Assuntos
Amianto/efeitos adversos , Asbestose/complicações , Pleura/diagnóstico por imagem , Doenças Pleurais/complicações , Atelectasia Pulmonar/etiologia , Tomografia Computadorizada por Raios X/métodos , Idoso , Asbestose/diagnóstico , Asbestose/cirurgia , Biópsia , Diagnóstico Diferencial , Humanos , Masculino , Doenças Pleurais/diagnóstico , Doenças Pleurais/cirurgia , Atelectasia Pulmonar/diagnóstico , Cirurgia Torácica VídeoassistidaRESUMO
Barrett's esophagus (BE) is a metaplastic process whereby the normal stratified, squamous esophageal epithelium is replaced by specialized intestinal epithelium. Barrett's is the only accepted precursor lesion for esophageal adenocarcinoma (EAC), a solid tumor that is rapidly increasing in incidence in western countries. BE evolves into EAC through intermediate steps that involve increasing degrees of dysplasia. Current histologic criteria are quite subjective and the clinical behavior of BE is highly variable and difficult to predict using these standards. It is widely believed that molecular alterations present in BE and EAC will provide more precise prognostic and predictive markers for these conditions than the current clinical and histologic features in use. In order to further define molecular alterations that can classify unique groups of BE and EAC, we utilized methylation microarrays to compare the global gene methylation status of a collection of normal squamous, BE, BE + high-grade dysplasia (HGD), and EAC cases. We found distinct global methylation signatures, as well as differential methylation of specific genes, that discriminated these histological groups. We also noted high and low methylation epigenotypes among the BE and EAC cases. Additional validation of those CpG sites that distinguished BE from BE + HGD and EAC may lead to the discovery of useful biomarkers with potential clinical applications in the diagnosis and prognosis of BE and EAC.
Assuntos
Adenocarcinoma/genética , Esôfago de Barrett/genética , Ilhas de CpG/genética , Metilação de DNA/genética , Neoplasias Esofágicas/genética , Adenocarcinoma/patologia , Idoso , Esôfago de Barrett/patologia , Biomarcadores Tumorais/genética , Progressão da Doença , Epigênese Genética/genética , Neoplasias Esofágicas/patologia , Regulação Neoplásica da Expressão Gênica , Humanos , Pessoa de Meia-Idade , Estadiamento de Neoplasias , Análise de Sequência com Séries de Oligonucleotídeos/métodos , Prognóstico , Análise de Sequência de DNARESUMO
Pseudolesions in the liver are caused by unusual/altered hemodynamics of the liver and can be confused with a true hepatic mass. In superior vena cava (SVC) obstruction. there is recruitment of the cavo-mammary-phrenic-hepatic-capsule-portal pathway. and the venous blood follows the internal mammary vein, the inferior phrenic vein, the hepatic capsule veins, and the intrahepatic portal system. causing a hypervascular pseudolesion in segment IV A of the liver. Recognizing the classic appearances of this hypervascular pseudolesion from the vein of Sappey in a CT study of the abdomen has prognostic implications in directing further evaluation of the chest for SVC obstruction. We present a case of a 54-year-old HIV-positive male smoker in whom identification of the hypervascular pseudolesion from the vein of Sappey on the abdominal CT led to the diagnosis of SVC syndrome.
