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Molecular pathways: digoxin use and estrogen-sensitive cancers--risks and possible therapeutic implications.

Robert J Biggar¹

¹Department of Epidemiology Research, Statens Serum Institut, Copenhagen, Denmark. rjbiggar@gmail.com

Clinical Cancer Research : an Official Journal of the American Association for Cancer Research

|February 28, 2012

Summary

Digoxin, a phytoestrogen, may increase breast and uterine cancer risks by mimicking estrogen. Its effects on estrogen-sensitive cancers warrant further investigation, especially in women with existing or high-risk conditions.

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Area of Science:

Endocrinology
Oncology
Pharmacology

Background:

Digoxin, a cardiac glycoside, exhibits phytoestrogen properties.
Estrogen receptors (ER) are implicated in the development of hormone-sensitive cancers.

Purpose of the Study:

To investigate the potential estrogenic effects of digoxin on cancer incidence.
To explore the implications for patients with or at risk of estrogen-sensitive malignancies.

Main Methods:

Observational analysis of cancer incidence in digoxin users versus non-users.
Comparison of cancer types based on estrogen sensitivity.

Main Results:

Increased incidence of ER-sensitive breast and uterine cancers (RR 1.3-1.5) in women using digoxin.
No significant change in ER-insensitive ovarian and cervical cancer rates.
Reduced prostate cancer risk (RR 0.76) in men using digoxin.
Cancer incidence normalized after digoxin cessation.

Conclusions:

Digoxin's effects suggest ER-mediated proliferation, potentially accelerating nascent ER-sensitive cancers.
Estrogen-like drugs like spironolactone require similar investigation.
Clinical management may need to consider drug interactions, particularly with tamoxifen versus aromatase inhibitors in women with ER-sensitive cancers.