Abstract 204P
Background
Breast cancer is the most common cancer among women, with incidence increasing after the age of 35 until it reaches a peak at 55-64 years. Metformin has an anti-proliferative effect and diabetic patients on metformin have been shown to have a 30% reduction in lifetime risk of all cancers This anti-proliferative effect is the result of direct inhibition of mammalian target of rapamycin (mTOR) activity and direct activation of adenosine monophosphate-activated protein kinase (AMPK). We aimed at evaluating this anti-proliferative effect in terms of overall pathological response (partial and complete), concurrent with standard neoadjuvant chemotherapy in breast cancer.
Methods
Sixty non-diabetic breast cancer patients receiving neoadjuvant chemotherapy (fluorouracil, epirubicin, cyclophosphamide (FEC) then docetaxel ± trastuzumab) were randomized into two arms (thirty in each arm): Arm A: metformin (850 mg bid) starting with neoadjuvant chemotherapy. Arm B: control group receiving neoadjuvant chemotherapy alone.
Results
There was a significant difference between the metformin and control arm in terms of overall pathological complete response(pCR) and partial pathological response (pPR) versus no response (P=0.03). pCR was higher in Arm A, but didn’t reach significance due to the small sample size (P=0.09). Multivariate analysis showed a significantly more pronounced response in the Luminal B subtype of breast cancer (P=0.03) and in grade II tumours (P=0.03). There was no significant difference in overall toxicity or ≥ grade 3 adverse events between both arms; the most common toxicities were vomiting (53.6%), nausea (30.4%) and neutropenia (30.4%).
Conclusions
Metformin has a significant anti-proliferative effect which appears to result in increased pathological response in stage II-III breast cancer when given with neoadjuvant chemotherapy.
Clinical trial identification
Editorial acknowledgement
Legal entity responsible for the study
Ain Shams University Clinical Oncology Department (ASCOD).
Funding
Ain Shams University Clinical Oncology Department (ASCOD).
Disclosure
All authors have declared no conflicts of interest.