Background: Recently, the immunohistochemical markers cytokeratin 17 (CK17) and SRY-box2 (SOX2) have been evaluated as adjuncts for the diagnosis of high-grade vulvar intraepithelial neoplasia (VIN). In the present study, the aim was to assess CK17 and SOX2 expression in VIN by studying 150 vulvar lesions, originally reported as high-grade VIN and to assess the diagnostic accuracy.
Methods: All slides (H&E, p16, p53, Ki-67, CK17, and SOX2 stains) were independently assessed by six pathologists and the final diagnosis was reached in consensus meetings, as follows: 46 human papillomavirus (HPV)-independent VIN (including 30 p53 mutant and 16 p53 wild-type lesions), 58 high-grade squamous intraepithelial lesions (HSILs), 4 low-grade SILs (LSILs), 37 non-dysplastic lesions, and 5 lesions where the histology was inconclusive.
Objective: To systematically explore vulvar pathology diagnosed prior to vulvar squamous cell carcinoma (VSCC), as well as the association with tumor characteristics, stage and survival outcome, with the aim of improving vulvar cancer prevention strategies.
Methods: VSCC diagnosed between 2005 and 2019 were identified from a population-based cohort provided by the Dutch Nationwide Pathology Databank. Pathology reports were reviewed to identify vulvar pathology diagnosed before primary VSCC.
Aims: Data on the clinical profiles of patients with transthyretin amyloidosis cardiomyopathy (ATTR-CM) in the post-approval era of tafamidis 61 mg are lacking. Study aims were characterization of contemporary ATTR-CM patients, analysis of potential eligibility for the 'Transthyretin Amyloidosis Cardiomyopathy Clinical Trial' (ATTR-ACT) and identification of factors associated with the decision on tafamidis 61 mg treatment.
Methods And Results: This retrospective study analysed ATTR-CM patients seen at eight University Hospitals in the first year after approval of tafamidis 61 mg for ATTR-CM in Germany (April 2020 to March 2021).
Aims: Myocardial inflammation and impaired mitochondrial oxidative capacity are hallmarks of heart failure (HF) pathophysiology. The extent of myocardial inflammation in patients suffering from ischaemic cardiomyopathy (ICM) or dilated cardiomyopathy (DCM) and its association with mitochondrial energy metabolism are unknown. We aimed at establishing a relevant role of cardiac inflammation in the impairment of mitochondrial energy production in advanced ischaemic and non-ischaemic HF.
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