Two prophylactic human papillomavirus (HPV) vaccines against types 6, 11, 16 and 18 have shown great promise in clinical trials with recent results demonstrating 100% efficacy against persistent HPV infection and development of cervical intraepithelial neoplasia up to five years of follow-up. Published data from the phase-IIb and III trials thus far indicate that the prophylactic HPV L1 virus-like particle vaccine is safe and well-tolerated. It offers HPV-naive women a very high level of protection against HPV persistent infection and cervical intraepithelial lesions associated with the types included in the vaccine. HPV vaccination should be also offered to girls before onset of sexual activity. But there are still questions about several issues of HPV prophylactic vaccination. Prolonged clinical trials should be performed for demonstration of these remaining questions. Finally, prophylactic vaccines against HPV will certainly reduce the incidence of the risk of developing cervical cancer.
Cervical Intraepithelial Neoplasia ; Female ; Follow-Up Studies ; Humans* ; Incidence ; Sexual Behavior ; Uterine Cervical Neoplasms ; Vaccination ; Vaccines

Human papillomavirus infection is often transient and spontaneously reversible. High-risk human papillomavirus persistence is the major cause of cancerous transformation in several tissues. For prophylactic vaccines there is first clinical evidence of effectivity (ie, 100% protection from HPV infection and dysplasia by virus-like particle (VLP) vaccine-induced neutralizing antibodies). Also, Therapeutic vaccines have entered clinical evaluation. While prophylactic VLP vaccines are immunogenic per se, therapeutic vaccines will need further adjuvants to guide T cell differentiation, expansion, survival, and homing to tumor sites. To enhance clinical outcome of successful T cell induction in patients, the susceptibility of the tumor cells for lysis must be addressed in the future, since tumor immune evasion is a severe problem in cervical cancer. Both preventive and therapeutic human papillomavirus vaccinations will probably change our approach to the screening and therapy of human papillomavirus-related diseases in the next few years. The mass vaccination of adolescent patients should lower the frequency of these very frequently lethal infections.
Adolescent ; Cell Differentiation ; Humans ; Mass Screening ; Mass Vaccination ; Papillomavirus Infections ; Tumor Escape ; Uterine Cervical Neoplasms* ; Vaccination ; Vaccines

No abstract available.
Drug Therapy* ; Gestational Trophoblastic Disease*

No abstract available.
Mass Screening* ; Uterine Cervical Neoplasms*

No abstract available.
DNA* ; Flow Cytometry* ; Gestational Trophoblastic Disease*

The aim of present study was to investigate the effects of kaempferol on cellular proliferation and cell cycle arrest and explore the mechanism for these effects in human breast carcinoma MDA-MB-453 cells. Cells were treated with kaempferol at various concentrations (ranging from 1 to 200 microM) for 24 and 48 hrs. Kaempferol significantly inhibited cancer cell growth in cells exposed to 50 and 10 microM of kaempferol and incubated for 24 and 48 hrs, respectively. Exposure to kaempferol resulted in cell cycle arrest at the G2/M phase. Of the G2/M-phase related proteins, kaempferol down-regulated CDK1 and cyclin A and B in cells exposed to kaempferol. In addition, small DNA fragments at the sub-G0 phase were increased by up to 23.12 and 31.90% at 10 and 50 microM incubated for 24 and 48 hrs, respectively. The kaempferol-induced apoptosis was associated with the up-regulation of p53. In addition, the phosphorylation of p53 at the Ser-15 residue was observed with kaempferol. Kaempferol inhibits cell proliferation by disrupting the cell cycle, which is strongly associated with the induction of arrest at G2/M phase and may induce apoptosis via p53 phosphorylation in human breast carcinoma MDA-MB-453 cells.
Apoptosis ; Breast ; Breast Neoplasms ; Cell Cycle ; Cell Cycle Checkpoints ; Cell Proliferation ; Cyclin A ; DNA ; Humans ; Kaempferols ; Phosphorylation ; Proteins ; Up-Regulation

