Purpose: To investigate the potential of computed tomography (CT) imaging features and texture analysis to differentiate between mass-forming pancreatitis (MFP) and pancreatic ductal adenocarcinoma (PDAC).Materials and Methods: Thirty patients with pathologically proved MFP and 79 patients with PDAC were included in this study. Clinical data and CT imaging features of the two lesions were evaluated. Texture features were extracted from arterial and portal phase CT images using commercially available software (AnalysisKit). Multivariate logistic regression analyses were used to identify relevant CT imaging and texture parameters to discriminate MFP from PDAC. Receiver operating characteristic curves were performed to determine the diagnostic performance of predictions.Results: MFP showed a larger size compared to PDAC (p = 0.009). Cystic degeneration, pancreatic ductal dilatation, vascular invasion, and pancreatic sinistral portal hypertension were more frequent and duct penetrating sign was less frequent in PDAC compared to MFP. Arterial CT attenuation, arterial, and portal enhancement ratios of MFP were higher than PDAC (p < 0.05). In multivariate analysis, arterial CT attenuation and pancreatic duct penetrating sign were independent predictors. Texture features in arterial phase including SurfaceArea, Percentile40, InverseDifferenceMoment_angle90_offset4, LongRunEmphasis_angle45_offset4, and uniformity were independent predictors. Texture features in portal phase including LongRunEmphasis_angle135_offset7, VoxelValueSum, LongRunEmphasis_angle135_offset4, and GLCMEntropy_angle45_offset1 were independent predictors. Areas under the curve of imaging feature-based, texture feature-based in arterial and portal phases, and the combined models were 0.84, 0.96, 0.93, and 0.98, respectively.Conclusions: CT texture analysis demonstrates great potential to differentiate MFP from PDAC.
Polo-like kinase 4 (PLK4), a key regulator of centriole biogenesis, has recently been shown to play key roles in tumorigenesis. Blocking PLK4 expression by interference or targeted drugs exhibits attractive potential in improving the efficacy of chemotherapy. Nevertheless, the role of PLK4 in diffuse large B-cell lymphoma (DLBCL) is still undefined. In this study, we discover that PLK4 is a potential target for the treatment of DLBCL, and demonstrate the efficacy of a PLK4 inhibitor when used in combination with doxorubicin. Pharmaceutical inhibition of PLK4 with CFI-400945 inhibited DLBCL cell proliferation and induced apoptotic cell death. The anti-tumor effects were accompanied by mitotic defects, including polyploidy and cytokinesis failure. Activation of p53 and Hippo/YAP tumor suppressor signaling pathway was identified as the potential mechanisms driving CFI-400945 activity. Moreover, CFI-400945 treatment resulted in activation of DNA damage response. Combining CFI-400945 with doxorubicin markedly delayed tumor progression in DLBCL xenografts. Finally, PLK4 was increased in primary DLBCL tissues and cell lines. High levels of PLK4 expression were associated with poor survival in the patients receiving CHOP-based treatment, implicating PLK4 as a predictive biomarker of DLBCL chemosensitivity. These results provide the therapeutic potential of CFI-400945 both as monotherapy or in combination with doxorubicin for the treatment of DLBCL.
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