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Chondrosarcomas of the sinonasal cavity and skull base are uncommon malignancies. We sought to provide long-term outcomes at two tertiary care centers.Patients with chondrosarcoma treated between 2000 and 2021 were included. The primary outcomes were overall survival (OS) and disease-specific survival (DSS).Thirty-eight patients met inclusion criteria. Fourteen patients had sinonasal (36.8%), 7 petroclival (18.4%), and 17 other primary skull base lesions (44.7%). Twenty-eight patients (73.7%) underwent radiation with an average dose of 67.3 ± 15.1 Gy. Eighteen patients (47.4%) required revision surgery for recurrence. 1, 5, and 10-year OS were 97.3%, 93.1%, and 74.7%. DSS at 5- and 10-year survival was 95.7%. Adjuvant radiation was associated with improved OS (HR: 0.12; 95% CI: 0.02-0.75, p = 0.023).We present our experience over the last 20 years treating chondrosarcomas. Favorable survival outcomes can be achieved but recurrence requiring repeat resection is common.

Supplementary Figure 1 from Inhibition of STAT3Tyr705 Phosphorylation by Smad4 Suppresses Transforming Growth Factor β–Mediated Invasion and Metastasis in Pancreatic Cancer Cells

The role of Smad4 in transforming growth factor β (TGFβ)–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 TGFβ-mediated EMT as determined by increased expression of vimentin and decreased expression of β-catenin and E-cadherin. TGFβ-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, TGFβ inhibited STAT3Tyr705 phosphorylation in Smad4-intact cells. The decrease in STAT3Tyr705 phosphorylation was linked to a TGFβ/Smad4-dependent and enhanced activation of extracellular signal-regulated kinases, which caused an increase in serine phosphorylation of STAT3Ser727. Down-regulating signal transducer and activator of transcription 3 (STAT3) expression by short hairpin RNA in Smad4-deficient cells prevented TGFβ-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 TGFβ-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 TGFβ from a tumor-suppressive to a tumor-promoting pathway in pancreatic cancer. [Cancer Res 2008;68(11):4221–8]

Supplementary Figure 1 Legend from Inhibition of STAT3Tyr705 Phosphorylation by Smad4 Suppresses Transforming Growth Factor β–Mediated Invasion and Metastasis in Pancreatic Cancer Cells

Pre-operative magnetic resonance imaging (MRI) studies are routinely ordered for trigeminal neuralgia (TN), though with contested reliability in contemporary literature. A potential reason for this disagreement is inconsistency in MRI reading methodologies. Here, we compare the rate of reported neurovascular compression on pre-operative MRI by radiologists employed in community or private practice settings and academic neuroradiologists.A retrospective review was conducted on patients who underwent endoscopic microvascular decompression (E-MVD) for TN with intra-operatively visualized neurovascular compression and primary read by a non-academic or community radiologist. Patient imaging was then re-read by a board-certified neuroradiologist practicing in an academic setting, who was blinded to the initial read and the side of TN symptoms.Non-academic radiologists reported vascular compression in 26.0% (20/77) of all patients, and mention was rarely made of the non-pathological side (sensitivity=26.0%). On academic neuroradiologist re-reads, vascular compression was noted in 87.0% (67/77) of patients on the pathological side and in 57.1% (44/77) on the non-pathological side (sensitivity=87.0%, specificity=42.9%). Isotropic/near isotropic 3D steady state or heavily T2-weighted sequences were read with 92.3% sensitivity and 36.9% specificity, compared to 58.3% sensitivity and 66.7% specificity using routine T2 weighted sequences.The frequency of vascular compression reported by non-academic radiologists is much lower than what is reported by academic neuroradiologists reading the same MRI scans. These results highlight the effect of practice setting on the predictive power of neuroimaging. Future studies are indicated to further investigate these relationships, as well as to trial newer imaging modalities.

After dedicated CT and MRI, Ga-DOTATATE PET/CT was performed in a patient with a temporal bone mass with primary diagnostic considerations of an endolymphatic sac tumor versus a glomus jugulotympanicum paraganglioma. The Ga-DOTATATE PET showed mild radiotracer uptake in the mass (SUVmax, 10.9). After surgical resection, pathology revealed an endolymphatic sac tumor. Immunohistochemical staining demonstrated somatostatin receptor type 2A expression in the vasculature of the mass, but not in the tumor cells.

