Adenocarcinoma, Follicular ; Adult ; Carcinoid Tumor ; metabolism ; pathology ; Carcinoma, Renal Cell ; metabolism ; pathology ; surgery ; Diagnosis, Differential ; Female ; Humans ; Keratin-7 ; metabolism ; Kidney Neoplasms ; metabolism ; pathology ; surgery ; Mucin-1 ; metabolism

Carcinoma, Squamous Cell ; metabolism ; pathology ; surgery ; Female ; Follow-Up Studies ; Humans ; Keratin-7 ; metabolism ; Keratins ; metabolism ; Kidney Neoplasms ; metabolism ; pathology ; surgery ; Kidney Pelvis ; Middle Aged ; Mucin-1 ; metabolism

Adenoma ; metabolism ; pathology ; surgery ; Humans ; Keratin-7 ; metabolism ; Kidney Neoplasms ; metabolism ; pathology ; surgery ; Kidney Transplantation ; Living Donors ; Male ; Mucin-1 ; metabolism ; Young Adult

OBJECTIVETo study the expression of Notch receptors, ligands and downstream target genes in hypertrophic scar and normal skin, and to investigate its role in the development of hypertrophic scar.

METHODSBy immunohistochemistry, the expression of epidermal differentiation markers- beta1 integrin, keratin 14 (K14) and keratin 19 (K19), as well as Notch 1-4 and Jagged1 were examined in hypertrophic scars and normal skins. The expression of Notch downstream genes- P21 and P63 was analyzed with real-time quantitative PCR and immunohistochemistry staining.

RESULTSHistological analysis revealed a significant epidermal thickening in the hypertrophic scars, with excessive cell layers above the basal layer. Compared to the normal epidermis, the expression of beta1 integrin, K19 and K14 decreased in hypertrophic scars (P <0.05). Positive expression rate of Notch1 and Jagged1 in keratinocytes was significantly higher in hypertrophic scar than in normal skin (P < 0.05), while there was no difference in Notch2 and 3 positive expression rate. Furthermore, the expression of P21 was significantly up-regulated, while the expression of P63 was down-regulated in keratinocytes of hypertrophic scar (P < 0.05).

CONCLUSIONSNotch signal may play an important role in hypertrophic scar pathogenesis. Over-differentiation of Keratinocytes in hypertrophic scar may be related to the overexpression of Notch1 and Jagged1, up-regulation of P21 gene and down-regulation of P63 gene.

Adult ; Calcium-Binding Proteins ; metabolism ; Case-Control Studies ; Cicatrix, Hypertrophic ; metabolism ; pathology ; Down-Regulation ; Epidermis ; metabolism ; pathology ; Female ; Humans ; Integrin beta1 ; metabolism ; Intercellular Signaling Peptides and Proteins ; metabolism ; Jagged-1 Protein ; Keratin-14 ; metabolism ; Keratin-19 ; metabolism ; Male ; Membrane Proteins ; metabolism ; Receptor, Notch1 ; metabolism ; Serrate-Jagged Proteins ; Signal Transduction ; Up-Regulation ; Young Adult

OBJECTIVETo screen the regulatory proteins involved in Nox1 promoter activation in a cell model of inflammation and oxidative stress.

METHODSA cell model of inflammation and oxidative stress was established by stimulating A549 cells with tumor necrosis factor-α (TNF-α). The differential proteins binding to Nox1 promoter were screened by DNA pull-down and the binding proteins were separated by 2D electrophoresis and selected according to the their differential expression levels (with over 1.5-fold changes relative to the control level). The screened proteins were finally identified by MALDI-TOF/TOF-MS.

RESULTSSeven differentially expressed protein spots (all upregulated in the cell model) were obtained, among which GLE1, DDX19A, KRT1 and KRT10 were identified by mass spectrometry.

CONCLUSIONGLE1, DDX19A, KRT1 and KRT10 participate in the activation of Nox1 promoter in TNF-α-induced A549 cells, and this result provides new insights into the biological roles of the regulatory proteins of Nox1 promoter in inflammation and oxidative stress.

