The Role of Inflammation in Breast and Prostate Cancer Metastasis to Bone.

Tumor metastasis to bone is a common event in multiple forms of malignancy. Inflammation holds essential functions in homeostasis as a defense mechanism against infections and is a strategy to repair injured tissue and to adapt to stress conditions. However, exaggerated and/or persistent (chronic) inflammation may eventually become maladaptive and evoke diseases such as autoimmunity, diabetes, inflammatory tissue damage, fibrosis, and cancer.

Anti-tumor effects of mevalonate pathway inhibition in ovarian cancer.

Background: Ovarian cancer remains the most fatal gynecological malignancy. Current therapeutic options are limited due to late diagnosis in the majority of the cases, metastatic spread to the peritoneal cavity and the onset of chemo-resistance. Thus, novel therapeutic approaches are required.

Plasma levels of Semaphorin 4D are decreased by adjuvant tamoxifen but not aromatase inhibitor therapy in breast cancer patients.

Background: Semaphorin 4D (Sema4D) is a glycoprotein that inhibits bone formation and has been associated with cancer progression and the occurrence of bone metastases. Recently, Sema4D expression has been linked to estrogen signaling in breast cancer. Endocrine therapies like tamoxifen and aromatase inhibitors (AI) are a standard therapeutic approach in hormone receptor positive breast cancers.

The potential predictive role of nuclear NHERF1 expression in advanced gastric cancer patients treated with epirubicin/oxaliplatin/capecitabine first line chemotherapy.

Cellular resistance in advanced gastric cancer (GC) might be related to function of multidrug resistance (MDR) proteins. The adaptor protein NHERF1 (Na(+)/H(+) exchanger regulatory factor) is an important player in cancer progression for a number of solid malignancies, even if its role to develop drug resistance remains uncertain. Herein, we aimed to analyze the potential association between NHERF1 expression and P-gp, sorcin and HIF-1α MDR-related proteins in advanced GC patients treated with epirubicin/oxaliplatin/capecitabine (EOX) chemotherapy regimen, and its relation to response.

Adrenergic stimulation decreases osteoblast oxytocin synthesis.

Oxytocin (OT) regulates bone mass by inducing the differentiation of osteoblasts to a mature, mineralizing phenotype. We have shown recently that osteoblasts can synthesize OT. In view of known interactions between OT-ergic and adrenergic neurons in the central nervous system, we questioned whether the negative regulation of osteoblast differentiation by adrenergic nerves was mediated through its suppression of OT synthesis.

Regulated production of the pituitary hormone oxytocin from murine and human osteoblasts.

Oxytocin (OT) is a primitive neurohypophyseal hormone that plays a primary and indispensible role in mammalian lactation. We have shown recently that OT also regulates bone remodeling, mainly bone formation, with remarkable sensitivity. We now show that OT, apart from its neurohypophyseal origin, is produced in abundance by both human and murine osteoblasts.

Effect of shock wave treatment on platelet-rich plasma added to osteoblast cultures.

The aim of this study was to verify the effects on osteoblast cultures of adding a platelet-rich plasma (PRP) concentrate pretreated with 500 shock wave (SW) at an energy flow density of 0.17 mJ/mm(2), emitted by an electromagnetic generator Minilith SL1 (STORZ, Germany), reproducing the conditions of our previous study in which we apply SW directly on osteoblasts. Real-time PCR showed that in osteoblast cultures with added PRP pretreated with SW, there was an increased expression at 48 h of insulin-like growth factor binding protein 3 (IGFBP-3) and runt-related transcription factor 2 (RUNX2) and at 72 h, of collagen type I, osteocalcin, insulin-like growth factor 1 (IGF-1) as well as IGFBP-3.

Extracorporeal shock waves stimulate osteoblast activities.

The extracorporeal shock wave therapy (ESWT) is an extensively applied treatment for musculoskeletal disorders because it promotes bone repair. The aim of this study was to evaluate the direct effect of ESWT on murine osteoblasts to clarify the cellular mechanism that leads to the induction of osteogenesis. Osteoblasts in culture flasks were treated with ESWT pulses (500 impulses of 0.