Variations in the venous drainage of the central nervous system can have imaging and clinical findings that mimic pathology, presenting a challenge for neuroimagers and clinicians. Patients with these variants may undergo unnecessary testing, and patients with pathology may receive delayed diagnoses because of overlap with benign findings. Consequently, the accurate identification of venous variations on cross-sectional imaging and angiography and their potential causes are critical for differentiating benign imaging variants from potential pathologic processes requiring further evaluation. For example, in the epidural space, benign dilation of the epidural venous plexus may be mistaken for evidence of a fistula, abscess, or metastasis. Hypoplasia of a dural venous sinus or an arachnoid granulation may mimic venous sinus thrombosis. The superior ophthalmic vein may demonstrate benign dilation in intubated patients, mimicking thrombosis, increased intracranial pressure, orbital varix, inflammatory pseudotumor, or other conditions. Furthermore, certain venous variations, such as the occipital sinus or emissary veins, may complicate surgery or herald pathology and should be reported. In addition, some supposedly benign variations, such as the developmental venous anomaly, can be complicated by pathology. The objective of this review article is to provide a descriptive and pictorial review of common anatomic and physiologic variations in the venous drainage system of the brain, spine, and orbits that can mimic pathology. Neuroimaging findings of related pathologies and differences in clinical presentations will also be discussed to assist in the approach to differential diagnosis.

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.

Objectives Guidelines for transoral robotic surgery (TORS) have generally regarded patients with retropharyngeal carotid arteries as contraindicated for surgery due to a theoretical risk of intraoperative vascular injury and/or perioperative cerebrovascular accident. We aimed to demonstrate that careful TORS-assisted resection and free flap coverage could not only avoid intraoperative injury and provide a physical barrier for vessel coverage but also achieve adequate margin control. Study design Retrospective cohort analysis. Methods Retrospective review of patients with oropharyngeal malignancies and radiologically confirmed retropharyngeal carotid arteries who underwent TORS, concurrent neck dissection, and free flap reconstruction between 2015 and 2019. Results Twenty patients were included, 19 (95.0%) with tonsillar tumors and one (5.0%) with a tongue base tumor with significant tonsillar extension. Eighteen patients (90.0%) received a radial artery forearm flap, one (5.0%) an ulnar artery forearm flap, and one (5.0%) an anteromedial thigh flap. All 20 (100%) flaps were inset through combined transcervical and transoral approaches without mandibulotomy. There were no perioperative mortalities, carotid injuries, oropharyngeal bleeds, cervical hematomas, or cerebrovascular accidents. One patient (5.0%) had a free flap failure requiring explant. All patients underwent decannulation and resumed a full oral diet. The mean length of hospitalization was 6.8 (standard deviation 1.2) days. One (5.0%) patient had a positive margin. Conclusion In this analysis, 20 patients with oropharyngeal malignancy and retropharyngeal carotid arteries underwent TORS, neck dissection, and microvascular reconstruction without serious complication (perioperative mortality, vascular injury, or neurologic sequalae) with an acceptable negative margin rate. These results may lead to a reconsideration of a commonly held contraindication to TORS. Level of evidence 3 Laryngoscope, 131:E821-E827, 2021.

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 18F-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, 18F-FDG PET shows both abnormality along the course of the involved nerve and muscular changes secondary to denervation. Assessment of PNS on 18F-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.

BACKGROUND AND PURPOSE: This study’s purpose is to correlate location and metabolic activity of developmental venous anomalies (DVAs) in epilepsy patients to the seizure focus as determined by ictal/interictal encephaloelectrogram (EEG). METHODS: A retrospective search was performed for epilepsy patients with DVAs who underwent brain (18)F-fluorodeoxyglucose positron emission tomography ((18)F-FDG-PET) and magnetic resonance imaging (MRI). MRI exams were analyzed to characterize DVA location and associated structural findings. MRI and PET images were co-registered and assessment of (18)F-FDG uptake in the DVA territory was performed. The electronic medical record was reviewed for each subject to determine seizure semiology and site of seizure focus by ictal/interictal EEG. RESULTS: Twenty-eight DVAs in 25 patients were included. Twelve DVAs demonstrated regional metabolic abnormality on (18)F-FDG-PET. There was no significant correlation between DVA site and seizure focus on EEG. DVA location was concordant with EEG seizure focus in three subjects, and all three demonstrated hypometabolism on (18)F-FDG-PET. This significance remains indeterminate, as one of these DVAs was associated with cavernoma, which could serve as the true seizure focus, and one of the patients underwent resection of the DVA without decrease in seizure frequency. Furthermore, there was no statistically significant relationship between DVA metabolic activity and DVA-EEG lobar or laterality concordance. CONCLUSIONS: In this sample, there is no significant correlation between location of DVA and seizure focus, and hypometabolism within the DVA territory is not predictive of EEG/DVA co-localization. As use of (18)F-FDG-PET for evaluation of epilepsy increases, knowledge of this poor correlation is important to avoid diagnostic confusion and potentially unnecessary surgery in epilepsy patients.

