Antineoplastic Combined Chemotherapy Protocols ; therapeutic use ; Breast Neoplasms ; drug therapy ; metabolism ; pathology ; Cyclophosphamide ; therapeutic use ; Dose-Response Relationship, Drug ; Epirubicin ; therapeutic use ; Female ; Fluorouracil ; therapeutic use ; Humans ; Methotrexate ; therapeutic use ; Neoadjuvant Therapy ; methods ; Neoplasm Invasiveness ; Neoplasm Staging ; Paclitaxel ; therapeutic use ; Receptor, ErbB-2 ; metabolism ; Receptors, Estrogen ; metabolism ; Receptors, Progesterone ; metabolism ; Tumor Burden

Antineoplastic Agents, Hormonal ; therapeutic use ; Bone Neoplasms ; diagnostic imaging ; secondary ; Breast Neoplasms ; pathology ; therapy ; Combined Modality Therapy ; Female ; Humans ; Neoplasm Recurrence, Local ; Neoplasm Staging ; Salvage Therapy ; methods ; Tomography, X-Ray Computed

Adult ; Androstadienes ; therapeutic use ; Aromatase Inhibitors ; therapeutic use ; Breast Neoplasms ; drug therapy ; Female ; Humans ; Middle Aged ; Nitriles ; therapeutic use ; Triazoles ; therapeutic use

Antineoplastic Agents, Hormonal ; therapeutic use ; Bone Neoplasms ; secondary ; Breast Neoplasms ; chemistry ; drug therapy ; pathology ; Disease Progression ; Female ; Humans ; Menopause ; Neoplasm Recurrence, Local ; Receptors, Estrogen ; analysis ; Receptors, Progesterone ; analysis ; Tamoxifen ; therapeutic use

Antibodies, Monoclonal ; administration & dosage ; Antibodies, Monoclonal, Humanized ; Antineoplastic Agents ; administration & dosage ; Carcinoma, Non-Small-Cell Lung ; drug therapy ; Cetuximab ; Drug Delivery Systems ; Humans ; Lung Neoplasms ; drug therapy ; Protein Kinase Inhibitors ; administration & dosage ; Quinazolines ; administration & dosage ; Receptor, Epidermal Growth Factor ; antagonists & inhibitors

Adenoviridae ; genetics ; Animals ; Bone Marrow Purging ; methods ; Genes, p53 ; Hematopoietic Stem Cell Transplantation ; methods ; Hematopoietic Stem Cells ; cytology ; virology ; Humans ; Receptors, Virus ; genetics ; Transplantation, Autologous ; methods

Gastric tuberculosis is a rare disease. It usually occurs secondarily to another lesions and mainly in the lungs. Only a few cases of primary gastric tuberculosis have been reported in the literature. Most commonly, gastric tuberculosis lesion locates in the lesser curvature side of the antrum. Therefore the clinical picture is similar to the peptic ulcer. A 24-year-old women visited to the Inha university hospital complaining of vomiting and epigastric discomfort. Gastrofiberscopy showed multiple polypoid mass around the pylorus with stenotic pyloric channel. Subtotal gastrectomy was performed and histologic examination revealed chronic granulomatous inflammation with caseation necrosis. That is compatible with tuberculosis. The patient was taken antituberculosis medication without complication. So we report the case of pyloric obstruction due to gastric tuberculosis with review of the literature.
Female ; Gastrectomy ; Humans ; Inflammation ; Lung ; Necrosis ; Peptic Ulcer ; Pyloric Stenosis ; Pylorus ; Rare Diseases ; Tuberculosis* ; Vomiting ; Young Adult

OBJECTIVETo study the effects of exogenous ER beta on the growth of breast cancer MCF-7 cells under different treatment.

METHODSAn eukaryotic expression vector containing 1.6 kb of human entire coding sequence of ER beta (pCDNA3-ER beta) was transfected into human breast cancer MCF-7 cells using lipofectamine 2000. The biological activity of ER beta was detected with the luciferase reporter containing estrogen responsive element (ERE) and the expression of ER beta protein by Western blot. The growth properties of MCF-7, pCDNA 3-transfected MCF-7 and pCDNA 3-ER beta-transfected MCF-7 cells under different treatment, including E2 (17beta-estradiol) and 4-OHT (4-hydroxytamoxifen), were observed.

RESULTSA stronger activation of the reporter by ER beta in the presence of E2 was observed in the pCDNA 3-ER beta-transfected MCF-7 cells than in the pCDNA 3-transfected MCF-7 and in MCF-7 cells. Western blot analysis showed that the protein level of ER beta in the pCDNA 3-ER beta-transfected MCF-7 cells was markedly increased. Exogenous ER beta expression did not change the growth properties and the morphology of MCF-7 cells under normal condition. The pCDNA 3-ER beta-transfected MCF-7 cells proliferated at the same rate as naive cells in the presence of 4-OHT, whereas a strong inhibition of the proliferation of the pCDNA 3-ER beta-transfected MCF-7 cells in the presence of E2 was observed.

