Humans ; Liver Neoplasms ; genetics ; immunology ; pathology ; Lymphoma, T-Cell ; genetics ; immunology ; pathology ; Receptors, Antigen, T-Cell, alpha-beta ; metabolism ; Receptors, Antigen, T-Cell, gamma-delta ; metabolism ; Splenic Neoplasms ; genetics ; immunology ; pathology

OBJECTIVETo study the clinicopathological features of thyrotropin-secreting pituitary adenoma (TSH adenoma).

METHODSClinical and pathological features of 7 TSH adenoma cases were studied by review of patients' medical records, light and electronic microscopy, and immunohistochemistry.

RESULTSAll seven patients presented with clinical hyperthyroidism and high levels of plasma free T3, free T4, total T3 and total T4. The levels of TSH failed to be suppressed by thyroxin administration. MRI showed macro or giant pituitary adenomas in all seven patients with tumor diameters ranging from 2.0 to 5.0 cm. Under light microscope, there were 5 cases of chromophobe cell adenoma, 1 case of acidophil cell adenoma, and 1 case of mixed acidophil and chromophobe cell adenoma. Immunohistochemical stains showed a strong positivity of TSH in all the tumors, PRL positive cells in 1 tumor, GH positive cells in 2 tumors and scattered GH and PRL double positive cells in 3 tumors. Ki-67 proliferation index ranged from 0 approximately 0.4%. P53 immunostain was negative in all tumors. After initial surgery, 2 cases had recurrences. However, the Ki-67 proliferation index was not elevated in these two tumors.

CONCLUSIONSThe histological features of TSH pituitary adenomas are heterogeneous with chromophobe as the most common subtype. Secretion of TSH was detected by immunohistochemistry in all cases. P53 mutation is not a feature of TSH adenoma and the proliferation marker, such as Ki-67, may not predict clinical behavior of the tumor. Recurrence is likely due to incomplete resection.

Adenoma ; pathology ; secretion ; Adult ; Aged ; Female ; Humans ; Hyperthyroidism ; blood ; etiology ; Ki-67 Antigen ; blood ; Magnetic Resonance Imaging ; Male ; Middle Aged ; Pituitary Neoplasms ; pathology ; secretion ; Thyrotropin ; secretion

OBJECTIVETo determine the expression status of survivin gene in pancreatic carcinoma.

METHODSExpression of survivin gene was evaluated by immunohistochemistry, Western Blot and RT-PCR in 59 cases of pancreatic carcinoma along with their corresponding adjacent benign tissues, 11 cases of chronic pancreatitis, and 7 pancreatic carcinoma cell lines.

RESULTSThe positive expression rate of survivin in pancreatic carcinoma was 72.8% (43/59). There was no relationship between the expression of survivin and tumor stage and differentiation. No expression of survivin was detected in benign tissue adjacent to the tumors as well as in samples of chronic pancreatitis. All 7 pancreatic carcinoma cell lines showed a positive expression of survivin mRNA and protein.

CONCLUSIONSThe expression of survivin appears to be tumor specific to some extent in our pancreatic carcinoma samples. Survivin may be an ideal target for therapy against pancreatic carcinoma.

Adenocarcinoma, Mucinous ; metabolism ; pathology ; Biomarkers, Tumor ; Carcinoma, Pancreatic Ductal ; metabolism ; pathology ; Cell Line, Tumor ; Female ; Gene Expression Regulation, Neoplastic ; Humans ; Inhibitor of Apoptosis Proteins ; Male ; Microtubule-Associated Proteins ; biosynthesis ; genetics ; Neoplasm Proteins ; biosynthesis ; genetics ; Neoplasm Staging ; Pancreatic Neoplasms ; metabolism ; pathology ; RNA, Messenger ; biosynthesis ; genetics

OBJECTIVESTo investigate the differences in morphology, immunohistochemistry, DNA ploidy status, LOH and MSI of 11q13 and 1p between benign and malignant pheochromocytomas, and to find the marker or markers useful in distinction between benign and malignant pheochromocytoma or for predicting the malignant potential of this tumor.

METHODSTwenty-two cases of clinically documented benign and malignant pheochromocytomas from the files of Peking Union Medical College Hospital were analyzed. Aside from histological study, Ki-67, p53, CgA, S-100, PCNA and survivin immunohistochemistry studies were performed. DNA ploidy status was assessed by flow cytometry on cell suspensions prepared from formalin-fixed, paraffin-embedded sections. Twelve tumors (7 benign and 5 malignant) with paired normal tissues were microdissected. Tumor and normal tissue DNA were extracted. The obtained DNAs and 8 microsatellite markers related to 11q13 and 1q were subjected to PCR amplification for analysis of LOH and MSI.

RESULTSNone of the tumors showed atypical mitosis, only 1 malignant tumor had a mitotic count > 1/10 HPF (2.3/10 HPF). Two malignant tumors exhibited confluent necrosis. Ki-67 index was low in benign tumors (average 0.73%), and high in malignant tumors (average 2.4%). The difference of Ki-67 index between benign and malignant tumors was statistically significant. DNA ploidy status did not correlate with malignancy. Although LOH and/or MSI of 11q13 and 1p were observed in several tumors, a statistically significant difference could not be reached due to the small number of tumors analyzed.

CONCLUSIONOnly Ki-67 index (> 3%) is an useful marker for distinguishing benign from malignant or for predicting the malignant potential of pheochromocytoma.

Adrenal Gland Neoplasms ; genetics ; metabolism ; pathology ; Adult ; Aged ; Biomarkers, Tumor ; metabolism ; DNA, Neoplasm ; genetics ; metabolism ; Female ; Humans ; Ki-67 Antigen ; genetics ; metabolism ; Loss of Heterozygosity ; Male ; Middle Aged ; Neoplasm Metastasis ; Pheochromocytoma ; genetics ; metabolism ; pathology ; Polymerase Chain Reaction ; Tumor Suppressor Protein p53 ; genetics ; metabolism ; Urinary Bladder Neoplasms ; genetics ; metabolism ; pathology

Objective: To investigate the protective effect of glucagon-like peptid-1 (GLP-1) against cardiac microvascular endothelial cell (CMECs) injured by high glucose. Methods: CMECs were isolated and cultured. Superoxide assay kit and dihydroethidine (DHE) staining were used to assess oxidative stress. TUNEL staining and caspase 3 expression were used to assess the apoptosis of CMECs. H89 was used to inhibit cAMP/PKA pathway; fasudil was used to inhibit Rho/ROCK pathway. The protein expressions of Rho, ROCK were examined by Western blot analysis. Results: High glucose increased the production of ROS, the activity of NADPH, the apoptosis rate and the expression level of Rho/ROCK in CMECs, while GLP-1 decreased high glucose-induced ROS production, the NADPH activity and the apoptosis rate and the expression level of Rho/ROCK in CMECs, the difference were statistically significant (. P<0.05). Conclusions: GLP-1 could protect the cardiac microvessels against oxidative stress and apoptosis. The protective effects of GLP-1 are dependent on downstream inhibition of Rho through a cAMP/PKA-dependent manner, resulting in a subsequent decrease in the expression of NADPH oxidase.