Objective: To evaluate the multi-parametric MRI in predicting chemotherapy response in pathologically proven cases of osteosarcoma and Ewing’s sarcoma. Correlation between the tumor size changes and internal breakdown using RECIST 1.1, modified RECIST, quantitative ADC and tumor volume as well as dynamic contrast enhanced MRI. Methods: The study included 104 patients pathologically proved osteosarcoma (53) and Ewing`s sarcoma (51) underwent MRI examinations; beforeand after chemotherapy. All patients were assessed using the RECIST 1.1 criteria, m-RECIST, quantitative ADC, and tumor volume evaluation. 21 patients underwent DCE-MRI curve type with quantitative parameters. Correlation between the different evaluations was carried out. Results were correlated with the postoperative pathology in 42 patients who underwent surgery and for statistical evaluation, Those patients were classified into responders (≥90% necrosis) and non-responders (<90% necrosis). Results: The initial mean ADC of 104 patients of osteosarcoma and Ewing’s sarcoma (0.90 ± 0.29) and (0.71 ± 0.16) respectively, differed significantly from that after treatment (1.62 ± 0.46) and (1.6 ± 0.39) respectively with (P<0.001). ADC variations (ADC%) in the non-progressive group were higher than those of the progressive group (128.3 ± 63.49 vs 36.34 ± 78.7) % with (P<0.001). ADC values and ADC variations were inversely correlated with morphologic changes, regardless of the effectiveness of chemotherapy expressed as changes in tumor size based on (RECIST 1.1, RECIST, and 3D volume). Linear regression analysis revealed a Pearson correlation coefficient of r=(-0.427, -0.498 and -0.408), respectively with (P<0.001). An increase in the ADC value was not always associated with a reduction in tumor volume. The disease control rate (defined as the percentage of CR+PR+SD patients) was 89.4% and 93.9% according to RECIST 1.1 and m-RECIST respectively. 42 out of the 104 patients had postsurgical histological evaluation as regards the chemotherapeutic response divided into two groups. ADC values showed a statistically significant difference between Group A and Group B being more evident with minimum ADC% (P<0.001). Conclusion: Quantitative DW imaging with ADC mapping and ADC % after chemotherapy allows a detailed analysis of the treatment response in osteosarcoma and Ewing’s sarcoma. The therapeutic response can be underestimated using RECIST 1.1, so the modified RECIST should be also considered. Advances in knowledge: Quantitative ADC especially ADC% provided an accurate non-invasive tool in the assessment of post-therapeutic cases of osteosarcoma and Ewing's sarcoma

[Purpose] This study was conducted to investigate the effect of Wiihabilitation on the ankle dorsiflexion/plantar flexion strength ratio in adults. [Subjects and Methods] Thirty-two healthy male volunteers were randomly assigned to two equal groups (experimental and control). Participants in the experimental group received a Wiihabilitation training program for six weeks. Data were collected using a Biodex system 3 Isokinetic dynamometer. Peak torques of the dorsiflexors and plantar flexors were measured at an angular velocity of 60°/sec which in turn were used to derive the ankle dorsiflexion/plantar flexion strength ratio. [Results] The mean values of the ankle dorsiflexion/plantar flexion strength ratio decreased significantly between before and after the training in the experimental group, meanwhile there was no significant difference between before and after the training period in the control group . [Conclusion] Wiihabilitation has an impact on the ankle dorsiflexion/plantar flexion strength ratio, so it can be considered an effective training tool in terms of the ankle strength ratio. Thus, it could be recommended for both prevention and rehabilitation of ankle instability patients.

