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

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

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

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

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

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

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

OBJECTIVETo investigate the clinical and pathological features of the mucinous tubular and spindle cell carcinoma (MTSCC) of the kidney.

METHODSSeven cases of MTSCC were analyzed by gross examination and light microscopy. Immunostaining was performed to detect the expression of CD10, CK7, CK18, CK19, Villin, EMA, P504S and vimentin. The literature on this tumor was reviewed to discuss the histological features of MTSCC and its clinical behavior.

RESULTSThree of 7 cases were male and the other 4 were female. The mean age of the patients was 48.2 years old, with a range from 39 to 61 years. All the patients presented no symptom and their tumors were found by health examination. Tumors averaged 5.5 cm in greatest dimension (range from 4.0 cm to 9.0 cm). The tumors were well-circumscribed without capsules, and the cut surfaces were solid and soft with white-tan color. By light microscopy, tumors were composed of tightly packed, small, elongated tubules with transitions to spindle cell components. Five cases had mucinous stroma. Clear cell clusters, focal sarcomatoid differentiation, papillations and foamy macrophages were seen in several cases. Immunohistochemically, all 7 cases showed positive for CK7, five of 5 cases positive for EMA, CK18 and P504S, four of 5 cases positive for CK19, but heterogeneous for CD10, villin and vimentin expression. No evidence of local recurrence or distant metastases was identified in the 5 patients with follow-up information.

CONCLUSIONSThe mucinous tubular and spindle cell carcinoma is a low-grade and polymorphic neoplasm. The morphology of these tumors may not be uniform with a wide histological spectrum. The tumors can be tubular predominant or spindle cells predominant with scant to abundant mucinous stroma, which coupled with the presence of other unusual features such as clear cells, papillations, foamy macrophages, necrosis and sarcomatoid differentiation. Immunohistochemically, MTSCC can express the markers from the proximal convoluted tubules to collecting tubules.

Adenocarcinoma ; metabolism ; pathology ; surgery ; Adenocarcinoma, Mucinous ; metabolism ; pathology ; surgery ; Adenoma ; pathology ; Adult ; Carcinoma ; metabolism ; pathology ; surgery ; Carcinoma, Renal Cell ; pathology ; Diagnosis, Differential ; Female ; Follow-Up Studies ; Humans ; Keratin-18 ; metabolism ; Keratin-7 ; metabolism ; Kidney Neoplasms ; metabolism ; pathology ; surgery ; Male ; Middle Aged ; Mucin-1 ; metabolism ; Nephrectomy ; Prognosis ; Racemases and Epimerases ; metabolism