Abstract: The metabolism of tumor cells which have .beta.-glucuronidase activity is inhibited by administering to a patient a conjugate of glucuronic acid and a thiocarbamate compound of the formula: ##STR1## wherein R.sup.1 and R.sup.2 are selected from the group consisting of C.sub.1 -C.sub.6 alkyl and C.sub.1 -C.sub.6 cycloaliphatic, and M is selected from the group consisting of hydrogen, an electropositive, ionically bonded metal, and the radical ##STR2## and R.sup.3 and R.sup.4 are selected from the group consisting of C.sub.1 -C.sub.6 alkyl and C.sub.1 -C.sub.6 cycloaliphatic groups.

Abstract: Saturated aliphatic straight chain dicarboxylic acids having a total number of carbon atoms which are divisible by four, are selectively toxic to certain tumor cells while non-toxic to normal cells of the same origin. Octacosanedioic acid is particularly preferred as it is a component of normal blood serum. Compositions containing these compounds may be used in the treatment of certain malignancies.

Abstract: The effectiveness of interferon for treatment against cancer may be increased by first administering an agent for inhibiting tyrosinase. In this manner the tyrosinase which is known to be produced by malignancies, and which may cause inactivation of the interferon, will be substantially inactivated prior to the interferon administration.

Abstract: Hyperacidified tumors having high .beta.-glucuronidase activity can be treated with glucuronides with aglycones toxic to the tumor cells with great safety toward the rest of the body by first administering an alkalinizing agent in an amount sufficient to maintain the pH level of non-tumor tissues at approximately 7.4 during the glucuronide treatment. This will cause inactivation of .beta.-glucuronidase activity in the rest of the body. Novel glucuronides are disclosed the aglycones of which exert a higher toxic effect in an acid environment or is water-soluble only in an alkaline environment. Such compounds have particular utility with the above process. By substituting radioisotopes into the aglycone, diagnosis and in situ radiation therapy may be accomplished. Bacterial cells having .beta.-glucuronidase activity may also be diagnosed and treated in accordance with the present invention.

Abstract: Mandelonitrile-.beta.-D-glucuronic acid can be produced by tritylating mandelonitrile-.beta.-D-glucoside, acetylating the obtained product, and then simultaneously detritylating and oxidizing in order to obtain mandelonitrile-.beta.-D-triacetyl glucuronic acid. This compound may then be deacetylated to obtain mandelonitrile-.beta.-D-glucuronic acid or the salt thereof.

Abstract: Hyperacidified tumors having high .beta.-glucuronidase activity can be treated with glucuronides with aglycones toxic to the tumor cells with great safety toward the rest of the body by first administering an alkalinizing agent in an amount sufficient to maintain the pH level of non-tumor tissues at approximately 7.4 during the glucuronide treatment. This will cause inactivation of .beta.-glucuronidase activity in the rest of the body. When nitrile-containing aglycones are used sodium thiosulfate is also administered to avoid cyanide poisoning. A loading dose of glucuronide greater than 2 mMoles per kilogram body weight is first administered with additional administration of one third the initial dose each hour as long as .beta.-glucuronidase activity remains at the tumor site. Bacterial cells having .beta.-glucuronidase activity may also be diagnosed and treated in accordance with the present invention.

Abstract: Mandelonitrile-.beta.-D-glucuronic acid is produced by condensing a mandelic amide with a tri-O-acetyl methyl ester of glucuronic acid and then reacting the product with acetic anhydride to produce the tri-O-acetyl methyl ester of mandelonitrile-.beta.-D-glucuronic acid. The protecting acetyl groups may be removed and the barium salt formed by reacting with barium hydroxide, which salt, when treated with sulfuric acid, will yield the mandelonitrile-.beta.-D-glucuronic acid. This compound, as well as methacrylonitrile .beta.-D-glucuronic acid may be used in the treatment of bacterial infections having .beta.-glucuronidase activity.

Abstract: A method of diagnosing the presence of tumors having .beta.-glucuronidase activity comprises administering a glucuronide which differs in color or color intensity from the aglycone thereof to a patient. The preferred glucuronide is phenolphthalein glucuronide. The urine is then collecting for a twenty four hour period and the amount of phenolphthalein glucuronides present in the urine is determined. If substantially all of the phenolphthalein glucuronide is expelled then it is apparent that the body has no tumors or bacterial infections exhibiting .beta.-glucuronidase activity. If however substantial amounts of phenolphthalein is retained, then this is an indication of the presence of tumors having .beta.-glucuronidase activity or a bacterial infection having .beta.-glucuronidase activity.

Abstract: Hyperacidified tumors having high .beta.-glucuronidase activity can be treated with glucuronides with aglycones toxic to the tumor cells with great safety toward the rest of the body by first administering an alkalinizing agent in an amount sufficient to maintain the pH level of non-tumor tissues at approximately 7.4 during the glucuronide treatment. This will cause inactivation of .beta.-glucuronidase activity in the rest of the body. When nitrile-containing aglycones are used sodium thiosulfate is also administered to avoid cyanide poisoning. Novel glucuronides are disclosed the aglycones of which exert a higher toxic effect in an acid environment or are water-soluble only in an alkaline environment. Such compounds have particular utility with the above process. By substituting radioisotopes into the aglycone, diagnosis and in situ radiation therapy may be accomplished. Bacterial cells having .beta.-glucuronidase activity may also be diagnosed and treated in accordance with the present invention.