Thyroid nodules are prevalent in the general population. Distinguishing benign and malignant thyroid nodules is a clinical challenge. Although ultrasonography is commonly used for the assessment of thyroid nodules, previous studies have found that its usefulness is controversial. Therefore, there is a need to assess the clinical value of ultrasonography reported in the literature. This article reviews the literature on the clinical value of greyscale ultrasonography, colour and power Doppler ultrasonography, and ultrasound elastography in differentiating benign and malignant thyroid nodules.
Brain tumor behavior is driven by aberrations in the genome and epigenome. Many of these changes, such as IDH mutations in diffuse low-grade glioma (DLGG), are common amongst the same class of tumour and can be incorporated into the diagnostic criteria. However, any given tumor may have other, less common genomic aberrations that are essential for its biological behavior and may inform on underlying aberrant cellular pathways, and potential therapeutic agents. Precision oncology is a genomics-based approach which profiles these alterations to better manage cancer patients and has established itself within the practice of oncology and is slowly making its way into neuro-oncology. The BC Cancer’s Personalized OncoGenomics (POG) program has profiled 16 adult tumours originating from the central nervous system using whole genome and transcriptome analysis (WGTA), for the first time, within a meaningful clinical timeframe/setting. As expected, primary genomic drivers were consistent with their respective diagnoses, though secondary drivers were found to be unique to each tumour. Although these analyses did not result in altered clinical management for these patients, primarily due to availability of drug or clinical trials, they highlight the heterogeneity of secondary drivers in cancers and provide clinicians with meaningful biological information. Lastly, the data generated by POG has highlighted the frequency and complexity of novel driver fusions which are predicted to behave similarly to canonical driver events in their respective tumours. The information available to clinicians through POG has provided paramount knowledge into the biology of each unique tumour.
Introduction The intervertebral disk is composed of three structures: a central gelatinous nucleus pulposus (NP), surrounded peripherally by a tough annulus fibrosus (AF), and flanked on either end by an endplate (EP). They function together to allow flexibility and confer weight-bearing properties to the spine. Under normal conditions, there is a constant turnover of the IVD matrix, in which protein is produced in balance to their degradation rate. IVD cells are the key to keeping this homeostasis of the matrix and thus the functionality of IVD. Degeneration initiates when IVD cells fail to effectively replace degraded matrix proteins. Hence if IVD cells could not be maintained, the disk will degenerate. It is therefore important to study the factors that could influence the normal phenotype of IVD cells. The niche in which IVD cells reside constantly interacts with the cells and is a main factor involved. Type II collagen is one of the major proteins expressed in this niche. It entraps proteoglycans to keep the structure hydrated. In normal turnover, its degradation is initiated at a single site (PQG775↓776LAG) within the triple helix. A mouse mutant (Col2a1cr) in which this site is altered has been generated. It exhibits a cartilage matrix less susceptible to degradation.1 Given the high expression level of type II collagen in the IVD, we postulate that this mouse will also show a reduced IVD matrix turnover rate. We therefore utilize this mouse to study the relationship between a normal matrix turnover and the IVD cellular differentiation. Materials and Methods Metachromatic histological analysis2 is performed on IVD sections at different stages from neonatal (P10) to maturity (1 year). Molecular and cellular changes are analyzed by immunohistochemical staining using IVD specific markers such as brachyury and Sox9. Results The IVD of the mutant is structurally similar to normal mouse at neonatal stages (Fig. A). However the cartilaginous EP thickens and becomes more cellular at later stages. Its complete ossification is also much delayed. Cells in the AF are less flattened and more chondrocyte-like at all stages examined (Fig. B). An enhanced type II collagen staining with simultaneous increase in safranin O staining is observed, indicating a change in proteoglycan distribution in the matrix. Closer examination using molecular markers reveals altered brachyury and Sox9 expression levels in IVD cells, which implicated a change in their differentiation state. Conclusion We have demonstrated that by impairing type II collagen degradation, IVD cellular phenotype is altered. This implies that matrix turnover may play a role in determining differentiation of IVD cells. A balance of all factors in IVD matrix is crucial in maintaining the phenotype and function of IVD cells. The altered matrix composition may have an effect on their early differentiation; whereas in later stages additional influence resulting from structural changes within the EP could modify nutrient supply to the cells. Further investigat...
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