Epithelial neutrophil-activating peptide-78 (CXCL5), a member of the CXC chemokine family, has been shown to be involved in angiogenesis, tumor growth, and metastasis. The objective of this study was to determine the relationship between CXCL5 expression and tumor progression in human pancreatic cancer and to elucidate the mechanism underlying CXCL5-mediated tumor angiogenesis and cancer growth. We report herein that CXCL5 is overexpressed in human pancreatic cancer compared with paired normal pancreas tissue. Overexpression of CXCL5 is significantly correlated with poorer tumor differentiation, advanced clinical stage, and shorter patient survival. Patients with pancreatic cancer and CXCL5 overexpression who underwent resection of cancer had a mean survival time 25.5 months shorter than that of patients who did not overexpress CXCL5. Blockade of CXCL5 or its receptor CXCR2 by small-interfering RNA knockdown or antibody neutralization attenuated human pancreatic cancer growth in a nude mouse model. Finally, we demonstrated that CXCL5 mediates pancreatic cancer-derived angiogenesis through activation of several signaling pathways, including protein kinase B (Akt), extracellular signal-regulated kinase (ERK), and signal transducer and activator of transcription (STAT) in human endothelial cells. These data suggest that CXCL5 is an important mediator of tumor-derived angiogenesis and that it may serve as a survival factor for pancreatic cancer. Blockade of either CXCL5 or CXCR2 may be a critical adjunct antiangiogenic therapy against pancreatic cancer.

The kidney is the most commonly transplanted solid organ. Advances in surgical techniques, immunosuppression regimens, surveillance imaging, and histopathologic diagnosis of rejection have allowed prolonged graft survival times. However, the demand for kidneys continues to outgrow the available supply, and there are efforts to increase use of donor kidneys with moderate-or highrisk profiles. This highlights the importance of evaluating the renal transplant patient in the context of both donor and recipient risk factors. Radiologists play an integral role within the multidisciplinary team in care of the transplant patient at every stage of the transplant process. In the immediate postoperative period, duplex US is the modality of choice for evaluating the renal allograft. It is useful for establishing a baseline examination for comparison at future surveillance imaging. In the setting of allograft dysfunction, advanced imaging techniques including MRI or contrastenhanced US may be useful for providing a more specific diagnosis and excluding nonrejection causes of renal dysfunction. When a pathologic diagnosis is deemed necessary to guide therapy, USguided biopsy is a relatively low-risk, safe procedure. The range of complications of renal transplantation can be organized temporally in relation to the time since surgery and/or according to disease categories, including immunologic (rejection), surgical or iatrogenic, vascular, urinary, infectious, and neoplastic complications. The unique heterotopic location of the renal allograft in the iliac fossa predisposes it to a specific set of complications. As imaging features of infection or malignancy may be nonspecific, awareness of the patient's risk profile and time since transplantation can be used to assign the probability of a certain diagnosis and thus guide more specific diagnostic workup. It is critical to understand variations in vascular anatomy, surgical technique, and independent donor and recipient risk factors to make an accurate diagnosis and initiate appropriate treatment. ©

Although a broad spectrum of entities can induce acute pathologic changes in the small bowel, there are relatively few imaging features that are characteristic of a specific diagnosis on the basis of CT findings. Specific clinical information, including time course and onset of disease, patient risk factors, and any recent pharmacologic or radiation therapy, is often instrumental in refining the differential diagnosis. A wide spectrum of disorders is reviewed in this article; however, given the breadth of disorders associated with the small bowel, neoplastic and infectious conditions affecting the small bowel that can manifest acutely are not specifically discussed. Vascular diseases that can affect the small bowel regionally or diffusely, including thromboembolic and hypoperfusion phenomena, as well as a spectrum of vasculitides, are reviewed. Iatrogenic causes of small bowel disorders are discussed, including angiotensin-converting enzyme inhibitor-induced angioedema, and chemotherapy- and radiation therapy-associated patterns of disease. Autoimmune and hereditary conditions that can affect the small bowel, including systemic lupus erythematosus and genetic C1 esterase inhibitor deficiency, respectively, are reviewed. RSNA, 2018.