The relationship between Epstein-Barr virus (EBV) and the germinal centre (GC) of the asymptomatic host remains an enigma. The occasional appearance of EBV-positive germinal centres in some patients, particularly those with a history of immunosuppression, suggests that EBV numbers in the GC are subject to immune control. The relationship, if any, between lymphoid hyperplasia with EBV-positive germinal centres and subsequent or concurrent lymphomagenesis remains to be clarified. As far as the development of EBV-associated Hodgkin's lymphoma is concerned, the suppression of virus replication, mediated by LMP1 on the one hand, and the loss of B-cell receptor signalling on the other, appears to be an important pathogenic mechanism. A further important emerging concept is that alterations in the microenvironment of the EBV-infected B-cell may be important for lymphomagenesis. IntroductionThe Epstein-Barr virus (EBV) infects most of the world's adult population. In most cases primary infection and virus persistence are asymptomatic, the virus having evolved a sophisticated strategy to exist long term in the B-cell pool. However, EBV can contribute to the development of several human B-cell lymphomas, which include Hodgkin's lymphoma (HL), Burkitt's lymphoma, and a subset of diffuse large B-cell lymphomas, and can potently transform resting B-cells in vitro (Young & Murray, 2003;Young & Rickinson, 2004;Oyama et al., 2003Oyama et al., , 2007. Two questions central to our understanding of the origins of EBVassociated B-cell lymphomas are (1) how the host and virus interact to allow benign persistent latent infection, and (2) how perturbation of this normal homeostasis leads to neoplastic transformation. This review will summarize current knowledge of how the EBV life cycle is regulated in the B-cells of the asymptomatic host. It will also discuss how the disruption of normal B-cell homeostasis can contribute to the development of B-cell lymphomas, focussing on several novel pathogenic mechanisms in EBV-associated HL, which include the suppression of the virus lytic cycle and the activation of collagen receptor signalling. In vitro transformation of B-cells by EBVMuch of what we know of the role of EBV in B-cell transformation comes from the study of lymphoblastoid cell lines (LCLs), cell lines generated by the in vitro infection of resting B-cells. These in vitro transformed B-cells express a limited subset of viral gene products, the so-called latent genes. They include six nuclear antigens (EBNAs 1, 2, 3A, 3B, 3C and -LP), three latent membrane proteins (LMPs 1, 2A and 2B), two major groups of viral microRNA (miRNA) (Amoroso et al., 2011) and the noncoding Epstein-Barr-encoded RNA (EBER); the latter of which is a target for in situ-based assays to detect EBV in tissue sections (Wu et al., 1990). This pattern of virus latency is often referred to as latency III or the growth programme (Fig. 1). Experiments with recombinant EBV lacking individual latent genes have shown that EBNA2 and LMP1 are required for the in vitro ...

Background: Colorectal cancer (CRC) in Egypt is a relatively high young onset disease. As a form of heterogeneous cancer, there is interplay between genetic and environmental factors. We aimed at probing the association of life style factors and Microsatellite Instability (MSI) status that could provide more insights on carcinogenic process of CRC. Methods: One hundred incident sporadic CRC patients were involved. Information on risk factors of CRC was obtained and microsatellite instability status was predicted through evaluation of MMR protein expression via immunohistochemistry (IHC). Results: Median age was 47.50 years, females represented 54.0% and 36% of patients were Microsatellite Instability High (MSI-H). Most patients with right sided colon cancer (78.3%) were MSI-H while mostly stable or low MSS/MSI-L for left-sided colon and rectum (78.6%, 74.3% respectively, p<0.001). Patients with low physical activity had higher risk of MSS/MSI-L than those with moderate or high activity p =0.026. Patients with BMI greater than 30 Kg/m 2 had higher MSS/MSI-L (75.5%) than those with BMI between 25-30 Kg/m 2 (60.6%) and those with normal BMI <25 (38.9%), p for trend = 0.006. On subgroup analyses, the association of high BMI with MSS/ MSI-L was only shown in patients younger than 40 years, females, stage III, non-mucin secreting adenocarcinoma and a significant interaction with physical activity. Conclusion: In Conclusion, the present study confirms the increased risk of MSS/MSI-L with increased BMI and speculates this association to be modified by patient's life style and tumor characteristics. Further research is needed to validate present results.

SLIT2 has been classified as a major tumour suppressor gene due to its frequent inactivation in different cancer types. However, alterations of SLIT2 expression and relation to patient outcomes in diffuse large B-cell lymphoma (DLBCL) remain undefined. The aim of this study was to investigate the expression and the methylation status of SLIT2 gene as well as its relation to patient outcomes in DLBCL. Immunohistochemical (IHC) staining was carried out to detect the expression of SLIT2 in a series of 108 DLBCL cases. Re-analysis of previously published dataset (GSE10846) that measured gene expression in DLBCL patients who had received CHOP or R-CHOP therapy was performed to identify associations between SLIT2 and patients survival. Laser capture microdissection was performed to isolate GC B cells and DLBCL primary tumor cells. Bisulfite treatment and methylation-specific PCR (MSP) analysis were done to assess SLIT2 promotor methylation status. The expression of SLIT2 protein was reduced in a subset of DLBCL cases and this was significantly correlated with advanced clinical stage (p= 0.041) and was an independent predictor of worse overall survival (OS) (p= 0.012). Re-analysis of published gene expression data showed that reduced SLIT2 mRNA expression was significantly correlated with worse OS in R-CHOP-treated ABC DLBCL patients (p= <0.01). Hypermethylation of the SLIT2 promotor was significantly correlated with low SLIT2 expression (p=0.009). Our results provide a novel evidence of reduced expression of SLIT2 that is associated with promoter hypermethylation and adverse outcomes in patients with DLBCL.