Prostate Cancer
Prostate cancer is a disease of aging,
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Prostate cancer is a disease of aging, brought about by changes in cellular biochemistry which result in an imbalance in the prooxidant-antioxidant balance, and in the cellular response to androgens which this brings about. No doubt there is also a genetic susceptibility underlying all this, but nevertheless, prostate cancer strikes as many as 75 percent of men by age 80, so there is more than genetics at work. Many advanced cases of prostate cancer become resistant to chemotherapy, making the prognosis for those men dismal. It has been shown that many multidrug resistance associated proteins are involved in this resistance to therapy, and if their exact role can be elucidated, perhaps it will be possible to break this resistance. Non-steroidal-antiinflammatory-drug-activated gene protein has been found consistently in prostate cancers, but not in benign prostate tissue, and rarely in other tumors. ItĘs role in tumorigenesis of prostate cancer remains to be elucidated. This paper will review some of recent biochemical investigations into mechanisms involved in prostate cancer, and discuss their findings.Non-steroidal antiinflammatory drug (NSAID), NSAID-activated gene (NAG-1), Sa-dihydrotestosterone (DHT) In the United States, prostate cancer is the most commonly diagnosed solid tumor in men, and can be found in a pre-clinical or clinical form in approximately 30 percent to 40 percent of men by age 30 to 50 years (1). This figure
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l-Anti-Inflammatory Drugs (NSAID)-activated gene (NAG-1) protein has been shown previously to be overexpressed in prostate cancer. These researchers used immunohistochemical techniques and Western blotting using rabbit polyclonal antibody to NAG-1 to examine 50 malignant tissues obtained at prostatectomy and 17 from benign cases (2). Deparafinized tissue samples were quenched in hydrogen peroxide in methanol, rinsed in water, tris-buffered-saline, and then exposed to Ventana, an inhibitor solution. The sections were reacted with rabbit polyclonal whole-serum antibody to NAG-1/PTGF(?) at a 1 in 300 dilution for 2 hours at room temperature. A secondary antibody LSAB was applied for 25 minutes. The chromagen was diaminobenzidine, and slides were counterstained with hematoxylin. The positive control for NAG-1 was placental tissue, and the negative control was prepared by applying nonimmune whole rabbit serum at a 1 in 300 dilution, or NAG-1 antiserum preincubated with synthetic NAG-1 protein to prostatectomy tissue.
Two observers, blinded to clinical data, rated the percentage of cytoplasmic reactivity and its intensity (2). They viewed specimens of cancer, high-grade prostatic intraepithelial neoplasia, atrophy/postatrophi
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Some common words found in the essay are:
Drugs NSAID-activated, DHT R1881, Ki57 Antibodies, Opti-4CN Bio-Rad, Van Bussell, Abstract Prostate, Introduction United, Sa-dihydroxytestosterone DHT, Rago Wilding, Upregulation Ki-67, prostate cancer, multidrug resistance, oxidative stress, -glutamyl transpeptidase, resistance associated, multidrug resistance associated, nsaid-activated gene, advanced prostate cancer, mitochondrial activity, gene nag-1, nag-1 protein, advanced prostate, resistance associated protein, increase oxidative stress, nsaid-activated gene nag-1,
Approximate Word count = 2268
Approximate Pages = 9 (250 words per page)
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