Search

Rationale and Objectives: To determine the metabolic effects of developmental venous anomalies (DVAs) and to correlate those effects with conventional magnetic resonance imaging (MRI) findings.Materials and Methods: We conducted a retrospective review of MRI and brain 18F-fluorodeoxyglucose positron emission tomography (18F-FDG-PET) examinations in subjects with DVAs. Conventional MRI was used to determine DVA number, location, size, and associated parenchymal findings such as atrophy, hemorrhage, cavernoma, capillary telangiectasia, cortical dysplasia/polymicrogyria, and white matter signal abnormality. Qualitative and quantitative measures of relative metabolism in the drainage territory of the DVA were measured on 18F-FDG-PET.Results: Fifty-four subjects with 57 DVAs were included in the analysis. 38% were associated with qualitative and quantitative metabolic abnormalities on 18F-FDG-PET, with decreased metabolism in the parenchyma surrounding all but one of these DVAs. DVAs draining gray matter were significantly more likely to be hypometabolic than those draining only white matter, suggesting that the metabolic effects of DVAs may be underestimated on 18F-FDG-PET.Conclusion: Altered metabolism is seen in the drainage territory of a significant proportion of DVAs, suggesting that these anomalies are vascular lesions with abnormal physiologic features. [ABSTRACT FROM AUTHOR]

Rationale and Objectives: To determine the metabolic effects of developmental venous anomalies (DVAs) and to correlate those effects with conventional magnetic resonance imaging (MRI) findings., Materials and Methods: We conducted a retrospective review of MRI and brain 18F-fluorodeoxyglucose positron emission tomography ( 18 F-FDG-PET) examinations in subjects with DVAs. Conventional MRI was used to determine DVA number, location, size, and associated parenchymal findings such as atrophy, hemorrhage, cavernoma, capillary telangiectasia, cortical dysplasia/polymicrogyria, and white matter signal abnormality. Qualitative and quantitative measures of relative metabolism in the drainage territory of the DVA were measured on 18 F-FDG-PET., Results: Fifty-four subjects with 57 DVAs were included in the analysis. 38% were associated with qualitative and quantitative metabolic abnormalities on 18 F-FDG-PET, with decreased metabolism in the parenchyma surrounding all but one of these DVAs. DVAs draining gray matter were significantly more likely to be hypometabolic than those draining only white matter, suggesting that the metabolic effects of DVAs may be underestimated on 18 F-FDG-PET., Conclusion: Altered metabolism is seen in the drainage territory of a significant proportion of DVAs, suggesting that these anomalies are vascular lesions with abnormal physiologic features., (Copyright © 2018 The Association of University Radiologists. Published by Elsevier Inc. All rights reserved.)

Perineural spread (PNS) refers to tumor growth along large nerves, a macroscopic analog of microscopic perineural invasion. This phenomenon most commonly occurs in the head and neck, but its incidence varies with histologic tumor subtype. PNS results from a complex molecular interplay between tumor cells, nerves, and connective stroma. PNS is clinically underdiagnosed despite its impact on patients' prognosis and management. The role of 18 F-FDG PET in assessment of PNS in head and neck cancer remains to be explored, in contrast to MRI as the established gold standard. In patients with PNS, 18 F-FDG PET shows both abnormality along the course of the involved nerve and muscular changes secondary to denervation. Assessment of PNS on 18 F-FDG PET requires knowledge of relevant neural pathways and can be improved by correlation with anatomic imaging, additional processing of images, and review of clinical context., (© 2019 by the Society of Nuclear Medicine and Molecular Imaging.)

The role of Smad4 in transforming growth factor beta (TGFbeta)-mediated epithelial-mesenchymal transition (EMT), invasion, and metastasis was investigated using isogenically matched pancreatic cancer cell lines that differed only in expression of Smad4. Cells expressing Smad4 showed an enhanced TGFbeta-mediated EMT as determined by increased expression of vimentin and decreased expression of beta-catenin and E-cadherin. TGFbeta-mediated invasion was suppressed in Smad4-intact cells as determined by in vitro assays, and these cells showed a reduced metastasis in an orthotopic model of pancreatic cancer. Interestingly, TGFbeta inhibited STAT3(Tyr705) phosphorylation in Smad4-intact cells. The decrease in STAT3(Tyr705) phosphorylation was linked to a TGFbeta/Smad4-dependent and enhanced activation of extracellular signal-regulated kinases, which caused an increase in serine phosphorylation of STAT3(Ser727). Down-regulating signal transducer and activator of transcription 3 (STAT3) expression by short hairpin RNA in Smad4-deficient cells prevented TGFbeta-induced invasion. Conversely, expressing a constitutively activated form of STAT3 (STAT3-C) in Smad4-intact cells enhanced invasion. This study indicates the requirement of STAT3 activity for TGFbeta-induced invasion in pancreatic cancer cells and implicates Smad4-dependent signaling in regulating STAT3 activity. These findings further suggest that loss of Smad4, leading to aberrant activation of STAT3, contributes to the switch of TGFbeta from a tumor-suppressive to a tumor-promoting pathway in pancreatic cancer.