Cancer

Patients with estrogen receptor (ER)-positive breast cancer are at risk of metastatic relapse for decades after primary tumor resection and treatment, a consequence of dormant disseminated tumor cells (DTCs) reawakening at secondary sites. Here we use syngeneic ER+ mouse models in which DTCs display a dormant phenotype in young mice but accelerated metastatic outgrowth in an aged or fibrotic microenvironment. In young mice, low-level Pdgfc expression by ER+ DTCs is required for their maintenance in secondary sites but is insufficient to support development of macrometastases.

Classic Hodgkin lymphoma (cHL) has a rich immune infiltrate, which is an intrinsic component of the neoplastic process. Malignant Hodgkin Reed-Sternberg cells (HRSC) create an immunosuppressive microenvironment by the expression of regulatory molecules, preventing T-cell activation. It has also been demonstrated that mononuclear phagocytes (MNPs) in the vicinity of HRSC express similar regulatory mechanisms in parallel, and their presence in tissue is associated with inferior patient outcomes.

Introducción: El virus linfotrópico de células T humanas tipo 1 es el retrovirus causal de la leucemia-linfoma de células T. Su escaso diagnóstico en fases agudas hace que encontrar un biomarcador acertado para conocer el desarrollo de la leucemia sea de interés clínico y científico. Objetivo: Presentar la proteína basic zipper protein como marcador diagnóstico y de seguimiento al tratamiento de la leucemia-linfoma de células T. Métodos: Se consultó material académico en diferentes bases de datos científicas tales como PubMed, Springerlink, Proquest y Sciencedirect.

Abstract Unavailable

Current approaches to staging chronic liver diseases have limited utility for predicting liver cancer risk. Here, we employed single-nucleus RNA sequencing (snRNA-seq) to characterize the cellular microenvironment of healthy and pre-malignant livers using two distinct mouse models. Downstream analyses unraveled a previously uncharacterized disease-associated hepatocyte (daHep) transcriptional state. These cells were absent in healthy livers but increasingly prevalent as chronic liver disease progressed.

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Malignant salivary gland tumours characterized by mucoepidermal differentiation with sclerotic stroma rich in lymphocytes and eosinophils have been designated the name sclerosing mucoepidermoid carcinoma with eosinophilia1-4 (SMECE). However, it has not been listed as an entity in the chapter on salivary gland, 2022 WHO Classification of Head and Neck Tumours5 . Some reports highlighted the lack of MAML2 translocation in these tumours, as distinct from classical mucoepidermoid carcinoma (MEC) of the salivary glands.

Cholangiocarcinoma is the second most common primary liver malignant neoplasm. It usually affects older individuals in their seventh decade of life with no gender predilection. Recently, a distinct subtype of cholangiocarcinoma has emerged with 2 proposed names: "cholangioblastic" and "solid tubulocystic." This variant predominantly occurs in younger women who lack the common risk factors for patients diagnosed with cholangiocarcinomas, such as older age and chronic liver disease or cirrhosis. We describe 3 new patients with a cholangioblastic variant of intrahepatic cholangiocarcinoma.

Objectives To investigate the upstream regulatory molecules of proteasomal activator 28γ (PA28γ), and explore its specific regulatory mechanism and potential clinical significance in OSCC. Materials and methods qPCR was used to examine miR-34a, circFANCA and PSME3 expression. Western blotting was adopted to detect PA28γ expression. Transwell experiments were conducted to evaluate OSCC cell migration and invasion ability. FISH was used to evaluate the subcellular localization of circFANCA and miR-34a, and RNA pull-down verified the interaction between them.

Tumor-elicited inflammation confers tumorigenic properties, including cell death resistance, proliferation, or immune evasion. To focus on inflammatory signaling in tumors, we investigated linear ubiquitination, which enhances the nuclear factor-κB signaling pathway and prevents extrinsic programmed cell death under inflammatory environments. Here, we showed that linear ubiquitination was augmented especially in tumor cells around a necrotic core. Linear ubiquitination allowed melanomas to tolerate the hostile tumor microenvironment and to extend a necrosis-containing morphology.