Abstract Title:

Actions of an endogenous antitumorigenic agent on mammary tumor development and modeling analysis of its capacity for interacting with DNA.

Abstract Source:

J Steroid Biochem. 1988 ;30(1-6):325-8. PMID: 3133525

Abstract Author(s):

L B Hendry, T G Muldoon

Article Affiliation:

Department of Medicine, Medical College of Georgia, Augusta 30912.


Antineoplaston A10 (3-phenylacetylamino-2,6-piperidinedione) is an agent derived from human urine which is remarkable for its antineoplastic activity and lack of toxicity. This study deals with the discovery of a hormonal component to the action of A10 on rodent tumor formation and approaches to the delineation of its mechanism of action. Oral administration of A10 dramatically delays onset of spontaneous mammary tumor incidence in female and orchidectomized male C3H+ mice. The action in the male qualitatively mimics that of androgens. In the rat, A10 ingestion is very effective in preventing carcinogen-induced mammary tumors, but does not cause regression of pre-established tumors. It selectively blocks the occurrence of the estrogen-sensitive subpopulation of tumors, acting in a fashion completely analogous to that of tamoxifen; in contrast to tamoxifen, however, A10 has no measurable affinity for the estrogen receptor. Modeling studies demonstrate a stereoselective capacity for interaction between A10 and specific deoxyribonucleotide base pair sequences. The potential affinity is lower than that for classical intercalating antitumor agents, and the stereospecificity differs from that which we have previously established for estrogens. We offer an interpretation of the data in terms of direct effect of A10 at the genomic level to alter the cellular responsiveness to steroid hormones.

Study Type : Review
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