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

To determine the metabolic effects of developmental venous anomalies (DVAs) and to correlate those effects with conventional magnetic resonance imaging (MRI) findings.We conducted a retrospective review of MRI and brain 18F-fluorodeoxyglucose positron emission tomography (Fifty-four subjects with 57 DVAs were included in the analysis. 38% were associated with qualitative and quantitative metabolic abnormalities onAltered metabolism is seen in the drainage territory of a significant proportion of DVAs, suggesting that these anomalies are vascular lesions with abnormal physiologic features.

We describe the computed tomographic (CT) and magnetic resonance imaging (MRI) features of a very rare renal neoplasm, a glomus tumor. Our patient was a 68-year-old woman with a history of high grade T1 stage bladder cancer, status post intravesical Bacillus Calmette-Guerin (BCG) therapy and left ureteral stent placement, who presented for routine follow-up imaging evaluation of the urothelial tract. Computed tomographic urography (CTU) incidentally demonstrated a 1.7 cm well-circumscribed, non-calcified, non-fat containing lesion in the left renal cortex with arterial phase continuous peripheral rim enhancement and central hypoattenuation relative to enhanced renal parenchyma. Subsequent MRI showed the lesion to be isointense in signal intensity relative to the renal parenchyma on T1-weighted imaging and hyperintense on T2-weighted imaging. No macroscopic fat or microscopic lipid was seen within the lesion, and there were no foci of susceptibility artifact on T1-weighted images. Diffusion-weighted and apparent diffusion coefficient images demonstrated no restricted diffusion. Contrast-enhanced images demonstrated continuous peripheral rim enhancement in the arterial phase and persistent rim enhancement with partial centripetal fill in of enhancement on venous phase images, similar to the pattern seen on CT. Partial left nephrectomy was performed for the suspected solid renal neoplasm. Histopathological assessment was diagnostic of a renal glomus tumor.

The classification of posterior fossa congenital anomalies has been a controversial topic. Advances in genetics and imaging have allowed a better understanding of the embryologic development of these abnormalities. A new classification schema correlates the embryologic, morphologic, and genetic bases of these anomalies in order to better distinguish and describe them. Although they provide a better understanding of the clinical aspects and genetics of these disorders, it is crucial for the radiologist to be able to diagnose the congenital posterior fossa anomalies based on their morphology, since neuroimaging is usually the initial step when these disorders are suspected. We divide the most common posterior fossa congenital anomalies into two groups: 1) hindbrain malformations, including diseases with cerebellar or vermian agenesis, aplasia or hypoplasia and cystic posterior fossa anomalies; and 2) cranial vault malformations. In addition, we will review the embryologic development of the posterior fossa and, from the perspective of embryonic development, will describe the imaging appearance of congenital posterior fossa anomalies. Knowledge of the developmental bases of these malformations facilitates detection of the morphological changes identified on imaging, allowing accurate differentiation and diagnosis of congenital posterior fossa anomalies.

A mechanism whereby water flow towards root surfaces is stimulated when exposed to nutrient patches may be evolutionarily desirable in environments with heterogeneous soils. Indeed, the presence of nitrate has been shown to increase root hydraulic conductance in a few agricultural species characterized by high nitrate demand. Does a similar stimulation of root conductivity in response to external nitrate addition exist among wild type organisms? To answer this question, we studied and compared the effect of a sudden increase of nitrate concentration on root hydraulic properties in seven species. These included three agricultural species (Cucumis sativus L., Solanum esculentum L., Zea mays L.) and four wild type species (Arabidopsis thaliana L., Festuca arundinacea Schreb., Populus trichocarpa Torr.&Gray, Nephrolepis exaltata L.). The selected species differed in overall nitrate demand and specific nitrate uptake rates. Changes in root hydraulic conductance induced by nitrate varied from non-existent (N. exaltata L.) to more than 50% increases (Z. mays L.). The magnitude of the hydraulic response to nitrate presence was significantly correlated with species nitrate uptake rate. This finding suggests an emergent physiological trait that links together plant nitrate needs, nitrate availability and root hydraulic properties.

The role of Smad4 in transforming growth factor β (TGFβ)–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 TGFβ-mediated EMT as determined by increased expression of vimentin and decreased expression of β-catenin and E-cadherin. TGFβ-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, TGFβ inhibited STAT3Tyr705 phosphorylation in Smad4-intact cells. The decrease in STAT3Tyr705 phosphorylation was linked to a TGFβ/Smad4-dependent and enhanced activation of extracellular signal-regulated kinases, which caused an increase in serine phosphorylation of STAT3Ser727. Down-regulating signal transducer and activator of transcription 3 (STAT3) expression by short hairpin RNA in Smad4-deficient cells prevented TGFβ-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 TGFβ-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 TGFβ from a tumor-suppressive to a tumor-promoting pathway in pancreatic cancer. [Cancer Res 2008;68(11):4221–8]