Expression of c-kit proto-oncogene product in breast cancer tissues.

BACKGROUND: The published results on expression of c-kit in benign and malignant breast tissues vary. MATERIALS AND METHODS: The immunohistochemical expression of c-kit proto-oncogene product in 52 invasive breast cancer tissues and 16 benign breast tumor (fibroadenoma) tissues was studied using anti-c-kit proto-oncogene product antibody. Its expression was evaluated by immunoreactive score (IRS). RESULTS: In breast cancer tissues, the mean IRS of c-kit proto-oncogene product expression was significantly increased compared to those of fibroadenoma (3.4 +/- 2 and 2.19 +/- 1.8, respectively,p = 0.035). The mean IRS of c-kit expression was higher in the group comprising estrogen (ER) positive tumor than in the group of ER negative (4.1 +/- 2.1 and 2.7 +/- 1.8, respectively,p = 0.012) but no statistically significant relationship was seen between the expression of c-kit proto-oncogene product and other clinicopathological parameters of breast cancer, including histologic type, tumor size, lymph node metastasis, distant metastasis, stage, progesterone receptor, c-erbB-2 expression, menopausal status and age of the patient (p > 0.05). CONCLUSIONS: Our results show that a high level of c-kit expression occurs frequently in invasive breast cancer, and its expression is associated with ER but unrelated to other clinico-pathological variables.

The effect of G-CSF in an experimental MRSA graft infection in mice.

Wound infection after prosthetic material implantation is a troublesome complication with an incidence of 2% to 10%. The effect of granulocyte colony-stimulating factor (G-CSF) was studied in an experimental methicillin-resistant Staphylococcus aureus (MRSA) graft infection model. Eighty adult mice were used. Under general anesthesia an abdominal incision of 2 cm in length was performed. A subcutaneous cavity of 2 x 2 cm in size was created. Polypropylene mesh pieces of 2 x 1 cm and MRSA solution of 0.1ml of 10(8) CFU/mL were used. G-CSF was applied systemically or locally in a dosage of 0.02 MU/30 g body weight. There were 8 groups: group I, wound + MRSA; group II, wound + mesh + MRSA; group III, wound + mesh + MRSA + G-CSF (ip, 48 h before operation); group IV, wound + mesh + MRSA + G-CSF (ip, 24 h before operation); group V, wound + mesh + MRSA + G-CSF (locally, into the cavity); group VI, wound + mesh (incubated in G-CSF solution for 4 h) + MRSA; group VII, wound + mesh + MRSA + G-CSF, ip, 24 h from operation; and group VIII (positive control group), wound + mesh + MRSA + Teicoplanin (0.03 mg/30 g body weight, ip, 1/2 h before operation). Three days after, animals were killed and incisions were examined for possible infection or abscess formation and wound failure. Meshes were removed; after vortexing and dilution, samples were incubated with 5% agar media. Results of bacterial incubation were evaluated 24 h and 48 h later. There were symptoms of wound infection and abscess formation in all groups except group VIII. In group VIII, MRSA was isolated in 7 events with a colony count below 10(3). Bacterial counts were above 10(6) (10(6)-10(8)) in all other groups. Thus, it was observed that wound infection could be created with this model, but G-CSF could not prevent the development of wound infection, whether it was administered systemically or locally. Teicoplanin decreased the number of colony-forming units of MRSA, and prevents wound infection in this MRSA wound infection model.