Theory of Beta-Glucuronidase |
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We
searched PubMed and found a twenty-year-old abstract on a concept for
cancer therapy: Most cancer cells
differ from normal cells in that they show higher beta-glucuronidase activity
and lower pH of their cytoplasm. Anti-cancer drugs can be designed which
take advantage of these gradients to deliver maximal toxicity to tumors
and minimal toxicity to normal tissue. Many design criteria are suggested
here, the most basic of which is the use of the glucuronide structure,
in which glucuronic acid acts as a protective carrier of a toxic fragment
which becomes active when split off by the beta-glucuronidase at the tumor
site. The high beta-glucuronidase activity in cancer cells is also discussed
here as a possible explanation for some of the pathognomonic features
of a malignant growth: the automatic proliferation of tumor tissue, the
invasion of tumors into adjacent tissue, the metastases to remote sites,
and the weak response of the immune system. Med
Hypotheses This paper, which supports some of David Rubin's later work on his drug, is consistent with a paper in Cancer Res 1979 Sep;39(9): 3485-3490 Serum tyrosinase in malignant disease . . . " Chen YM, Lim BT, Chavin W. Chen's paper reported higher serum tyrosinase "in many persons with metastatic diseases," i.e. in cancer generally, although "The highest activity was observed in melanoma and breast carcinoma." But a new assay had already found lack of higher tyrosinase activity except in melanoma. Int J Cancer 1977 Nov 5; 20 (5):689-693 Tyrosinase activity in the sera of patients with malignant melanoma: method and specificity. Nishioka K, Romsdahl MM, Fritsche HA Jr, McMurtrey MJ. Research on tryosinase
in melanoma continues to be very active but tyrosinase seems to be unimportant
for most other cancers including prostate cancer. Dr. Rubin, it seems
fair to say, has never modified his basic theory to bring it in line with
new technology and research (unless to use those for window-dressing). PubMed atNIH (National Institutes of Health). Search medical abstracts |
We
E-mailed The theory was that the enzyme, b-glucosidase was low in normal cells and higher in cancer cells, etc. This was a misinterpretation of the work of Anlyan et al in 1948 who reported higher b-glucuronidase in cancer cells. But both were subsequently proved incorrect, when all cells were found to have similar amounts of b-glucuronidase (and all mammalian cells have no b-glucosidase - cancer and normal). Differences in respiration (oxidative and non-oxidative) thought to be present (Warburg) between cancer and normal cells were also found later to be insignificant despite the Nobel Prize having been won for that "discovery." Cancer cells can respire in absence of oxygen (fermentation) but do not have to. Fermentation produces lactic acid which lowers the pH, but nothing has ever come of that quality. Medical Hypotheses is a journal that publishes anyone's ideas regardless of degree of connection to reality. It published Charles Gurchot's original laetrile ideas. But none of the above would give a rationale for why "glucuronides" would have anticancer effects. It is not surprising that followers and takers of glucuronides swear by them, as they did and do with laetrile, antineoplastons, etc. It is cult behavior, no matter which method is chosen, and none of them works. W. Sampson, MD Quackwatch Home Page Operated by Stephen Barrett, M.D. Quackwatch
"Where to Complain or Seek Help" NEXT: People told us David Rubin has a lot of patents. We took a look and found they began from a laetrile reading list. And ended up 15 years later being used to make drugs tested (one notch up from laetrile) in clinical trials in Mexico. |
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PSA Rising Magazine April 15, 1998 http://www.psa-rising.org © 1997-1998. |