Publications by authors named "Craig Lotterman"

Article Synopsis
  • Bloodstream infections (BSIs) are common and serious for kids with acute myeloid leukemia (AML), often linked to central venous access devices (CVADs) used during treatment.
  • This study analyzed the risk of bacterial BSIs in pediatric AML patients based on different types of CVADs (tunneled externalized catheter, peripherally inserted central catheter, and totally implanted catheter) using data from over 500 patients.
  • Results showed no significant difference in BSI rates among the CVAD types during neutropenia, suggesting that the risk factors for BSIs may be specific to patients with AML rather than the type of CVAD used.
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Importance: Pediatric acute myeloid leukemia (AML) requires multiple courses of intensive chemotherapy that result in neutropenia, with significant risk for infectious complications. Supportive care guidelines recommend hospitalization until neutrophil recovery. However, there are little data to support inpatient over outpatient management.

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The pathway involving the tumor suppressor gene TP53 can regulate tumor angiogenesis by unclear mechanisms. Here we show that p53 regulates hypoxic signaling through the transcriptional regulation of microRNA-107 (miR-107). We found that miR-107 is a microRNA expressed by human colon cancer specimens and regulated by p53.

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Aberrant expression of microRNAs (miRNAs) has emerged as an important hallmark of cancer. However, the putative mechanisms regulating miRNAs per se are only partially known. It is well established that many tumor suppressor genes in human cancers are silenced by chromatin alterations, including promoter methylation and histone deacetylation.

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A large body of evidence has documented abnormal microRNA (miRNA) expression patterns in diverse human malignancies. Given that miRNA expression is tightly regulated during development and cellular differentiation, aberrant miRNA expression in cancer cells is likely to be in part a consequence of the loss of normal cellular identity that accompanies malignant transformation. Nevertheless, it is now clear that miRNAs function as critical effectors of several canonical oncogenic and tumor suppressor pathways, including those controlled by Myc and p53.

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