Antidepressant Paxil May Promote Breast Cancer
19 Feb 2014
A troubling new study has found the popular antidepressant paroxetine — better known by its commercial name, Paxil — may promote the development and growth of breast tumors in women.
The finding, by researchers from the City of Hope in Duarte, resulted from a new way the scientists developed to identify drugs and chemicals that can disrupt the balance of sex hormones in human beings and influence the development and progress of breast cancer, the Los Angeles Times reports.
A trial screening of 446 drugs in wide circulation flagged Paxil as having a weak estrogenic effect that could promote breast cancer.
The researchers noted as many as a quarter of breast cancer patients suffer from depression, which is typically treated with antidepressants known as SSRIs (selective serotonin reuptake inhibitors), including Paxil, which has been on the market since 1992.
Almost a quarter of American women in their 40s and 50s are taking an antidepressant, mostly SSRIs.
Last year, the Food and Drug Administration approved a low dose of paroxetine — repackaged under the commercial name Brisdelle — as a nonhormonal treatment for hot flashes and other menopausal symptoms.
About 70 percent of breast cancers in women are fueled, at least in part, by estrogen.
The novel screening method developed at City of Hope is described in a forthcoming issue of the journal Toxicological Sciences. It also identified two antifungal medications — biconazole and oxyconazole — as having an anti-estrogenic effect similar to that of medications prescribed to prevent breast cancer and its recurrences in women.
In addition, the researchers identified bisphenol A — a compound used in the manufacture of plastics and epoxy resins — as an estrogen promoter capable of raising breast cancer risk.
The finding that paroxetine has estrogenic effects "has implications for patients with estrogen-sensitive breast cancer who are on other medications," said Shihuan Chen, professor and chairman of City of Hope's department of cancer biology and lead author of the study.