Faculty Research 1980 - 1989

Role of urinary beta-glucuronidase in human bladder cancer.

Document Type

Article

Publication Date

1984

Keywords

Aged, Alpha-Galactosidases: ur, Beta-Galactosidases: ur, Bladder-Neoplasms: en, Comparative-Study, Female, Glucuronidase: ur, Glycoside-Hydrolases: ur, Hexosaminidases: ur, Human, Lysosomes: en, Male, Middle-Age, Reference-Values, SUPPORT-NON-U-S-GOVT, SUPPORT-U-S-GOVT-P-H-S

First Page

3620

Last Page

3623

JAX Source

Cancer Res 1984 Aug; 44(8):3620-3.

Grant

RR05467

Abstract

It has been suggested that high levels of urinary beta-glucuronidase may increase an individual's risk of bladder cancer by releasing free carcinogens from their inactive glucuronide conjugates in the bladder. The hypothesis derives in part from the high levels of urinary beta-glucuronidase observed in bladder cancer patients. Because most of the individual variation in levels of urinary beta-glucuronidase and other lysosomal enzymes in the normal population is genetically determined, we would expect that, if high glucuronidase levels were a predisposing factor in the disease, bladder cancer patients would transmit this trait to their progeny. We have tested this hypothesis and find that levels of urinary beta-glucuronidase and three other lysosomal enzymes, alpha-galactosidase, beta-galactosidase, and beta-hexosaminidase, are not significantly elevated in 34 progeny of bladder cancer patients compared to 34 matched controls. Additionally, 15 bladder cancer patients judged to be disease free for a median time of 5 years did not have elevated levels of urinary beta-glucuronidase when compared to a normal population of 125 individuals. Thus, the high levels of glucuronidase observed in bladder cancer patients are most likely a consequence of disease rather than a cause.

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