Day 2 :
National Hospital Organization Kure Medical Center and Chugoku Cancer Center, Japan
Keynote: Aberrant DNA methylation as a predictive marker for disease progression of LSIL in uterine cervix
Time : 09:15-09:45
Taniyama completed his PhD in Pathology at the Hiroshima University School of Medicine in Japan in 1985, and he learnt molecular techniques and laser capture microdissection at the University of California, San Diego Cancer Center in 1998-99. He joined the National Hospital Organization (NHO), Kure Medical Center and Chugoku Cancer Center in 2002, and he became the president of this center in July 2014.
In the present study, 113 patients were classified into four groups according to their cervical cytology, HPV infection and follow up. Cytology samples were examined for aberrant DNA methylation (abMet) of DLX4 and SIM1 genes and their protein expressions. CaSki cells were treated with 5-Aza-2´-deoxycytidine (5-aza-dC). Of 113 samples, 40 in Group 1 were negative for intraepithelial lesion or malignancy. 21 low-grade squamous intraepithelial lesions (LSILs) in Group 2 showed a continuance of LSIL for longer than 365 days, and 12 LSILs in Group 3 showed an up-grading to high-grade (H) SIL+ within 365 days after the diagnosis of LSIL. 40 in Group 4 were squamous cell carcinoma. All but Group 1 were infected with high-risk HPV. Significant difference existed in frequency of abMet between groups 2 and 3 (p = 0.044), between groups 3 and 4 (p = 0.020) for DLX4, and between groups 1 and 3 (p = 0.0003), as well as between groups 2 and 3 (p = 0.005) for SIM1 gene. DLX4 protein expression was significantly reduced in the DLX4 abMet positive tissues, as compared to the negative tissues (p = 0.008), and 5-aza-dC treatment extracted DLX4 protein expression of CaSki cells in a dose-dependent manner (p < 0.005). The LSIL cases with abMet of SIM1 gene or both genes progressed faster to HSIL+ than others (p = 0.033 or p = 0.048). Therefore, AbMet of DLX4 and SIM1 genes should be a useful and novel progression marker of uterine cervical LSIL with HPV infection.
Key Laboratory of Antibody Technique of Ministry of Health, Nanjing Medical University China
Time : 09:45-10:15
Guo-Min Deng has obtained MD in China and PhD in Gothenburg University, Sweden in 2001. He worked as research fellow in NIH, USA during 2002-2006 and worked as instructor and assistant professor in Harvard University during 2006-2014. He is distinguished professor and the director of key Lab of antibody techniques of ministry of health in Nanjing Medical University. He has published more than 25 papers in reputed journals including Nature Medicine, Nature reviews Rheumatology and has been serving as an editorial board member of repute.
Skin is the second most common manifestation in patients with Systemic lupus erythematosus (SLE) yet the etiology and the mechanisms which are involved in the expression of injury remain unclear. We discuss the role of ultraviolet light (UV), immune cells, cytokines and the deposition of immunoglobulin in the development of inflammation and damage. UV represents the most typical environmental factor which triggers the expression of skin lesions in areas where immunoglobulin has been deposited and various components of the immune system have been amassed. Understanding of the interplay of environmental and immune factors has led to the identification of key molecules which can be targeted therapeutically. These include IgG/Fc receptor, tumor necrosis factor (TNF)/TNF receptor and interferon (IFN)/IFN receptor-initiated cell signaling. A number of intracellular kinases (spleen tyrosine and calcium/calmodulin 4) and transcription factors have also been demonstrated to be involved in the expression of skin lesions in lupus-prone mice. The possibility to apply small drugs locally with limited side-effects calls for further studies to eliminate the burden of skin inflammation in SLE patients.