Peripherally inserted central catheter-related bloodstream infections in patients with hematological malignancies: A retrospective 7-years single-center study.

OBJECTIVES: We sought to investigate the nature and incidence of bloodstream infection complications and to identify the risk factors of central catheter-related bloodstream infections (CRBSI). METHODS: During the study period, 291 consecutive patients with hematological malignancies who underwent PICC placement were retrospectively enrolled. We analyzed the covariates that were specified a priori for their association with CRBSI through multivariate Cox proportional hazards regression models. The association between each predictor and the related outcome was expressed using hazard ratios (HRs) with corresponding 95% confidence intervals (CIs). RESULTS: Of 391 peripherally inserted central catheter (PICCs) were inserted in 291 patients for a total of 63,714 catheter days during 7 years, with an infection rate of 0.71/1,000 catheter days. Among the patients with hematological malignancies, those with acute leukemia were prone to CRBSI. Having previous bloodstream infection (BSI) (HR 18.139; 95% CI, 8.19-40.174; P < .0001), the number of PICCs insertions (HR 4.695; 95% CI, 1.842-11.967; P = .001) (twice), (HR 6.794; 95% CI, 1.909-24.181; P = .003) (≥3 times) were significantly associated with CRBSI. Not accompanied by chronic comorbidities (HR 0.34; 95% CI, 0.131-0.887; P = .028) and longer duration of PICC use (days) (HR 0.997; 95% CI, 0.994-0.999; P = .008) might be protective factors preventing CRBSI. CONCLUSIONS: Our finding suggests that previous BSI and a higher number of PICC insertions are associated with an increased risk of CRBSI. A lack of chronic comorbidities may help prevent CRBSI.

miR-150 Suppresses the Proliferation and Tumorigenicity of Leukemia Stem Cells by Targeting the Nanog Signaling Pathway.

Proliferation, a key feature of cancer cells, accounts for the majority of cancer-related diseases resulting in mortality. MicroRNAs (miRNAs) plays important post-transcriptional modulation roles by acting on multiple signaling pathways, but the underlying mechanism in proliferation and tumorigenicity is unclear. Here, we identified the role of miR-150 in proliferation and tumorigenicity in leukemia stem cells (LSCs; CD34+CD38- cells). miR-150 expression was significantly down-regulated in LSCs from leukemia cell lines and clinical samples. Functional assays demonstrated that increased miR-150 expression inhibited proliferation and clonal and clonogenic growth, enhanced chemosensitivity, and attenuated tumorigenic activity of LSCs in vitro. Transplantation animal studies revealed that miR-150 overexpression progressively abrogates tumor growth. Immunohistochemistry assays demonstrated that miR-150 overexpression enhanced caspase-3 level and reduced Ki-67 level. Moreover, luciferase reporter assays indicated Nanog is a direct and functional target of miR-150. Nanog silencing using small interfering RNA recapitulated anti-proliferation and tumorigenicity inhibition effects. Furthermore, miR-150 directly down-regulated the expression of other cancer stem cell factors including Notch2 and CTNNB1. These results provide insights into the specific biological behavior of miR-150 in regulating LSC proliferation and tumorigenicity. Targeting this miR-150/Nanog axis would be a helpful therapeutic strategy to treat acute myeloid leukemia.