Objectives of this study were to establish a leukemia mouse model in the Balb/c mouse based upon the A20 cell line (murine B-lymphoma/leukemia cell line, H-2d). Here we demonstrate for the first time that A20 cells were infiltrated into tissue and bone marrow, thereby evaluate the feasibility of using A20 leukemic cells as a leukemia model. In the study, changes of behavior, survival rate and histological changes of major organs after intravenous injection of A20 cells (1x105, 1x106 or 1x107) into Balb/c mice were observed. After inoculation of 1x106 cells, animals survived up to 38.3 days, although there were no significant correlation between the number of injected cells and life-span. At 21 and 28 days post-injection, both hematoxylin-eosin and CD45R immunohistochemical stains showed diffuse large B-cell lymphoma in the liver. FACS analysis was performed after injection of fluorescent nanomaterial (MNPs@SiO2 RITC)-labeled A20 cells. The labeled A20 cells were detected in bone marrow from 6 hours post-inoculation, indicative of the cellular infiltration. This is the first study that demonstrated the invasion of A20 cells into the bone marrow of Balb/c model using A20 cells. With the occurrence of systemic lesions following metastasis of the cells into lymph nodes and neighboring tissues via bone marrow infiltration, it is suggested that the A20 cell-inoculated Balb/c miouse could be an animal model of acute lymphocytic leukemia.
Animals ; Bone Marrow ; Cell Line ; Coloring Agents ; Injections, Intravenous ; Leukemia ; Liver ; Lymph Nodes ; Lymphoma, B-Cell ; Mice ; Models, Animal ; Nanostructures ; Neoplasm Metastasis ; Precursor Cell Lymphoblastic Leukemia-Lymphoma ; Survival Rate

BACKGROUND: For the detection of HLA antibodies, solid-phase tests using purified HLA antigens are increasingly used. In this study, we analyzed the panel reactive antibody (PRA) test results using ELISA and Luminex methods, and the results were compared with those of crossmatch test. METHODS: A total of 111 sera including 90 sera from kidney transplanted patients were tested. ELISA-PRA was performed using Lambda Antigen Tray Class I and II Mixed kits (One Lambda Inc., USA) and additional test was performed to identify HLA specificities. Luminex-PRA tests were performed using LABScreen Mixed kits (One Lambda Inc., USA) and LIFECODES LifeScreen Deluxe kits (Tepnel Co., USA). RESULTS: The positive rates of PRA were higher in Tepnel (P=0.006) and One Lambda Luminex (P<0.001) methods than ELISA, without significant difference between two Luminex methods (P=0.087). The overall concordance rate among the three PRA tests was 62.2% (69/111). The positive and negative predictive values of PRA tests for the flow cytometric crossmatch were 33.3-45.7% and 85.7-89.5%, respectively. Of the two Luminex methods, One Lambda showed higher positive rate than Tepnel for the detection of class I antibodies. The sensitivity of pretransplant PRA for the detection of posttransplant acute rejection episodes was higher in Luminex (P=0.007 for Tepnel, P=0.003 for One lambda) than ELISA method. CONCLUSIONS: Different methods used to detect HLA antibodies showed discrepant results. As the Luminex method was more sensitive than ELISA for the detection of HLA antibodies, it can be used as a routine test in the transplantation laboratory.
Enzyme-Linked Immunosorbent Assay/*methods ; Flow Cytometry ; Histocompatibility Antigens Class I/*immunology ; Histocompatibility Antigens Class II/*immunology ; Humans ; Isoantibodies/*blood ; Kidney Transplantation/immunology ; Reagent Kits, Diagnostic ; Sensitivity and Specificity

No abstract available.
Diagnosis*

PURPOSE: We investigated the expressions of E- Cadherin and p53 in soft tissue tumors to determine their significance in sarcoma development and/or progression and to assess their potential correlation with epithelial features. MATERIALS AND METHODS: A total of 79 soft tissue sarcomas, including 10 tumors comprising epithelial components, were studied immunohistochemically in paraffin-embedded tissue sections. Further analysis was performed on 61 tumors by the application of a polymerase chain reaction technique and a direct sequence analysis procedure applied to exons 5 through 8 in the p53 gene. RESULTS: E-Cadherin was expressed at the cell-cell boundaries in 8 (10%) tumors: 5 of grade 2 and 3 of grade 3. Of these, six (being 60% of the total of 10 tumors containing epithelial elements) contained and two did not contain histologic evidence of epithelial differentiation. Overexpression of p53 was detected in 26 (33%) samples, 7 of which demonstrated mutations in the p53 gene. No association was established between E-Cadherin immunoreactivities and p53 abnormalities. Tumor grade was found to be strongly correlated with p53 alterations (p=0.01) but not with E-Cadherin expression (p=0.09). CONCLUSION: These data confirm a role for altered p53 in the pathogenesis of soft tissue sarcomas and suggest a possible role for E-Cadherin in the maintenance of epithelial architecture in these tumors regardless of p53 status.
Cadherins* ; Exons ; Genes, p53 ; Polymerase Chain Reaction ; Sarcoma* ; Sequence Analysis