Cell Line, Tumor ; DEAD-box RNA Helicases ; metabolism ; Electrophoresis, Gel, Two-Dimensional ; Humans ; Inflammation ; Keratin-1 ; metabolism ; Keratin-10 ; metabolism ; Mass Spectrometry ; NADPH Oxidase 1 ; NADPH Oxidases ; genetics ; metabolism ; Nucleocytoplasmic Transport Proteins ; metabolism ; Oxidative Stress ; Promoter Regions, Genetic ; Tumor Necrosis Factor-alpha ; adverse effects

Adult ; Diagnosis, Differential ; Female ; Humans ; Keratin-18 ; metabolism ; Mucin-1 ; metabolism ; Omentum ; metabolism ; pathology ; Peritoneal Neoplasms ; metabolism ; pathology ; ultrastructure ; Pregnancy ; Trophoblastic Neoplasms ; metabolism ; pathology ; ultrastructure ; Trophoblastic Tumor, Placental Site ; pathology ; Vimentin ; metabolism

Antigens, CD34 ; metabolism ; Choriocarcinoma ; pathology ; Diagnosis, Differential ; Female ; Hemangioma ; metabolism ; pathology ; Humans ; Keratin-18 ; metabolism ; Mesenchymoma ; pathology ; Placenta ; pathology ; Placenta Diseases ; metabolism ; pathology ; Platelet Endothelial Cell Adhesion Molecule-1 ; metabolism ; Pregnancy ; Pregnancy Complications, Neoplastic ; metabolism ; pathology ; Young Adult

Adenocarcinoma ; metabolism ; pathology ; surgery ; Adult ; Choriocarcinoma ; metabolism ; pathology ; surgery ; Diagnosis, Differential ; Endometrial Neoplasms ; metabolism ; pathology ; surgery ; Female ; Humans ; Keratin-7 ; metabolism ; Mucin-1 ; metabolism ; Ovarian Neoplasms ; metabolism ; pathology ; surgery

Adult ; Carcinoma, Embryonal ; drug therapy ; metabolism ; pathology ; surgery ; Diagnosis, Differential ; Endodermal Sinus Tumor ; drug therapy ; metabolism ; pathology ; surgery ; Humans ; Keratin-19 ; metabolism ; Ki-1 Antigen ; metabolism ; Male ; Orchiectomy ; methods ; Testicular Neoplasms ; drug therapy ; metabolism ; pathology ; surgery ; alpha-Fetoproteins ; metabolism

OBJECTIVETo study the pathologic features, diagnosis, differential diagnosis and molecular characteristics of intraductal tubulopapillary neoplasm of the pancreas (ITPN).

METHODSThe clinical findings, morphologic features, immunophenotype (by EnVision method) and KRAS gene alterations (by reverse transcriptase-polymerase chain reaction) of 6 cases of ITPN encountered during the period from January, 2001 to June, 2010 were analyzed.

RESULTSThere were altogether 2 males and 4 females. The mean age of the patients was 64 years. Gross examination showed that the tumors were located in large pancreatic ducts and appeared as polypoid nodules with ductal obstruction. Solid tumor nodules associated with adjoining dilated ducts were identified in one case. Histologically, the tumors were characterized by tubulopapillary growth pattern without luminal mucin. The tumor cells showed high-grade nuclear atypia with scanty intracytoplasmic mucin. Intraductal necrotic foci were frequently observed. Immunohistochemical study showed that the tumor cells expressed CK7 and CK19. Focal positivity for MUC5AC was demonstrated. Two cases expressed MUC1. The staining for MUC2 was negative. KRAS gene mutations were identified in 2 cases, with a single-amino-acid substitution in codon 12 (35G > A and 35G > T/34G > A).

CONCLUSIONSITPN is a newly described pancreatic intraductal neoplasm and different from intraductal papillary mucinous neoplasm. ITPN is characterized by intraductal tubulopapillary growth pattern, severe cytologic atypia and scanty mucin secretion.

Aged ; Amino Acid Substitution ; Carcinoma, Pancreatic Ductal ; genetics ; metabolism ; pathology ; surgery ; Carcinoma, Papillary ; genetics ; metabolism ; pathology ; surgery ; Female ; Follow-Up Studies ; Humans ; Keratin-19 ; metabolism ; Keratin-7 ; metabolism ; Ki-67 Antigen ; metabolism ; Male ; Middle Aged ; Mucin 5AC ; metabolism ; Mucin-1 ; metabolism ; Pancreatectomy ; Pancreatic Neoplasms ; genetics ; metabolism ; pathology ; surgery ; Treatment Outcome