AE rates in pediatric inpatients are high and did not improve from 2007 to 2012. Pediatric AE rates were substantially higher in teaching hospitals as well as in patients with more chronic conditions.
BACKGROUND AND OBJECTIVE: Efforts to advance patient safety have been hampered by the lack of high quality measures of adverse events (AEs). This study's objective was to develop and test the Global Assessment of Pediatric Patient Safety (GAPPS) trigger tool, which measures hospital-wide rates of AEs and preventable AEs.
Inflammatory breast cancer (IBC) is an extremely lethal cancer that rapidly metastasizes. Although the molecular attributes of IBC have been described, little is known about the underlying metabolic features of the disease. Using a variety of metabolic assays, including 13 C tracer experiments, we found that SUM149 cells, the primary in vitro model of IBC, exhibit metabolic abnormalities that distinguish them from other breast cancer cells, including elevated levels of N-acetylaspartate, a metabolite primarily associated with neuronal disorders and gliomas. Here we provide the first evidence of N-acetylaspartate in breast cancer. We also report that the oncogene RhoC, a driver of metastatic potential, modulates glutamine and N-acetylaspartate metabolism in IBC cells in vitro, revealing a novel role for RhoC as a regulator of tumor cell metabolism that extends beyond its well known role in cytoskeletal rearrangement. Inflammatory breast cancer (IBC)3 is a highly aggressive cancer that affords the lowest 5-year survival rate of any breast cancer diagnosis, with a large proportion of patients exhibiting nodal metastases at diagnosis (1). IBC disproportionally affects both younger women and African American women and is typically characterized by rapid and specific changes in skin appearance, such as peau d'orange, erythema, skin thickening, and rapid enlargement of the affected breast (2). Instead of forming solid masses, IBC cells tend to form abundant tumor emboli that have the capacity to rapidly invade the lymphatic system and spread to distant sites. Although the molecular attributes of IBC are well described and are suggestive of constitutive adaptation to hypoxia (3), little is known about the underlying metabolic features of the disease.Metabolic reprogramming is increasingly recognized as a fundamental hallmark of cancer, and efforts to identify clinically viable drugs that target cancer metabolism are underway (4). It is well established that many tumor cells consume glucose and produce lactate at significantly higher rates than the surrounding tissue, even when sufficient oxygen is present, via a phenomenon known as aerobic glycolysis or the Warburg effect (5). It was originally hypothesized that cancer cells utilize aerobic glycolysis because of mitochondrial respiratory dysfunction. However, even though a number of mitochondrial defects in tumor cells have been reported, evidence suggests that most tumor cells have functional tricarboxylic acid (TCA) cycles and electron transport chains (6, 7).In addition to increased glucose uptake, many cancer cells also consume glutamine at higher rates than normal cells, both in culture and in vivo (8, 9). The Rho GTPase family of proteins has recently been linked to the regulation of glutaminase activity (10). The oncogene RhoC, a GTPase involved in cytoskeletal rearrangement and cell motility, is a driver of the metastatic phenotype exhibited by IBC (11,12). RhoC expression increases with tumor stage, is a robust predictor of breast cancer aggressiveness and surv...
Recent large-scale GWAS and large epidemiologic studies have accelerated the discovery of genes and environmental factors that contribute to the risk of keratinocyte carcinoma (KC), which includes basal cell carcinoma (BCC) and squamous cell carcinoma (SCC). This Review summarizes the genomic regions associated with SCC and BCC risk, examines the genetic overlap between SCC and BCC, and discusses biological pathways involved in SCC and BCC development. Next, we review environmental factors that are associated with KC risk, including those that are shared between SCC and BCC as well as others that associated with only one type of KC. We conclude with a critical appraisal of current research and potential directions for future research.
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