrst's Avatar
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    Default Woops! Study Accidentally Finds Chemotherapy Makes Cancer Far Worse

    Woops! Study Accidentally Finds Chemotherapy Makes cancer worse

    NaturalSociety
    August 6, 2012

    A team of researchers looking into why cancer cells are so resilient accidentally stumbled upon a far more important discovery. While conducting their research, the team discovered that chemotherapy actually heavily damages healthy cells and subsequently triggers them to release a protein that sustains and fuels tumor growth. Beyond that, it even makes the tumor highly resistant to future treatment.
    Reporting their findings in the journal Nature Medicine, the scientists report that the findings were ‘completely unexpected’. Finding evidence of significant DNA damage when examining the effects of chemotherapy on tissue derived from men with prostate cancer, the writings are a big slap in the face to mainstream medical organizations who have been pushing chemotherapy as the only option to cancer patients for years.
    The news comes after it was previously ousted by similarly-breaking research that expensive cancer drugs not only fail to treat tumors, but actually make them far worse. The cancer drugs were found to make tumors ‘metasize’ and grow massively in size after consumption. As a result, the drugs killed the patients more quickly.
    Known as WNT16B, scientists who performed the research say that this protein created from chemo treatment boosts cancer cell survival and is the reason that chemotherapy actually ends lives more quickly. Co-author Peter Nelson of the Fred Hutchinson Cancer Research Center in Seattleexplains:
    “WNT16B, when secreted, would interact with nearby tumour cells and cause them to grow, invade, and importantly, resist subsequent therapy.”
    The team then complimented the statement with a word of their own:
    “Our results indicate that damage responses in benign cells… may directly contribute to enhanced tumour growth kinetics.”
    Meanwhile, dirt cheap substances like turmeric and ginger have consistently been found to effectively shrink tumors and combat the spread of cancer. In a review of 11 studies, it was found that turmeric use reduced brain tumor size by a shocking 81%. Further research has also shown that turmeric is capable of halting cancer cell growth altogether. One woman recently hit the mainstream headlines by revealing her victory against cancer with the principal spice used being turmeric.
    This accidental finding reached by scientists further shows the lack of real science behind many ‘old paradigm’ treatments, despite what many health officials would like you to believe. The truth of the matter is that natural alternatives do not even receive nearly as much funding as pharmaceutical drugs and medical interventions because there’s simply no room for profit. If everyone was using turmeric and vitamin D for cancer (better yet cancer prevention), major drug companies would lose out.

    Additional sources:

    http://www.ncbi.nlm.nih.gov/pubmed/21775121
    http://www.ncbi.nlm.nih.gov/pubmed/1913898
    Last edited by houghchrst; 08-09-2012 at 08:37 AM.

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    Distinguished Community Member gpawelski's Avatar
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    Default Treatment-induced damage to tumor microenvironment promotes chemoresistance

    "In the lab, you can cure almost any cancer: you just give a huge dose of toxic chemotherapy to the cancer cells in the petri dish. But you can't do that to patients, because the high dose would not only kill cancer cells but also healthy cells." How many times have I seen this happen with labs using single-endpoint assays (and basic leukemic type assays).

    By examining drug-induced cell death events in native-state three-dimensional (3D) microclusters, the functional profiling platform recognizes the interplay between cells, not only stromal, but vascular elements, cytokines, macrophages, lymphocytes, mesenchymal cells, fibroblasts, smooth muscle cells, pericytes and other microenviromental factors known to be crucial for clinical response prediction. The human tumor primary culture microspheroid contains all of these elements.

    The (slippery) polypropylene material prevents the attachment of fibroblasts and epithelial cells and encourages the tumor cells to remain in the form of three-dimensional (3D) floating clusters. Our body is already 3D (not 2D) in form, making this novel step better replicate that of the human body. When allowed to grow in vitro, "fresh" living cancer cells develop into these tiny microspheroid clusters that form a complex biosystem in which each malignant cell reacts upon it fellow colonists in subtle but important ways.

    The microclusters recapitulate the human tumor environment, while the "3D" advancement recreates the extracellular matrix (metalloproteinases). The functional profiling platform studies cancer response to drugs within this microenvironment, enabling it to provide a snapshot of cancer's behavior within the human body and provides a more accurate representation of how cancer cells are likely to respond to treatment in the clinic.

    Researchers at the University of Washington School of Medicine in Seattle have found that when cells become cancerous, they also become 100 times more likely to genetically mutate than regular cells. The findings may explain why cells in a tumor have so many genetic mutations, but could also be bad news for cancer treatments that target a particular gene controlling cancer malignancy.

    If cancer cells do indeed become "mutator" cells, traditional chemotherapy and other "targeted" drugs may never be very effective against advanced tumors. This means that cancer cells in a tumor will have mutations that protect them from therapeutics.

    A chemotherapy drug may target a particular oncogene, which is a gene that affects the malignancy of a particular cell. But if cancer cells are mutator cells, a single tumor may have cells with many different types of oncogenes and drug-resistant genes.

    A chemotherapy drug may kill off some of the cancerous cells, but millions of other cells in the tumor will live on. To be effective, a chemotherapy treatment may have to target more than one oncogene: so-called combination chemotherapy. The more mutations, the further along the tumor may be in its development to malignancy or metastasis.

    To lay the foundation for personalized cancer treatment, the ultimate "driver" could be the "functional" profiling platform. Cells speak to each other and the messages they send are interpreted via intracellular pathways. You wouldn't know this using genotype analysis. Phenotype analysis provides the window. It can test various cell-death signaling pathways downstream.
    Gregory D. Pawelski

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