RESUMO
The preponderance of pancreatic tumors is adenocarcinoma of the ductal type; carcinomas with multiple lineage differentiation are extremely rare. We report an unusual case of pancreatic carcinoma with combined acinar and neuroendocrine differentiation and minor ductal component with concurrent acinar-ductal metaplasia (ADM), an early lesion implicated in ductal carcinogenesis. The patient is a 56-year-old man with vague complaints of dull left upper quadrant pain with radiation across the mid-portion of his abdomen. A computer tomography scan revealed an irregular enlargement of the distal 3.2 cm of the pancreatic body. A distal pancreatectomy was then performed. Histologic examination revealed a pancreatic carcinoma with cellular features of eosinophilic granular cytoplasm and salt-pepper nuclei. The acinar differentiation of the carcinoma was confirmed by positivity on periodic acid-Schiff stain resistant to diastase digestion (dPAS), positivity for antitrypsin on immunohistochemistry (IHC), and presence of zymogen granules on electron microscopy (EM). The neuroendocrine differentiation was evident by positive synaptophysin and chromogranin stain on IHC and neuroendocrine granules on EM. The ductal component was only visible by PAS stain and immunostains for CEA and CK19A and accompanied by a number of the acinar-ductal metaplasia lesions adjacent to the main tumor. Thus, the histological, histochemical, immunohistochemical and electron-microscopic evidence all suggested that the pancreatic carcinoma underwent trilineage differentiation.
RESUMO
The modulation of vascular smooth muscle cells (VSMCs) from the quiescent phenotype to the proliferative and migratory phenotype is a critical event in the pathogenesis of atherosclerosis. To-date several growth factors, including platelet-derived growth factor, PDGF, have been shown to induce VSMC proliferation and migration. To further understand the mechanism of PDGF-induced VSMC activation, quiescent human coronary artery SMC were treated with PDGF, and the genes that displayed transcriptional changes within 3 and 8 h were identified using differential display RT-PCR, real-time PCR, nucleotide sequencing and bioinformatics. Eleven genes that were highly upregulated or down-regulated at 3 and/or 8 h by PDGF, designated growth-factor regulated VSMC genes (GRSG1-11), were analyzed. GRSG5 and GRSG9-1 were identified as cortactin and cytochrome c oxidase subunit II, respectively. The remaining nine GRSGs were novel. GRSG3, 4, 5 and 9-2 showed wide tissue distribution whereas GRSG10-1, 10-2, and 11 were tissue specific. Cortactin was localized by immunohistochemical staining to the neointima and fibrous cap of human coronary artery atherosclerotic plaques. Domain analysis of open reading frames suggest that the novel GRSGs may participate in signaling, metabolic, translational or migrational processes during PDGF-induced VSMC activation.
