Deficiency in DDR1 Induces Pulmonary Hypertension and Impaired Alveolar Development.

Pulmonary hypertension (PH) is a multifaceted condition characterized by elevated pulmonary arterial pressure, which can result in right ventricular dysfunction and failure. Disorders of lung development can present with secondary PH, which is a leading cause of mortality in infants with bronchopulmonary dysplasia (BPD). DDR1 (discoidin domain receptor 1) is a collagen-binding receptor that regulates tissue fibrosis and inflammation and controls cellular growth and migration.

PD-L1 assessment in cytology samples predicts treatment response to checkpoint inhibitors in NSCLC.

Background: Testing for tumor programmed death ligand-1 (PD-L1) expression was initially developed with histology specimens in non-small cell lung cancer (NSCLC). However, cytology specimens are widely used for primary diagnosis and biomarker studies in clinical practice. Limited clinical data exist on the predictiveness of cytology-derived PD-L1 scores for response to immune checkpoint inhibitor (ICI) therapy.

Clinicopathological, immunophenotypic and genetic studies of mediastinal paragangliomas†.

Objectives: Paragangliomas have unique features in the mediastinum, in part due to their location. Because of their paucity, they have not been thoroughly investigated. We studied the clinical, pathological, immunohistochemical and molecular features of mediastinal paragangliomas.

The c-Jun and JunB transcription factors facilitate the transit of classical Hodgkin lymphoma tumour cells through G.

Classical Hodgkin Lymphoma (cHL) is primarily a B cell lymphoid neoplasm and a member of the CD30-positive lymphomas. cHL and the other CD30-positive lymphomas are characterized by the elevated expression and/or constitutive activation of the activator protein-1 (AP-1) family transcription factors, c-Jun and JunB; however, the specific roles they play in the pathobiology of cHL are unclear. In this report we show that reducing either c-Jun or JunB expression with short-hairpin RNAs (shRNAs) reduced the growth of cHL cell lines in vitro and in vivo, primarily through impairing cell cycle transition through G.

MELAS syndrome and cardiomyopathy: linking mitochondrial function to heart failure pathogenesis.

Heart failure remains an important clinical burden, and mitochondrial dysfunction plays a key role in its pathogenesis. The heart has a high metabolic demand, and mitochondrial function is a key determinant of myocardial performance. In mitochondrial disorders, hypertrophic remodeling is the early pattern of cardiomyopathy with progression to dilated cardiomyopathy, conduction defects and ventricular pre-excitation occurring in a significant proportion of patients.

Molecular transplantation pathology: the interface between molecules and histopathology.

Purpose Of Review: In the last decade, high-throughput molecular screening methods have revolutionized the transplantation research. This article reviews the new knowledge that has emerged from transplant patient sample-derived 'omics data by examining the interface between molecular signals and allograft pathology.

Recent Findings: State-of-the-art molecular studies have shed light on the biology of organ transplant diseases and provided several potential molecular tests with diagnostic, prognostic, and theranostic applications for the implementation of personalized medicine in transplantation.

Sumoylated SnoN represses transcription in a promoter-specific manner.

The transcriptional modulator SnoN controls a diverse set of biological processes, including cell proliferation and differentiation. The mechanisms by which SnoN regulates these processes remain incompletely understood. Recent studies have shown that SnoN exerts positive or negative regulatory effects on transcription.