CONCLUSIONExogenous ER beta expression does not increase the resistance to 4-OHT, and a strong inhibition of the proliferation may occur in the presence of E2.

Breast Neoplasms ; metabolism ; pathology ; Cell Line, Tumor ; Cell Proliferation ; drug effects ; Estradiol ; pharmacology ; Estrogen Antagonists ; pharmacology ; Estrogen Receptor beta ; genetics ; metabolism ; Female ; Humans ; Tamoxifen ; analogs & derivatives ; pharmacology ; Transfection

OBJECTIVETo study the prevalence and clinical characteristics of the A to G mutation at nucleotide 3243 of the mitochondrial tRNA(Leu(UUR)) gene in familial diabetes in Shanghai, Jiangsu and Zhejiang Province of China.

METHODSThe mt3243 A to G mutation in 770 randomly selected, unrelated probands of diabetic pedigrees were screened by PCR-RFLP technique and PCR-direct sequencing. Genetic and clinical analyses were further performed in the probands and their family members.

RESULTSThirteen diabetic patients (13/770, 1.69%) with mt3243 A to G mutation were detected. Eleven diabetic patients and 8 normal glucose tolerance (NGT) first-degree relatives of these 13 probands were also found bearing the mutation. Seventeen patients were associated with sensory hearing loss. In the 24 patients harboring the mutation, the majority had lower body mass index (BMI), 18 showed typical maternal inheritance, 15 had sensory hearing loss, 13 had insulin resistance and 14 required insulin therapy due to secondary failure to oral hypoglycemic agents.

CONCLUSIONThe mutation of mt3243 A to G in the mitochondrial tRNA(Leu(UUR)) gene is an important cause of diabetes in Shanghai, Jiangsu and Zhejiang Province of China. Mitochondrial gene mutation diabetes (MDM) is clinically characterized by early onset, emaciation, maternal inheritance, sensorineural hearing loss, and lower islet beta cell function, and some have insulin resistance.

Asian Continental Ancestry Group ; genetics ; China ; epidemiology ; DNA, Mitochondrial ; genetics ; Deafness ; genetics ; Diabetes Mellitus ; genetics ; Genetic Testing ; Hearing Loss, Sensorineural ; genetics ; Humans ; Insulin Resistance ; genetics ; Molecular Sequence Data ; Mutation ; Prevalence ; RNA, Transfer, Amino Acyl ; genetics

OBJECTIVETo observe the anti-proliferation effect of bevacizumab and SN-38 (active metabolite of irinotecan), and investigate the possible mechanisms of these two agents.

METHODSHuman colon cancer LoVo cells were cultured under hypoxic conditions. Inhibition of cell proliferation was evaluated by MTT assay. The drug modulation on HIF-1alpha, VEGF, ERK and AKT were assessed by the following assays. The mRNA expression of HIF-1alpha and VEGF were measured by RT-PCR. The protein expression of HIF-1alpha, ERK and AKT were evaluated by Western blot analysis, and VEGF by ELISA assay.

RESULTSAmong different combination schedules, Bevacizumab given after SN-38 show most synergistic anti-proliferation effect. Under hypoxic conditions, the expression of HIF-1alpha and VEGF increased as time accumulated, Bevacizumab combined with SN-38 almost completely inhibited the expression of HIF-1alpha and VEGF. Moreover, the MAP kinase pathway was involved in the drug modulation of HIF-1alpha and VEGF.

CONCLUSIONThese findings suggest the anti-proliferation effect of bevacizumab and SN-38 was schedule-dependent, and the synergistic effect of Bevacizumab and SN-38 was related to drug modulation of the HIF-1alpha and MAP kinase pathway.

Antibodies, Monoclonal ; pharmacology ; Antibodies, Monoclonal, Humanized ; Antineoplastic Agents, Phytogenic ; pharmacology ; Bevacizumab ; Camptothecin ; analogs & derivatives ; pharmacology ; Cell Hypoxia ; Cell Line, Tumor ; Cell Proliferation ; drug effects ; Colonic Neoplasms ; metabolism ; pathology ; Drug Synergism ; Extracellular Signal-Regulated MAP Kinases ; metabolism ; Humans ; Hypoxia-Inducible Factor 1, alpha Subunit ; genetics ; metabolism ; RNA, Messenger ; metabolism ; Signal Transduction ; Time Factors ; Vascular Endothelial Growth Factor A ; genetics ; metabolism