Glioblastoma multiforme is a central nervous system tumor of grade IV histological malignancy according to the WHO classification. Over 90% of diagnosed glioblastomas multiforme cases are primary gliomas, arising from normal glial cells through multistep oncogenesis. The remaining 10% are secondary gliomas originating from tumors of lower grade. These tumors expand distinctly more slowly. Although genetic alterations and deregulations of molecular pathways leading to both primary and secondary glioblastomas formation differ, morphologically they do not reveal any significant differences. Glioblastoma is a neoplasm that occurs spontaneously, although familial gliomas have also been noted. Caucasians, especially those living in industrial areas, have a higher incidence of glioblastoma. Cases of glioblastoma in infants and children are also reported. The participation of sex hormones and viruses in its oncogenesis was also suggested. Progression of glioblastoma multiforme is associated with deregulation of checkpoint G1/S of a cell cycle and occurrence of multiple genetic abnormalities of tumor cells. Metastases of glioblastoma multiforme are rarely described. Treatment of glioblastoma multiforme includes tumor resection, as well as radiotherapy and chemotherapy. Drugs inhibiting integrin signaling pathways and immunotherapy are also employed. Treatment modalities and prognosis depend on the tumor localization, degree of its malignancy, genetic profile, proliferation activity, patient's age and the Karnofsky performance scale score. Although the biology of glioblastoma multiforme has recently been widely investigated, the studies summarizing the knowledge of its development and treatment are still not sufficient in terms of comprehensive brain tumor analysis.

The interaction between silver nanoparticles and herpesviruses is attracting great interest due to their antiviral activity and possibility to use as microbicides for oral and anogenital herpes. In this work, we demonstrate that tannic acid modified silver nanoparticles sized 13 nm, 33 nm and 46 nm are capable of reducing HSV-2 infectivity both in vitro and in vivo. The antiviral activity of tannic acid modified silver nanoparticles was size-related, required direct interaction and blocked virus attachment, penetration and further spread. All tested tannic acid modified silver nanoparticles reduced both infection and inflammatory reaction in the mouse model of HSV-2 infection when used at infection or for a post-infection treatment. Smaller-sized nanoparticles induced production of cytokines and chemokines important for anti-viral response. The corresponding control buffers with tannic acid showed inferior antiviral effects in vitro and were ineffective in blocking in vivo infection. Our results show that tannic acid modified silver nanoparticles are good candidates for microbicides used in treatment of herpesvirus infections.

Recently, it has been shown that silver nanoparticles (AgNPs) provide a unique approach to the treatment of tumors, especially those of neuroepithelial origin. Thus, the aim of this study was to evaluate the impact of AgNPs on proliferation and activation of the intrinsic apoptotic pathway of glioblastoma multiforme (GBM) cells cultured in an in ovo model. Human GBM cells, line U-87, were placed on chicken embryo chorioallantoic membrane. After 8 days, the tumors were divided into three groups: control (non-treated), treated with colloidal AgNPs (40 μg/ml), and placebo (tumors supplemented with vehicle only). At the end of the experiment, all tumors were isolated. Assessment of cell proliferation and cell apoptosis was estimated by histological, immunohistochemical, and Western blot analyses. The results show that AgNPs can influence GBM growth. AgNPs inhibit proliferation of GBM cells and seem to have proapoptotic properties. Although there were statistically significant differences between control and AgNP groups in the AI and the levels of active caspase 9 and active caspase 3, the level of these proteins in GBM cells treated with AgNPs seems to be on the border between the spontaneous apoptosis and the induced. Our results indicate that the antiproliferative properties of silver nanoparticles overwhelm proapoptotic ones. Further research focused on the cytotoxic effect of AgNPs on tumor and normal cells should be conducted.Electronic supplementary materialThe online version of this article (doi:10.1186/s11671-015-0823-5) contains supplementary material, which is available to authorized users.

