Cervical cancer is one kind of many cancers that cause death to women around the world. Many studies had support the statement that inflammation has a strong linkage with cancer development. Several factors like proinflammatory factor can influence tumor cell microenvironment, and induce a faster proliferation. TNF-α is suspected can induce proliferation. While cancer itself can induce inflammation, which is marked by several marker. One of them is HMGB1, released from the cell as active secretory lysosomes or passive diffusion. Genistein has demonstrated growth inhibitory effects of various types of cancer cells. It inhibits tyrosine kinase pathway, which can be activated by TNF -α. One of those pathways that have the link with proliferation is p38. This study tries to reveal about inhibitory effect of genistein toward p38 pathway that had been activated by TNF-α. This research was conducted by exposing cultured HeLa cells with various doses of genistein for 90 minutes, and then exposed to TNF-α 10 ng / mL for 20 minutes. Observations were made with a confocal microscope, by staining the cells with pp38-TRITC and HMGB1 antibody. The intensity was measured and analyzed by Fluoview software. The results suggest that there be significant differences between pp38 intranuclear intensity and HMGB1 extranuclear intensity of each dose of genistein (p = 0.000, ANOVA). pp38 and HMGB1 intensity were increased along with increasing genistein dose, but at high dose there were noted decreasing of pp38 and HMGB1 intensity. At apoptotic dose, pp38 and HMGB1 intensity w ere increased markedly, showing the effect of apoptosis. In general, increasing doses of genistein increase intranuclear p38 activation and HMGB1 extranuclear translocation. So there were a strong linkage between p38 activation and HMGB1 translocation in this study.

Background There is increasing evidence that toll-like receptors (TLR) play a key role in the mediation of systemic responses to invading pathogens during sepsis. Saliva is an important body fluid for detecting physiological and pathological conditions of the human body. Neutrophils are participants in the acute response against pathogens in many tissues, and their influx into the oral cavity may occur at any time.Objective To compare mean neutrophils and the expression of TLR2 and TLR4 in saliva and blood of newborns at risk for sepsis to those of healthy newborns.Methods This cross-sectional study was conducted from July to December 2011 in the Division of Neonatology, Department of Child Health, Ulin General Hospital, Lambung Mangkurat University Medical School, Banjarmasin. Case subjects were newborns with sepsis risk factors (30 infants), while 30 healthy infants were in the control group. Saliva and blood specimen examinations were performed in the Biomedical Laboratory of Brawijaya University Medical School, Malang. We used T-test for statistical analyses.Results From saliva specimens, mean neutrophils were significantly higher in the case group than in the control group [14.43 (SD 12.21) % vs. 5.63 (SD 6.78) %, respectively, (P=0.021)]. In addition, mean TLR2 and mean TLR4 saliva levels were significantly higher in the case group than in the control group [TLR2: 64.97 (SD 26.42) % vs. 40.06 (SD 6.23) %, respectively, (P=0.011); TLR4: 1.5 (SD 1.61) % vs. 0.57 (SD 0.53) %, respectively, (P=0.044)]. From blood specimens, mean neutrophils were also significantly higher in the case group than in the control group [1.09 (SD 0.61)% vs. 0.21 (SD 0.09)%, respectively, (P=0.000)]. Similarly, mean blood TLR2 and TLR4 levels were significantly higher in the case group than in the control group [TLR2: 92.51 (SD 5.51) % vs. 81.74 (SD 11.79) %, respectively, (P=0.003); TLR4: 0.71 (SD 1.42) % vs. 0.12 (SD 0.06) %, respectively, (P=0.000)].Conclusion There are significant increases in neutrophils, as well as neutrophil expression of TLR2 and TLR4 in the saliva and blood from newborns with sepsis risk factors compared to those of healthy newborns. [Paediatr Indones. 2013;53:132-7.]

Introduction: This study aimed to investigate the escape mechanism of tumor cell to host immune system via CD80, CD86, MHC Class I and CD8 in advanced stage nasopharynx carcinoma.