Background and purpose:Resistance to antitumor agents is a major cause of treatment failure in patients with breast cancer. Research has shown that, tumor stem cell marker aldehyde dehydrogenase 1 (ALDH1) is related with some anticancer drugs (such as cyclophosphamide, cisplatin) resistance, and the content of ALDH1 in tumor cells after treatment is higher than that before treatment. Breast cancer resistance protein (BCRP) is not expressed in normal tissues, but high expressed in breast cancer of after treatment, it may be associated with the mechanism of tumor drug resistance. This study was to investigate the correlation between expression and the relationship between these two kinds of protein ALDH1, BCRP and clinical pathological characteristics. Methods:Immunohistochemistry was performed to detect the expression of ALDH1 and BCRP in breast inifltrating ductal carcinoma tissues, and whether there is a correlation between and explore their relationship with clinical pathological features and their expression. Results:The expression of ALDH1 protein and BCRP protein in breast cancer and paracarcinoma breast tissues has signiifcant difference(χ2=14.685, P=0.000;χ2=12.243, P=0.000).The expression of ALDH1 with patients age, pathologic stage, axillary lymph node metastasis, histological grading, ER, PR, and HER-2 state were not relevant(P>0.05). HER-2, BCRP protein, expression was higher in cancer tissue (χ2=5.289, P=0.021). There were no relevant with the expression of BCRP with patients age, pathologic stage, axillary lymph node metastasis and histological grading, estrogen receptor (ER), progesterone receptor (PR), human epidermal growth factor receptor (HER-2) (P>0.05). Conclusion:ALDH1 proteins may be an independent factor compared with occur drug resistant protein, and participate breast cancer drug resistance in the chemotherapy and tumor invasion and metastasis of malignant biological behavior.

Objective To observe the effect of serum containing Dahuang Zhechong Pills on vascular endothelial growth factor ( VEGF) expression in K562 cells of chronic myelogenous leukemia ( CML) and to develop new antiangiogenic drugs for CML treatment. Methods Enzyme-linked immunosorbent assay ( ELISA) was used for the detection of serum VEGF content in 38 CML patients, 11 acute myelogenous leukemia patients and 9 healthy volunteers. SD rats were used for the preparation of serum containing Dahuang Zhechong Pills, and then ELISA was applied for the detection of VEGF content in K562 cells pretreated with serum containing Dahuang Zhechong Pills. Results Compared with the healthy volunteers, myelogenous leukemia patients at chronic phase and acute phase had high serum VEGF content ( P<0.05 or P<0.01) . Compared with blank serum control group, the secretion of VEGF in K562 cells pretreated with serum containing Dahuang Zhechong Pills was decreased obviously ( P<0.01) , and VEGF expression decreased with the increase of drug concentration. Conclusion VEGF content is increased in myelogenous leukemia patients at chronic phase and acute phase, which may be related to the pathogenesis, progress and prognosis of chronic myelogenous leukemia. Serum containing Dahuang Zhechong Pills can inhibit the expression of VEGF in chronic myelogenous leukemia K562 cells and decrease VEGF protein expression in concentration-dependent manner.

Objective To explore the clinic character of immune thrombocytopenia (ITP) children infected with helicobacter py‐lori (Hp) and the effects of anti‐helicobacter pylori treatment on those children .Methods One hundred and forty‐two ITP children and 92 healthy children were conducted the 13C‐Urea breath test to determine the infections of Hp .The ITP children infected with Hp were divided into two groups :single drug group (48 cases ,treated only with corticosteroid ) and combined drugs group (49 ca‐ses ,treated with corticosteroid and anti‐helicobacter pylori treatment) .The platelet parameters ,platelet associated immunoglobulin and some lymphocyte subsets were analyzed .Results Ninety seven children infected with Hp were found in 142 ITP children (69 . 7% ) .In the mean time ,37 children infected with Hp were observed in 92 healthy children (40 .2% ) .After treatment of 6 months , the PLT ,PCT ,CD3+ ,CD3+CD4+ and CD3+ CD4+ /CD3+ CD8+ of ITP children in both group were increased ,and the increased degree of those parameters were much higher in combined drug group than those in single drug group (P< 0 .01) .However ,the MPV ,PDW ,PAIgG ,PAIgA and CD3+ CD8+ were more decreased than that of the single drug group(P<0 .01) .Conclusion The ITP children have a higher infection rate of Hp ,which may be involved in the pathogenesis of ITP .Anti‐helicobacter pylori therapy would improve the therapy efficacy of ITP children infected with Hp by improving their immunity .

