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Cardiac Tumours
Published in Mary N. Sheppard, Practical Cardiovascular Pathology, 2022
Arguments concerning the origin of myxomas continue. It is now accepted that they are true neoplasms. DNA analysis of myxomas has shown to be mostly diploid and aneuploid. The cell of origin remains contentious. Ultrastructural studies suggest the tumour cells are most like primitive multipotential mesenchymal cells. The concept that this cell is capable of a wide range of phenotypic differentiation is supported by the reported expression of a wide range of antigens. The myxoma tumour cells often cluster around cells marking as endothelial cells with CD34 (Fig. 7.18), but whether these are just a supporting stroma or an integral part of the tumour is unclear. Cytokeratin may be focally positive if there is a glandular pattern of differentiation. Vimentin is usually positive in the tumour cells. Desmin is most frequently described as negative but smooth muscle actin can be positive in the myxoma cells as well as the stroma. Neuron-specific enolase, S-100 and synaptophysin have all been reported as variably positive (Fig. 7.19). Calretinin is the most useful marker and is strongly positive in all myxoma cells and very useful in differentiating from myxosarcomas which are usually negative (Fig. 7.20).9 Histiocytic/macrophage markers are positive in the stroma. The cells of the embryonic endocardial cushions resemble myxoma cells, and a widely held view is that nests of such cells persist in the endocardium, particularly in the region of the foramen ovale where they may give rise to myxomas but definitive identification of these in adults is lacking.
Breast Imaging with Radiolabeled Peptides
Published in Raymond Taillefer, Iraj Khalkhali, Alan D. Waxman, Hans J. Biersack, Radionuclide Imaging of the Breast, 2021
Eric P. Krenning, Marion de Jong, Roelf Valkema, Casper H.J. van Eijck
Between 1977 and 1982 several reports demonstrated a variety of argyrophilic breast tumors containing dense-core secretory granules and showing the typical features of carcinoids. Bussolati et al. also found argyrophilic chromogranin-positive cells immunocytochemically in part of human breast cancers with the mouse monoclonal antibody LK2H10 directed against human chromogranin [38]. Immunoreactivity for neuron-specific enolase, which is present in neurons, neuroendocrine cells, and tumors with neuroendocrine differentiation, was found in more than 30% of breast carcinomas. However, expression of this marker in mammary gland tissues does not appear to be always related to endocrine differentiation, as defined by ultrastructural demonstration of secretory granules. Other markers such as chromogranin A (CgA) and B and synaptophysin were later found to be more specific for neuroendocrine differentiation. In 391 patients with various tumors who underwent somatostatin receptor scintigraphy, we were recently able to make a comparison between serum values of CgA, neuron-specific enolase (NSE) and a-subunits of glycoprotein hormones (a-SU). Of 62 patients with breast cancer, elevated serum levels of CgA, NSE, and a-SU were found in 8%, 37%, and 10%, respectively; in 208 patients with various classical neuroendocrine tumors the mean figures were 50%, 43%, and 24%, respectively [39].
Degenerative Diseases of the Nervous System
Published in Philip B. Gorelick, Fernando D. Testai, Graeme J. Hankey, Joanna M. Wardlaw, Hankey's Clinical Neurology, 2020
James A. Mastrianni, Elizabeth A. Harris
Neuron-specific enolase (NSE) concentrations may be increased early (> 35 ng/mL; sensitivity 80%, specificity 92%) and when myoclonus and periodic sharp complexes appear, and return to normal in the late stage. Raised NSE in CSF is also reported in brain trauma, tumor, and acute stroke including subarachnoid hemorrhage. The enzyme is localized in neurons and neuroendocrine cells and is synthesized completely in the CNS.
