Colorectal carcinoma is a major cause of death throughout the Western world. It is increasingly recognized that any reduction in mortality must be achieved through the detection and removal of early and precancerous lesions. The primary attention for such a preventive strategy has been the polypoid adenoma and surveillance studies have shown a significant reduction in the incidence of carcinoma through systematic polypectomy of suspicious lesions. A potential problem with such a program, however, is raised by reports from Japan that some carcinomas seem to arise without a precursor polypoid adenoma, that is de novo. Although the histopathologic findings in such reports seem to clearly support this idea, this concept is not widely accepted in the Western world. We undertook a series of immunohistochemical (p53, bcl-2, Mib-1, E-cadherin, CD44, Stromelysin-3), and microsatellite analysis studies (on 17p (p53), 18q (DCC), 5q (APC), 8p, 2p and 1p), on groups of de novo and ex adenoma carcinomas in order to see if differences between the two groups of lesions exist. The results of these studies demonstrate that de novo carcinomas share several phenotypic and genotypic features with ex adenoma carcinoma (similar CD44 in the carcinomas, similar rates of LOH at APC and DCC loci), but have significantly higher rates of LOH at 17p, p53 over-expression and ST-3 expression indicating that tumor progression in de novo carcinoma is accelerated. These findings should help clarify the concept of de novo carcinoma and contribute to wider recognition of this important clinicopathologic entity.
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Purpose: To evaluate the effect of osilodrostat and hypercortisolism control on blood pressure (BP) and glycemic control in patients with Cushing's disease.
Methods: Pooled analysis of two Phase III osilodrostat studies (LINC 3 and LINC 4), both comprising a 48-week core phase and an optional open-label extension. Changes from baseline in systolic and diastolic BP (SBP and DBP), fasting plasma glucose (FPG), and glycated hemoglobin (HbA) were evaluated during osilodrostat treatment in patients with/without hypertension or diabetes at baseline.
Int J Mol Sci
January 2025
Department of Neurosurgery, Odense University Hospital, DK-5000 Odense, Denmark.
Pituitary adenomas are a diverse group of neoplasms with variable clinical behavior. Despite advances in genetic analysis, understanding the role of epigenetic modifications, particularly DNA methylation, remains an area under investigation. This scoping review aimed to update and synthesize the current body of literature on DNA methylation in pituitary adenomas, focusing on methodological advancements and clinical correlations.
View Article and Find Full Text PDFNat Rev Dis Primers
January 2025
Endocrine Division, Department of Medicine, Centre hospitalier de l'Université de Montréal (CHUM), Montreal, Québec, Canada.
Cushing syndrome (CS) is a constellation of signs and symptoms caused by excessive exposure to exogenous or endogenous glucocorticoid hormones. Endogenous CS is caused by increased cortisol production by one or both adrenal glands (adrenal CS) or by elevated adrenocorticotropic hormone (ACTH) secretion from a pituitary tumour (Cushing disease (CD)) or non-pituitary tumour (ectopic ACTH secretion), which stimulates excessive cortisol production. CS is associated with severe multisystem morbidity, including impaired cardiovascular and metabolic function, infections and neuropsychiatric disorders, which notably reduce quality of life.
View Article and Find Full Text PDFBMJ Case Rep
January 2025
Department of Maxillofacial Surgery, Dubrava University Hospital, Zagreb, Croatia
Myoepithelial carcinoma (MC) is a rare salivary gland malignancy that usually affects people over the age of 50. The incidence is similar in both men and women. MC might develop de novo or within a pre-existing benign myoepithelioma or pleomorphic adenoma.
View Article and Find Full Text PDFMol Oncol
January 2025
Department of Molecular Medicine, Aarhus University Hospital, Denmark.
The presence of circulating tumor DNA (ctDNA) in patients with colorectal adenomas remains uncertain. Studies using tumor-agnostic approaches report ctDNA in 10-15% of patients, though with uncertainty as to whether the signal originates from the adenoma. To obtain an accurate estimate of the proportion of patients with ctDNA, a sensitive tumor-informed strategy is preferred, as it ensures the detected signal originates from the adenoma.
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