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Metformin may affect breast cancer proliferation

Issue: July 2012

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Metformin may affect breast cancer proliferation depending on a woman’s insulin resistance, with decreased proliferation occurring in women with an increased homeostasis model assessment index, according to phase 2 study results.

Researchers evaluated women with stage I to stage IIa breast cancer who were candidates for elective surgery. Researchers measured Ki-67 levels in a pretreatment biopsy and then again in a post-treatment surgical specimen. Ki-67 is used as a marker because of its postulated role in predicting drug efficacy.

Patients were randomly assigned to treatment with metformin 850-mg tablets (n=100) or placebo (n=100). The primary endpoint of the study was the change in Ki-67 at 4 weeks.

The study failed to meet its primary endpoint. Metformin had a nonsignificant effect on Ki-67 compared with placebo.

In a subgroup analysis, the researchers measured the effect of metformin on Ki-67 according to insulin resistance status (P for interaction =.045). They found a nonsignificant 10.5% decrease of proliferation in women with elevated homeostasis model assessment (HOMA) index (>2.8), and a nonsignificant 11.1% increase in proliferation in women with no insulin resistance (HOMA ≤2.8).

The researchers also discovered that metformin did have a significant effect on Ki-67 in a subgroup of 119 women with luminal B tumors (P for interaction =.05).

Although researchers said the effect of metformin according to HOMA index had only a nominal statistical significance of P=.045, “the qualitative interaction between metformin and insulin resistance may have important clinical implications and warrants confirmation in independent studies.”

In an accompanying editorial, Matthew Martin, PhD, a postdoctoral fellow at The Institute of Cancer Research, and Richard Marais, PhD, director of the Paterson Institute for Cancer Research, both in the United Kingdom, noted recent studies in mice demonstrated that metformin and doxorubicin cooperate to suppress breast cancer growth, and that a combination of metformin and VEGF receptor signaling inhibitors help suppress the growth of some types of melanoma.

“As we move into the era of personalized medicine, it is not difficult to imagine how novel targeted agents could be combined with metformin to inhibit tumor-cell growth directly and simultaneously normalize the pathologic microenvironment that induces and maintains tumor growth,” they wrote.