Anoctamin-1 ; Antineoplastic Agents ; administration & dosage ; Benzamides ; Biomarkers, Tumor ; metabolism ; Chloride Channels ; Drug Delivery Systems ; methods ; Gastrointestinal Neoplasms ; genetics ; metabolism ; pathology ; therapy ; Gastrointestinal Stromal Tumors ; genetics ; metabolism ; pathology ; therapy ; Humans ; Imatinib Mesylate ; Indoles ; administration & dosage ; Membrane Proteins ; metabolism ; Neoplasm Proteins ; metabolism ; Piperazines ; administration & dosage ; Proto-Oncogene Proteins c-kit ; metabolism ; Pyrimidines ; administration & dosage ; Pyrroles ; administration & dosage ; Receptor, Platelet-Derived Growth Factor alpha ; genetics ; metabolism ; Vascular Endothelial Growth Factor A ; metabolism

Aged ; Antineoplastic Combined Chemotherapy Protocols ; therapeutic use ; CD4 Antigens ; metabolism ; CD56 Antigen ; metabolism ; Cyclophosphamide ; therapeutic use ; Dendritic Cells ; pathology ; Diagnosis, Differential ; Doxorubicin ; therapeutic use ; Female ; Humans ; Leukemia, Myeloid ; metabolism ; pathology ; Lymphoma, Extranodal NK-T-Cell ; metabolism ; pathology ; Plasmacytoma ; drug therapy ; metabolism ; pathology ; Precursor Cell Lymphoblastic Leukemia-Lymphoma ; metabolism ; pathology ; Prednisone ; therapeutic use ; Skin Neoplasms ; drug therapy ; metabolism ; pathology ; Vincristine ; therapeutic use

Hepatectomy ; Humans ; Liver Neoplasms ; surgery ; Preoperative Care ; Safety

12E7 Antigen ; Adult ; Antigens, CD ; metabolism ; Cell Adhesion Molecules ; metabolism ; Desmin ; metabolism ; Desmoplastic Small Round Cell Tumor ; metabolism ; pathology ; surgery ; Diagnosis, Differential ; Female ; Humans ; Neoplasm Recurrence, Local ; Neuroblastoma ; metabolism ; pathology ; Ovarian Neoplasms ; metabolism ; pathology ; surgery ; Phosphopyruvate Hydratase ; metabolism ; Rhabdomyosarcoma, Embryonal ; metabolism ; pathology ; Sarcoma, Ewing ; metabolism ; pathology ; Vimentin ; metabolism

Adenocarcinoma ; drug therapy ; genetics ; metabolism ; pathology ; surgery ; Adenocarcinoma, Bronchiolo-Alveolar ; drug therapy ; genetics ; metabolism ; pathology ; surgery ; Adenocarcinoma, Papillary ; metabolism ; pathology ; Cadherins ; metabolism ; Diagnosis, Differential ; Genes, erbB-1 ; genetics ; Humans ; Lung Neoplasms ; drug therapy ; genetics ; metabolism ; pathology ; surgery ; Lymphatic Metastasis ; Mucin-1 ; metabolism ; Mutation ; Neoplasm Invasiveness ; beta Catenin ; metabolism

Animals ; Genes, BRCA2 ; Genes, erbB-1 ; Genes, erbB-2 ; Genes, p16 ; Genes, p53 ; Genes, ras ; Genetic Predisposition to Disease ; genetics ; Humans ; Pancreatic Neoplasms ; classification ; genetics ; pathology

Acid Anhydride Hydrolases ; metabolism ; Apoptosis ; Biomarkers, Tumor ; metabolism ; Caspases ; metabolism ; Cell Adhesion Molecules ; metabolism ; Chromosome Deletion ; Drug Delivery Systems ; GPI-Linked Proteins ; metabolism ; Humans ; Hyaluronoglucosaminidase ; metabolism ; In Situ Hybridization, Fluorescence ; methods ; Lung Neoplasms ; diagnosis ; drug therapy ; genetics ; metabolism ; Neoplasm Proteins ; metabolism ; Neoplasm Staging ; Receptor, Epidermal Growth Factor ; metabolism ; Vascular Endothelial Growth Factor A ; metabolism