Objective:This study aimed to explore the effects of trichosanthin on the proliferative inhibition and apoptosis induc-tion in human lung carcinoma A549 cells. Methods:A549 cells were treated with various concentrations of TCS. The inhibitory effects in proliferation were detected by the MTT method. The microfilament changes were observed by transmission electron microscopy. Apoptosis rate and cell cycle were determined by flow cytometry. Results:A549 cells treated with TCS presented apoptotic changes and decreased cell activity. When the concentration increased and time was prolonged, the inhibition rate increased correspondingly. Conclusion:Pharmacological doses of TCS inhibited the proliferation and differentiation in lung carcinoma A549 cells and affected the function in A549 cells by changes in the cytoskeleton.

Objective To study on chronic myelogenous leukemia on the basis of protein interaction network to further explore its development mechanism.Methods Chronic myelogenous leukemia-related genes were screened from Online Mendelian Inheritance in Man database (OMIM) of genetic.After text mining by Cytoscape software and Agilent Literature Search,the protein interaction networks of chronic myelogenous leukemia were established.Then the molecular complexes contained in the network were analyzed by Clusterviz plug.The biological pathways of molecular complexes were enriched based on DAVID.Results There were 79 chronic myelogenous leukemia genes in OMIM.The protein-protein interaction network of chronic myelogenous leukemia contained 638 nodes,1 830 edges and maybe 5 molecular complexes.Conclusions Pathways underlying complexes 1 are involved in cytokines and inflammation,cytokines-receptor binding,cytokine receptor signaling.Complexes 3 has relation to complex biological behavior of the tumors and other broad relevance,which can provide the bioinformatic foundation for further understanding the development mechanisms of chronic myelogenous leukemia.

Immunotherapy has become a common means of cancer treatment. In immunotherapy, PD-1/PD-L1 inhibitors have significant efficacy. Cancer and various opportunistic infections are common complications in patients with AIDS. Owing to the special immune situation of these patients, AIDS is regarded as an exclusion standard in most clinical trials for cancer immunotherapy, conferring immunotherapy difficulty in treating patients with AIDS. The popularity of effective antiretroviral drugs has prolonged the lifetime of people with AIDS. Therefore, exploiting the opportunity of using immunotherapy in AIDS with cancer is urgent.

Objective: Analysis of the effect of triggering receptor-1 expressed on myeloid cells (TREM-1) in nonalcoholic fatty liver disease (NAFLD) and the mechanism. Methods: The oleic acid-treated HepG2 cells were divided into model group, overexpression group, interference group A, interference group B and negative control group. The mouse model of NAFLD was generated and randomly divided into (nuclear factor-κB) NF-κB inhibition group, protein kinase B (AKT) inhibition group, knockout group A, knockout group B and control group. The expression of inflammatory factors and TREM-1 in liver tissue was detected by PCR, and fat accumulation was detected by oil red O staining. Western blotting was used to detect the expression of TREM-1 and signaling pathway proteins, and HE staining was used to detect liver tissue changes. Results: TREM-1 was up-regulated in liver tissue of NAFLD mice [(0.936±0.127) vs. (0.432±0.105)] and in oleic acid-treated HepG2 cells. In oleic acid-treated HepG2 cells, overexpression of TREM-1 increased inflammatory factor expression and increased lipid droplets; inhibition of TREM-1 expression decreased inflammatory factor expression, and lipid droplets decreased. Knockout of TREM-1 and inhibition of NF-κB in NAFLD mice reduced hepatocyte inflammatory factor expression and reduced liver damage; knockout of TREM-1 and inhibition of AKT reduced liver tissue lipids and drops accumulate. Conclusions The overexpression of TREM-1 in NAFLD mice liver tissue can regulate inflammatory factor expression and lipid droplets through NF-κB and AKT signal pathway. TREM-1 might be a potential therapeutic target of NAFLD.