Abstract. Totally implantable venous access port systems (TIVAPS) are widely used in breast cancer patients. However, complications are frequent and may necessitate device replacement or removal, resulting in additional patient stress and treatment delays. The aim of the present study was to investigate possible risk factors for complications. A total of 2,996 consecutive female breast cancer patients, with a median age of 50.2 years (range, 21.2-85.5 years) were enrolled in this observational, single-centre study between December, 2008 and April, 2014. TIVAPS implantation was principally performed using local anaesthesia and the blind puncture or Seldinger technique through internal jugular or subclavian vein access. A retrospective chart review was conducted to obtain information associated with TIVAPS and patient data. Insertion performed by blind puncture and Seldinger technique had a success ratio of 96.34 and 99.80%, respectively (χ 2 =29.905, P<0.001). However, the success ratio of the puncture technique group was 99.76% when the TIVAPS was implanted in the right internal jugular vein. The most common complications were late complications, with an overall incidence rate of 5.41% (162/2,996) during the entire device duration. The most common late complications included fibrin formation (1.84%, 55/2,996), port-related bacteraemia (1.44%, 43/2,996) and deep vein thrombosis (0.63%, 19/2,996). No patient died during the study. Our results demonstrated that insertion of TIVAPS by blind puncture or the Seldinger technique through internal jugular or subclavian vein access is convenient, and insertion by the Seldinger technique through the right internal jugular vein is the preferred method. Therefore, TIVAPS is safe for continuous infusional chemotherapy regimens for breast cancer patients.

Abstract. The mitochondrial GTPase mitofusin-2 (Mfn2) gene is a novel gene characterized as a cell proliferation inhibitor. Mfn2 has previously been reported to play a role in regulating cell proliferation, apoptosis and differentiation in a number of cell types. However, there are no studies on the effect of Mfn2 in breast cancer. In this study, we aimed to elucidate the function and mechanism of Mfn2 in breast cancer. A plasmid encoding the complete Mfn2 open reading frame (pEGFP-Mfn2) was used to infect breast cancer cells. The effect of Mfn2 on proliferation was assessed by methyl thiazolyl tetrazolium and bromodeoxyuridine incorporation analyses. Flow cytometry, immunofluorescence and western blot analyses were used to test the effects of Mfn2 on cell cycle distribution and apoptosis. Additionally, the PI3K/Akt signaling pathway was analyzed after pEGFP-Mfn2 was transfected into MCF-7 cells. The results revealed that Mfn2 suppressed the proliferation of MCF-7 cells by regulating more cells at the G0/G1 phase and decreasing proliferating cell nuclear antigen and cyclin A expression. The results also demonstrated that the PI3K/Akt signaling pathway is involved in Mfn2-regulated proliferation and apoptosis. Taken together, this indicates that Mfn2 mediates MCF-7 cell proliferation and apoptosis via the PI3K/Akt signaling pathway. Mfn2 may thus be a significant therapeutic target in the treatment of breast cancer. IntroductionThe mitochondrial GTPase mitofusin-2 (Mfn2) gene, which is also called the hyperplasia suppressor gene, was originally identified in vascular smooth muscle cells from spontaneously hypertensive rats, which exhibited markedly lower expression than Wistar-Kyoto rats (1). Mfn2 localizes to the mitochondrial outer membrane and plays an essential role in mitochondrial fusion, thus regulating mitochondrial morphology and function. Further research has indicated that Mfn2 has a potential apoptotic effect mediated by the mitochondrial apoptotic pathway (1-3). Chen et al (4) demonstrated that Mfn2 notably suppresses cell growth and proliferation in a number of tumor cell lines through the inhibition of the Ras-ERK MAPK signaling pathway. Recently, Mfn2 has become a focal point in tumor research. Several studies have investigated the function of Mfn2 in various malignancies, including hepatocellular, urinary bladder and gastric cancers, and Mfn2 is considered to perform pro-apoptotic and anti-proliferative functions (5-7).Clinical and epidemiological evidence reveals that estrogens participate in the initiation and development of human breast cancer (8,9). Understanding the role of estrogen receptor (ER) α and β in the pathogenesis of breast cancer is essential, since the effects of estrogen are mediated through these two ERs (10). Although the function of ERα has been established and this receptor remains the most significant marker of the response to hormonal therapy in breast cancer, the role of ERβ remains elusive as a result of a number of conflicting studies (11). Our previous study demonstrat...