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Background: Because of the decreasing effect of metformin on insulin resistance, it has been suggested as an anti-obesity and anti-cancer drug. So, we aimed to study the effect of metformin therapy on tumor cell proliferation in non-diabetic breast cancer patients. Methods: We conducted a prospective clinical trial and studied the effect of metformin therapy on the level of Ki67 as a measure of tumor cell proliferation. Our primary endpoint was to evaluate the changes in Ki67. The intervention group consisted of 25 non-diabetic breast cancer patients with no indication for neoadjuvant chemo- therapy. They were followed up from the time of biopsy to operation. Metformin (1500 mg/day) was prescribed in the intervention group from the date of diagnosis until the surgery (2.8 weeks). Controls were 20 early breast cancer patients who had been followed up with no prescription from biopsy until operation. Results: We could not find any statistically significant difference between the two groups regarding baseline clinical or tumor characteristics such as age, stage, grade, estrogen receptor, HER2 status or time, and type of surgery. However, the immuno- histochemistry (IHS) study showed a decrease in median Ki67 from 35.14 to 29.6 in the intervention group (P-value= 0.02). While an increase from 24.5 to 30.6 was detected in the control group (P-value= 0.02). Both of these changes were statistically significant. Although mild gastrointestinal symptoms were seen in approximately 50% of cases, generally, patients tolerated metformin well. There was a correlation between the score of HOMA, a metabolic factor, and the changes in KI67. Conclusion: Metformin prescription in a short period of time between biopsy and definitive surgery leads to the inhibition of breast cancer cell growth. We found a relationship between metformin anti-proliferative effect and glucose and insulin metabolism.

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To date, no specific pattern of chromosomal abnormalities has been established in gastric cancer (GC). Cytogenetic analysis was performed using G-banding and fluorescence in situ hybridization (FISH) in 9 ascetic fluids from GC patients, and the clustering patterns of chromosomal abnormalities were studied. Twenty-six different types of chromosomal abnormalities were identified. In contrast to structural abnormalities, the gain or loss of chromosomes was infrequent. Moreover, five main clusters of chromosomal abnormalities were identified by clustering analysis. Extensive cytogenetic complexity, specific chromosomal abnormalities and karyotype heterogeneity are the main characterizations of GC. Some of the recurrent and novel chromosomal abnormalities with distinct clustering patterns identified in this study may play important roles for GC initiation and progression and could serve as promising diagnostic and prognostic markers in GC patients.