Human fetal esophageal epithelial tissue were cultured in vitro and treatedwith mycotoxins of Alternaria alternata (AME or AOH) for 4 h. The genomic DNAwere extracted from these tissues. Genomic DNA was isolated from normal human fetalesophageal epithelium (as blank control), DNA from malignant tissue and its adjacentnormal mucosa was obtained from esophagectomy patients. DNA was amplified with PCRreaction, using genomic DNA as templet. The PCR products was a 104bp fragment from which the 12 codon of c-Ha-ras gene was contained. The excition point of restriction en-zyme Hpe Ⅱ was located in this fragment. The PCR amplified 104bp fragment was diges-ted by Hpa Ⅱ and analysed by agarose gel electrophoresis. The results showed that the104bp fragment amplified from genomic DNA of blank control and esophagectomy patientcould be digested by Hpa Ⅱ ; but that from genomic DNA of human fetal esophagealepithelium treated by AME or AOH could not. These results indicated that a mutationhad taken place at 12-codon of c-Ha-ras gene after it was treated by AME, AOH for ashort time. The mutation of Ha-ras gene might be the early event during esophageal car-cinogenesis. The effect of AME and AOH during the onset of esophageal cancer and themolecular machanisms of the effect were worth of further study.

Abortifacient Agents, Nonsteroidal ; pharmacology ; Animals ; Drugs, Chinese Herbal ; pharmacology ; Female ; Pinellia ; chemistry ; Plant Proteins ; pharmacology ; Pregnancy

Hyperthermia is a means of adjuvant therapy, which have a sensitizing effect to radiotherapy and chemotherapy. In recent years, the molecular biology, cell and animal experimental research of tumor thermochemotherapy progressed very quickly, which provide theoretical foundation and guidance for us to further develop hyperthermia combined with chemotherapy in clinical trials. In this paper, the studies with the mechanism of thermo-chemotherapy treatment of tumor, different ways of thermochemotherapy and commonly used drugs in thermochemotherapy are reviewed.

Humans ; Occupational Diseases ; diagnosis

Female ; Humans ; Hydrocarbons, Chlorinated ; poisoning ; Male ; Middle Aged ; Occupational Diseases

A Kinase Anchor Proteins ; Cardiomegaly ; metabolism ; Humans

OBJECTIVETo study the over-expression of mutant p53 protein in non-mucinous adenocarcinoma in-situ (NMAIS) and invasive adenocarcinoma, NOS of lung.

METHODSImmunohistochemical study for p53 protein was performed on 17 cases of NMAIS and 70 cases of invasive adenocarcinoma, NOS of lung. The difference in p53 over-expression between the two tumor subtypes was analyzed.

RESULTSThe over-expression of mutant p53 protein was observed in 0 case (0%) of NMAIS and 37 cases (52.9%) of invasive adenocarcinoma, NOS of lung. The difference was of statistical significance (P = 0.000).

CONCLUSIONMutant p53 protein over-expression may play a role in the progression of NMAIS to invasive adenocarcinoma, NOS.

Adenocarcinoma ; metabolism ; Adenocarcinoma in Situ ; metabolism ; Humans ; Immunohistochemistry ; Mutant Proteins ; genetics ; metabolism ; Tumor Suppressor Protein p53 ; genetics ; metabolism

Animals ; Drugs, Chinese Herbal ; pharmacology ; therapeutic use ; Endotoxemia ; blood ; drug therapy ; immunology ; Humans ; Lipopolysaccharide Receptors ; blood ; Lipopolysaccharides ; blood ; Phytotherapy ; Shock, Septic ; blood ; drug therapy ; immunology

Recombinant human endostatin (Endostar) is a broad spectrum molecular targeted drug on anti-angiogenesis that the main evidence-based data is combined chemotherapy treatment of advanced non-small cell lung cancer (NSCLC).In recent years,the researches of recombinant human endostatin used in the treatment of various malignant tumors are on the increase and achieve good effect.In addition,the researches about combined treatment methods,routes of administration,methods of medication are carried out gradually,which will be conducive to the reasonable application in clinical.

Purpose:To determine the efficacy of paclitaxel in human bladder cancer lines and to investigate the mechanism by which paclita xel induce apoptosis in human bladder cancer cells. Methods:BIU-87, 5637, T24 and EJ bladder cancer cell lines wer e cultured by techniques of cell culture in vitro. The cytotoxic activity an d apoptosis induction abilities of paclitaxel were analyzed by MTT and Annexin- V assay as well as DNA cytometry , respectively. The effects on the cell cycle w ere assessed by flow cytometry of propidium iodide. The expressions of Bcl-2, B ax, p53 and Caspase3 proteins were determined by flow cytometry immunofluorescen ce. Results:Paclitaxel dose-dependent inhibition of cell prolifera tion was seen.Paclitaxel induced G_2/M arrest (71.29% and 64.57%) which was maximal in 5637 and EJ cell lines. While paclitaxel at 1?g/ml concentration ex posure to 5637 12h, 14h and 48h respectively, the apoptosis rates of the respect ive times were 5.0%, 12.9%, 27.6%. The expression of genes p53 and Bcl-2 was no t influenced, whereas the expression of Bax and Caspase3 had increases time-dep endently after exposure to paclitaxel. The analysis of Annexin-V showed a drama tic dose-dependent increase of apoptosis. Conclusions:Paclitaxel inhibited bladder cancer cells prolifera tion and had more effect on those cells whose grade was lower and doubling time was longer. Paclitaxel could block G_2/M arrest, and induce apoptosis by th e path of Bcl-2/Bax in bladder cancer cell lines.