Interleukin-18 (IL-18, interferon [IFN]-gamma-inducing factor) is a proinflammatory cytokine converted to a biologically active molecule by interleukin (IL)-1beta converting enzyme (caspase-1). A wide range of normal and cancer cell types can produce and respond to IL-18 through a specific receptor (IL-18R) belonging to the toll-like receptor family. The activity of IL-18 is regulated by IL-18-binding protein (IL-18bp), a secreted protein possessing the ability to neutralize IL-18 and whose blood level is affected by renal function and is induced by IFNgamma. IL-18 plays a central role in inflammation and immune response, contributing to the pathogenesis and pathophysiology of infectious and inflammatory diseases. Because immune-stimulating effects of IL-18 have antineoplastic properties, IL-18 has been proposed as a novel adjuvant therapy against cancer. However, IL-18 increases in the blood of the majority of cancer patients and has been associated with disease progression and, in some cancer types, with metastatic recurrence risk and poor clinical outcome and survival. Under experimental conditions, cancer cells can also escape immune recognition, increase their adherence to the microvascular wall and even induce production of angiogenic and tumor growth-stimulating factors via IL-18-dependent mechanism. This is particularly visible in melanoma cells. Thus, the role of IL-18 in cancer progression and metastasis remains controversial. This review examines the clinical correlations and biological effects of IL-18 during cancer development and highlights recent experimental insights into prometastatic and proangiogenic effects of IL-18 and the use of IL-18bp against cancer progression.
BackgroundDeviations in the amount of genomic content that arise during tumorigenesis, called copy number alterations, are structural rearrangements that can critically affect gene expression patterns. Additionally, copy number alteration profiles allow insight into cancer discrimination, progression and complexity. On data obtained from high-throughput sequencing, improving quality through GC bias correction and keeping false positives to a minimum help build reliable copy number alteration profiles.ResultsWe introduce seqCNA, a parallelized R package for an integral copy number analysis of high-throughput sequencing cancer data. The package includes novel methodology on (i) filtering, reducing false positives, and (ii) GC content correction, improving copy number profile quality, especially under great read coverage and high correlation between GC content and copy number. Adequate analysis steps are automatically chosen based on availability of paired-end mapping, matched normal samples and genome annotation.ConclusionsseqCNA, available through Bioconductor, provides accurate copy number predictions in tumoural data, thanks to the extensive filtering and better GC bias correction, while providing an integrated and parallelized workflow.Electronic supplementary materialThe online version of this article (doi:10.1186/1471-2164-15-178) contains supplementary material, which is available to authorized users.
Introduction Low surface contamination levels of hazardous drugs in compounding areas can be used as indicators of exposure and efficacy of cleaning procedures. We report the efficacy results of the KIRO® Oncology self-cleaning automated compounding system for decontamination of cytotoxic drugs, assessed in an oncology health center using a sanitizing method and an alkaline method. Methods The study was conducted for six-days over a three-week period. A mixture with known levels of 5-fluorouracil, ifosfamide, cyclophosphamide, gemcitabine, etoposide, methotrexate, paclitaxel, docetaxel and carboplatin was added to the KIRO® Oncology’s compounding area surface before each self-cleaning method was used. Contamination levels were determined, with a surface wipe sampling kit, at the end of the self-cleaning process. Results Background surface contamination for quantified levels of cytotoxic drugs during routine use of KIRO® Oncology was below limit of quantification (<LOQ) for all drugs, except for carboplatin, which has a very low LOQ (0.2 ng/sample). The quantified drug levels detected on surface wipe samples after self-cleaning using both methods in the KIRO® Oncology’s compounding area surface sections were all <LOQ when spiking with 1 ng/cm2 (ten times the ‘safe’ reference value), except for carboplatin (alkaline method only), although its levels were still below the ‘safe’ reference value (0.1 ng/cm2). For surface contamination levels when spiking with 100 ng/cm2, both self-cleaning methods had decontamination efficacies >99.8% for all cytotoxic drugs analyzed. Conclusion This study provides evidence on the efficacy of the KIRO® Oncology automatic self-cleaning system for surface area decontamination during the preparation of cytotoxic drugs.
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