The evaluation of an on-site monitoring program for activity meter quality assurance with exemption-level sources.

This paper discusses the feasibility of a monitoring program for the quality assurance status of activity meters. We sent a questionnaire to clinical nuclear medicine departments of medical institutions, requesting information on their activity meters and quality assurance practices. On-site visits were conducted with exemption-level standard sources (Co-57, Cs-137 and Ba-133) for dose calibrators in nuclear medicine departments including physical inspection, accuracy and reproducibility. A method offering a quick check on the detection efficiency of the space dimension inside the activity meters was also introduced. For dose calibrator quality assurance, the daily checks had the highest implementation. However, annual checks and upon acceptance/after a repair check were reduced to 50% and 44%, respectively. The accuracy results of dose calibrators showed that all models exceeded the ±10% criteria with Co-57 and Cs-137 sources. The reproducibility results showed that some models exceeded the ±5% criteria with Co-57 and Cs-137 sources. The appropriate application of exemption-level standard sources considering the uncertainty that affects the measurement is discussed.

Apelin Promotes Prostate Cancer Metastasis by Downregulating TIMP2 via Increases in miR-106a-5p Expression.

Prostate cancer commonly affects the urinary tract of men and metastatic prostate cancer has a very low survival rate. Apelin belongs to the family of adipokines and is associated with cancer development and metastasis. However, the effects of apelin in prostate cancer metastasis is undetermined. Analysis of the database revealed a positive correlation between apelin level with the progression and metastasis of prostate cancer patients. Apelin treatment facilitates cell migration and invasion through inhibiting tissue inhibitor of metalloproteinase 2 (TIMP2) expression. The increasing miR-106a-5p synthesis via c-Src/PI3K/Akt signaling pathway is controlled in apelin-regulated TIMP2 production and cell motility. Importantly, apelin blockade inhibits prostate cancer metastasis in the orthotopic mouse model. Thus, apelin is a promising therapeutic target for curing metastatic prostate cancer.

CXCR3 isoform A promotes head and neck cancer progression by enhancing stem-like property and chemoresistance.

BACKGROUND: The chemokine network orchestrates the cancer stem-like property and consequently participates in cancer progression. CXCR3 contributes cancer progressive property and immunomodulation in the tumor microenvironment. The two major isoforms of CXCR3 are scrutinized and the divergence is showed that CXCR3A promotes cancer cell growth and motility while CXCR3B functions contrarily in many studies. However, rare studies illustrate the role of CXCR3 isoforms in cancer stem-like property and chemoresistance, especially in head and neck cancer (HNC). METHODS: Levels of CXCR3, CXCR3B, and Sox2 were determined in HNC tissue microarray by immunohistochemistry staining to explore potential clinical relevance. Lentivirus-mediated CXCR3-isoform overexpression with MTS assay, clonogenic assay, transwell migration, sphere formation, and chemo-drug susceptibility were implemented to investigate the role of CXCR3-isofoms in HNC. RESULTS: High levels of CXCR3 were significantly associated with advanced stage (p < 0.01), regional lymph node metastasis (p < 0.05), and poor differentiation (p < 0.005) and further correlated with worse survival rate in oral cancer patients (p = 0.036). Higher levels of CXCR3B were found in regional lymphatic invasion of HNC and progressive stage of squamous cell carcinoma. Elevated Sox2 expression was significantly associated with the advanced stage of HNC in the oral cavity, and demonstrated a co-expression pattern with CXCR3B. Furthermore, lentivirus-mediated overexpression of CXCR3A and CXCR3B in SAS human oral cancer cells promoted cell mobility. CXCR3A overexpression enhanced sphere-forming ability and chemoresistance of CSCs by upregulating stemness-related genes. CONCLUSION: This study first provides a novel insight of CXCR3 isoform A in HNC cancer progression via regulating cancer stem-like properties and chemoresistance, suggesting that CXCR3A may be a prognostic marker and novel target for HNC therapy.