Animals ; Annexin A2 ; chemistry ; genetics ; metabolism ; physiology ; DNA Replication ; Endocytosis ; Exocytosis ; Humans ; Neoplasm Invasiveness ; Neoplasm Metastasis ; Neoplasms ; metabolism ; pathology ; Prognosis ; Tissue Plasminogen Activator ; metabolism ; physiology

Adult ; Diagnosis, Differential ; Histiocytoma, Malignant Fibrous ; pathology ; Humans ; Laryngeal Neoplasms ; diagnostic imaging ; metabolism ; pathology ; surgery ; Laryngectomy ; Leiomyosarcoma ; pathology ; Male ; Rhabdomyosarcoma ; diagnostic imaging ; metabolism ; pathology ; surgery ; Tomography, X-Ray Computed ; Vimentin ; metabolism

Adenocarcinoma, Follicular ; epidemiology ; genetics ; metabolism ; pathology ; Carcinoma, Papillary ; pathology ; DNA-Binding Proteins ; metabolism ; Diagnosis, Differential ; Genes, ras ; genetics ; Humans ; Point Mutation ; Prognosis ; Thyroglobulin ; metabolism ; Thyroid Neoplasms ; epidemiology ; genetics ; metabolism ; pathology ; Transcription Factors

Biomarkers, Tumor ; metabolism ; Carcinoma, Papillary ; metabolism ; Cathepsin B ; metabolism ; Cell Cycle Proteins ; metabolism ; HSP27 Heat-Shock Proteins ; metabolism ; Humans ; Proteomics ; Repressor Proteins ; metabolism ; S100 Calcium Binding Protein A6 ; S100 Proteins ; metabolism ; Serpins ; metabolism ; Thyroid Neoplasms ; metabolism

Adenocarcinoma, Clear Cell ; pathology ; Female ; Humans ; Middle Aged ; Ovarian Neoplasms ; pathology

Primary thyroid lymphomas (PTLs) are closely correlated with the autoimmune reaction of thyroid. However, the molecular mechanisms of PTLs are still unclear. It is really necessary to improve the ability to differentiate between benign and malignant PTLs along with the introduction of some new molecular biology methods. The diagnosis and prognosis of PTLs depend on their histological features, pathological classification, and clinical stages. Customized therapy of PTLs becomes possible with the further advances in lymphoma's pathological classification, clinical stages, and international prognosis index standard.
Humans ; Lymphoma ; diagnosis ; pathology ; therapy ; Thyroid Neoplasms ; diagnosis ; pathology ; therapy

OBJECTIVETo establish an appropriate animal model of uterine leiomyoma and to understand the pathogenesis of this disease.

METHODSMature female rats were intramuscularly injected with estradiol benzoate at 200 μg or 300 μg twice a week. After injection for 8 or 10 weeks, the rats were sacrificed. We measured the serum levels of estrogen (E(2)) and progesterone (P), evaluated ER and PR expression, and calculated the leiomyoma forming rate and mortality of the rats. Histological changes were compared between rat uterine leiomyoma and human uterine leiomyoma with HE staining. The optimal dose and duration of E(2) for induction of uterine leiomyoma in rat were determined.

RESULTSIn the rats treated with estradiol benzoate 200 μg for 8 weeks ìn the serum E(2) level increased significantly (P<0.01). Uterine nodules were visible in some of the tested rats. Based on the pathohistological Results , the uterine leiomyoma developed in the treated rats demonstrated similar features as in human uterine leiomyoma. The expressions of ER and PR were increased in the leiomyoma tissues.

CONCLUSIONThe rat model of uterine leiomyoma can be established by intramuscular injection of estradiol benzoate at 200 μg twice per week for 8 weeks, with similar features as those of human uterine leiomyoma. The high concentrations of ER and PR in uterine tissue might be related with the development of uterine leiomyoma in animal.

Animals ; Disease Models, Animal ; Estrogens ; administration & dosage ; adverse effects ; Female ; Leiomyoma ; chemically induced ; Rats ; Uterine Neoplasms ; chemically induced

A large number of data derived from molecular analyses support the hypothesis that human cancer is a genetic disease and a distinct subset of genes have been found to be genetically changed in most tumors. Molecular alterations in pancreatic cancer include: (1) oncogenes such as K-ras, c-myc, c-fos, and c-erbB-2; (2) tumor suppressor genes such as p53, p16, DPC4/SMAD4, and DCC; and (3) growth factors such as EGF, FGF, HGF, PDGF, VEGF, TGF-beta. Genetic alterations of K-ras and p53 are common in human pancreatic cancer, but the occurrence of pancreatic cancer is a multi-step phenomenon in which the accumulation of genetic changes is extremely important.
Epidermal Growth Factor ; genetics ; Fibroblast Growth Factors ; genetics ; Genes, Tumor Suppressor ; Genes, myc ; genetics ; Genes, p16 ; Genes, p53 ; genetics ; Genes, ras ; genetics ; Growth Substances ; genetics ; metabolism ; Humans ; Oncogenes ; genetics ; Pancreatic Neoplasms ; genetics

Adenocarcinoma, Follicular ; genetics ; metabolism ; pathology ; Biomarkers, Tumor ; genetics ; Diagnosis, Differential ; Humans ; Matrix Metalloproteinase 1 ; biosynthesis ; genetics ; Telomerase ; biosynthesis ; genetics ; Thyroid Neoplasms ; genetics ; metabolism ; pathology ; ras Proteins ; biosynthesis ; genetics

Increasing evidences have demonstrated the roles of epithelial-mesenchymal transition in tumor invasion and metastasis. In the invasive front of papillary thyroid carcinoma, the expressions of adhesion molecules are often lost. In anaplastic thyroid carcinoma, tumor cells showing cancer stem cell characteristics have been identified. Epithelial-mesenchymal transition may thus play a key role in the progression of thyroid cancer. Therefore, it provide new insight for the development of targeted drugs for anaplastic thyroid carcinoma.
Cadherins ; metabolism ; Epithelial-Mesenchymal Transition ; Humans ; Thyroid Neoplasms ; pathology ; Transcription Factors ; metabolism