Objective To analyze the clinical and ultrasonic features of primary squamous cell carcinoma of the thyroid(PSCCT)and diagnostic value of ultrasonography (US) in PSCCT in order to improve the cognition of PSCCT.Methods The clinical data and ultrasonic characters of 5 patients with PSCCT confirmed by pathology post surgery were retrospectively reviewed.Results The average age of the 5 patients was 62 years (range from 46 to 79).All of 5 patients with PSCCT were presented with a painless neck mass in clinical palpation examination.Of them,2 patients had different degrees of difficulty in breathing and swallowing,2 patients had hoarseness.Four of 5 patients had died after surgery with average survival time of 9.5 months.On US,the size of lesions was large(a maximum diameter of 2.9-5.5 cm),all of 5 lesions appeared as single solid mixed-echogenicity mass including irregular lamellate marked hypoechoic region,with irregular margin and undefined boundary.Of them,2 lesions presented with lobulated,only 1 lesion exhibited microcalcification and another 4 lesions had no calcification,3 lesions exhibited a? sign of breakthrough thyroid envelope.Color Doppler flow imaging showed few blood flow (3/5) and moderate blood flow (2/5),a higher vascular resistance spectrum was detected in 4 lesions (RI 0.72-0.88).Three patients exhibited suspicious cervical lymph nodes.Conclusions The characteristic ultrasonic appearance combined with the clinical features enables a confident preoperative diagnosis of PSCCT.

Carcinoma, Non-Small-Cell Lung ; genetics ; metabolism ; pathology ; DNA Mutational Analysis ; DNA, Neoplasm ; genetics ; isolation & purification ; Genes, erbB-1 ; Humans ; Lung Neoplasms ; genetics ; metabolism ; pathology ; Mutation ; Paraffin Embedding ; methods ; Polymerase Chain Reaction ; methods ; Real-Time Polymerase Chain Reaction ; methods ; Receptor, Epidermal Growth Factor ; genetics

OBJECTIVETo explore the effects of cyclopamine on the proliferation and apoptosis of LNCaP cells and the expression of the PCA3 gene in human prostate cancer in vitro.

METHODSLNCaP cells were treated with cyclopamine at the concentrations of 1, 5, 10 and 15 micromol/L for 24, 48 and 72 hours. The inhibitory effects of cyclopamine on the proliferation and apoptosis of the LNCaP cells were detected by MTT and flow cytometry respectively, the morphological changes of the cells observed by Hoechst 33258 staining, and the expression of the PCA3 gene determined by real-time fluorescence quantitative reverse transcriptase polymerase chain reaction (FQ-RT-PCR).

RESULTSCompared with the blank control group, cyclopamine significantly inhibited the proliferation of the LNCaP cells at 5, 10 and 15 micromol/L (P <0.01), reaching IC50 at 10 micro mol/L at 48 hours. The apoptosis rates of the LNCaP cells at 24, 48 and 72 hours were 37.21%, 57.38% and 57.98% in the 10 micromol/L group and 21. 16% , 71.31% and 72.90% in the 15 micro.mol/L group, significantly different from those in the control (P <0. 01). The cell apoptosis showed a rising trend with the increase of cyclopamine concentration and acting-time, while the expression of the PCA3 gene was decreasing with the increased concentration of cyclopamine, significantly lower than that of the blank control group (P <0.01) , and extremely low in the 10 micromo/L group

CONCLUSIONCyclopamine intervention at 10 and 15 micromol/L for 48 and 72 hours could significantly inhibit the at all time points. Proliferation and induce the apoptosis of LNCaP cells and reduce the expression level of PCA3.

Antigens, Neoplasm ; genetics ; Apoptosis ; drug effects ; Cell Line, Tumor ; Cell Proliferation ; drug effects ; Humans ; Male ; Prostatic Neoplasms ; genetics ; pathology ; Veratrum Alkaloids ; pharmacology