Sinonasal undifferentiated carcinoma with metastasis to the extradural spine
Published in British Journal of Neurosurgery, 2023
Samuel Jones, Heather O’Connor, Fraser Henderson, Adriana Olar, Sunil Patel
SNUC is diagnosed by histopathological examination. Grossly, these tumors are usually larger than four centimeters with fungating, ill-defined margins. Invasion into adjacent structures and anatomic compartments with bone destruction is common. Histologically, the tumor is characterized by a submucosal cellular proliferation with lobular and trabecular growth patterns predominating. The cellular infiltrate consists of polygonal medium- to large-sized cells with a high nuclear-to-cytoplasmic ratio, eosinophilic cytoplasm, and well-defined borders. The nuclei can be hyperchromatic or vesicular with variably prominent nucleoli. SNUCs have a high mitotic rate with prominent confluent tumor necrosis and individual cell apoptosis. As seen in our case, lymph-vascular and perineural invasion are common.7 These tumors are consistently positive for neuron specific enolase.8 About 50% of cases will also express epithelial membrane antigen.7 We present here the histopathological features of this SNUC tumor (Figure 2) from the original resection specimen (day +8) and the cervical spine metastasis (day +302).
Neuromarkers which can predict neurodevelopmental impairment among children with congenital heart defects after cardiac surgery: A systematic literature review
Published in Developmental Neurorehabilitation, 2023
Lacramioara Eliza Chiperi, Cristina Tecar, Rodica Toganel
Neuron-specific enolase: NSE is a glycolytic enzyme, the main enolase found in neuronal and neuroendocrine tissues. Due to this neural-neuroendocrine specificity and a short half-life (approximately 24 h), its concentrations in cerebrospinal fluid and serum are elevated in disorders with rapid neuronal destruction (h/days) thus representing a useful diagnostic tool for neuron-destructive disorders.13 It is used as a tumor marker in various types of neoplasia (neuroblastoma, carcinoid tumor, Wilms tumor, small cell lung cancer) and also reaches high levels in degenerative diseases of the nervous system, intracranial hemorrhage and cerebral hypoxia representing a biomarker of neuronal damage.14 Various studies have demonstrated that NSE serum levels increase after CBP for 24 h before it returns to normal levels and that NSE can predict neurodevelopmental impairment following cardiac surgery. A couple of studies correlated NSE levels with neurodevelopmental impairment pattern in children with congenital heart defects requiring cardiac surgery. In a study published by Sanchez-de-Toledo et al. which included 39 subjects,19 a correlation was investigated between NSE and immediate post-operative neurologic event, but no correlation was found. In another study by Schmitt conducted on 27 patients,23 the role of NSE in predicting brain injury was unclear. In Trakas’s study including 18 neonates,18 short term levels of NSE after surgery were unassociated with brain injury.
Comparison of frequency of silent cerebral infarction as assessed by serum neuron specific enolase in patients with non-valvular atrial fibrillation: Warfarin versus direct oral anticoagulant
Published in Acta Cardiologica, 2023
Huseyin Goksuluk, Nil Ozyuncu, Irfan Veysel Duzen, Veysel Kutay Vurgun, Turkan Seda Tan, Sadi Gulec
Atrial fibrillation (AF) is an important risk factor for thromboembolic events. Asymptomatic neurologic injury may account for a greater percentage of thromboembolic complications [1,2]. Silent cerebral infarction (SCI) is defined as the evidence of cerebral infarction in the absence of a any clinically apparent stroke or transient ischaemic attack. The importance of the SCI has been highlighted in previous studies linking them to neurologic deficits [3,4], cognitive decline [5,6], psychiatric disorders (i.e. depression) [4,7], clinically apparent stroke [8,9] and increased mortality [8,10]. These findings revealed that the definition is neither silent nor innocuous. Silent cerebral infarction can be identified by means of imaging modalities as gold standard tests, but an acute event can also be detected by serum neuron specific enolase (NSE), which is suggested to be a valid, sensitive, neuronal ischaemia marker, detectable in the serum in 2–4 h after the insult and remaining positive for 3 days [11–13]. The relationship of neuron-specific enolase with ischaemic cerebral events and SCI has been investigated in previous studies [14–18]. The risk of SCI in the context of anticoagulant treatment in NVAF patients is still controversial. Therefore, we designed a cross-sectional study to compare the incidence of recent SCI in NVAF patients who take either warfarin or direct oral anticoagulant (DOAC).