作者: Elisabetta Trevellin , Marco Scarpa , Amedeo Carraro , Francesca Lunardi , Andromachi Kotsafti
关键词: Adipose tissue macrophages 、 Endocrinology 、 Adenocarcinoma 、 Tumor progression 、 Biology 、 Adipocyte 、 Pathology 、 Adiponectin 、 Leptin 、 Adipose tissue 、 Metastasis 、 Internal medicine
摘要: // Elisabetta Trevellin 1,* , Marco Scarpa 2,* Amedeo Carraro 3 Francesca Lunardi 4 Andromachi Kotsafti 2 Andrea Porzionato 5 Luca Saadeh Matteo Cagol Rita Alfieri Umberto Tedeschi Fiorella Calabrese Carlo Castoro and Roberto Vettor 1 Department of Medicine, Internal Medicine 3, Endocrine-Metabolic Laboratory, University Padova, Italy Surgical Oncology Unit, Veneto Oncological Institute (IOV-IRCCS), General Surgery Odontoiatrics, Hospital Verona, Cardiothoracic Vascular Sciences, Molecular Normal Anatomy * These authors contributed equally to this work Correspondence to: Trevellin, email: Keywords : Esophageal adenocarcinoma, adipose tissue, peritumoral microenvironment, metastasis obesity Received January 05, 2015 Accepted February 19, Published March 14, Abstract Obesity is associated with cancer risk in esophageal adenocarcinoma (EAC). Adipose tissue directly stimulates tumor progression independently from body mass index (BMI), but the mechanisms are not fully understood. We studied morphological, histological molecular characteristics distal 60 patients EAC, investigate whether depot-specific differences affect behavior. observed that increased adipocyte size (a hallmark obesity) was leptin expression, angiogenesis (CD31) lymphangiogenesis (podoplanin); however, these parameters were nodal only patients. treated OE33 cells conditioned media (CM) collected cultured biopsies we mRNA levels adiponectin receptors, as well two key regulator genes epithelial-to-mesenchymal transition (EMT): alpha-smooth muscle actin (α-SMA) E-cadherin. This effect greater CM partially blunted by a antagonist. Therefore, may exert direct on EAC secreting paracrine factors, player crosstalk.