Fas receptor-Fas ligand (FasL) signalling is involved in apoptosis of immune cells as well as of the virus infected target cells but increasing evidence accumulates on Fas as a mediator of apoptosis-independent processes such as induction of activating and proinflammatory signals. In this study, we examined the role of Fas/FasL pathway in inflammatory and antiviral response in lungs using a mousepox model applied to C57BL6/J, B6. MRL-Faslpr/J, and B6Smn.C3-Faslgld/J mice. Ectromelia virus (ECTV) infection of Fas- and FasL-deficient mice led to increased virus titers in lungs and decreased migration of IFN-γ expressing NK cells, CD4+ T cells, CD8+ T cells, and decreased IL-15 expression. The lungs of ECTV-infected Fas- and FasL-deficient mice showed significant inflammation during later phases of infection accompanied by decreased expression of anti-inflammatory IL-10 and TGF-β1 cytokines and disturbances in CXCL1 and CXCL9 expression. Experiments in vitro demonstrated that ECTV-infected cultures of epithelial cells, but not macrophages, upregulate Fas and FasL and are susceptible to Fas-induced apoptosis. Our study demonstrates that Fas/FasL pathway during ECTV infection of the lungs plays an important role in controlling local inflammatory response and mounting of antiviral response.

The tumour suppressor p53 plays a key role in DNA damage and repair. It is the most frequently altered gene in human cancers and these mutations may implicate the genesis and/or progression of tumours. Mutations of the p53 gene were also found in a number of canine cancers, although it is poorly estimated in canine lymphomas. Thus, the aim of this study was to investigate the p53 status in these types of tumours. We have shown that the expression of p53 in canine lymphomas is rare, however significantly differs between lymphomas of T- and B-cell origin.

Recently, it has been shown that silver nanoparticles (AgNPs) provide a unique approach to the treatment of tumors, especially those of neuroepithelial origin. Thus, the aim of this study was to evaluate the impact of AgNPs on proliferation and activation of the intrinsic apoptotic pathway of glioblastoma multiforme (GBM) cells cultured in an in ovo model. Human GBM cells, line U-87, were placed on chicken embryo chorioallantoic membrane. After 8 days, the tumors were divided into three groups: control (non-treated), treated with colloidal AgNPs (40 μg/ml), and placebo (tumors supplemented with vehicle only). At the end of the experiment, all tumors were isolated.Assessment of cell proliferation and cell apoptosis was estimated by histological, immunohistochemical, and Western blot analyses. The results show that AgNPs can influence GBM growth. AgNPs inhibit proliferation of GBM cells and seem to have proapoptotic properties. Although there were statistically significant differences between control and AgNP groups in the AI and the levels of active caspase 9 and active caspase 3, the level of these proteins in GBM cells treated with AgNPs seems to be on the border between the spontaneous apoptosis and the induced. Our results indicate that the antiproliferative properties of silver nanoparticles overwhelm proapoptotic ones. Further research focused on the cytotoxic effect of AgNPs on tumor and normal cells should be conducted.

Forty five lymphomas, 14 of T cell origin, 28 of B cell and 3 with null-cell phenotype, were included in this study. Tumors were classified according to the updated Kiel classification system adapted to canine lymphomas. 3.33). Moreover, high positive correlation between the expression of Ki67 and MI was found (r = 0.668; P ≤ 0.001). In T-cell tumors the correlation was very high (r = 0.83; P ≤ 0.001) and in B-cell lymphomas the correlation was high (r = 0.61; P ≤ 0.001). There were also differences between mean MI values in the lymphomas of different morphological subtypes, but in some of them high variations in the range of MI values were identified and wide overlaps of MI between individual cases from different subtypes were observed. Because of differences in the proliferation activity in single cases of the same subtype of lymphoma, the proliferation activity assessment may be helpful to chose appropriate scheme of treatment and should be commonly performed during routine histopathological diagnosis of canine lymphomas.

Survivin is a member of apoptosis inhibiting proteins family. Apart from its antiapoptotic activity it plays a critical role in regulating the cell cycle and mitosis. It is overexpressed in most human malignancies. While the prognostic significance of survivin expression is widely investigated in human non-Hodgkin's lymphomas, little is known about its expression in canine lymphomas. The aim of the study was to evaluate the expression of survivin in canine lymphomas in relation to proliferation markers (mitotic index and percentage of Ki67-positive cells). Survivin was found in all examined lymphomas belonging to 6 different morphological subtypes with nuclear immunoreactivity. In most of lymphomas (18/25) survivin expression ranged 10%-25% of positive cells. Only single cases had lower (0-10% positive cells, 1/25) or higher (25-50% and >50% positive cells, 5/25 and 1/25, respectively) index of survivin. Neither mitotic index nor proliferative index correlated with survivin expression when the values quantified randomly in whole specimens were compared. However, when survivin expression were quantified in selected tumor areas of low and high proliferation activity the high correlations between survivin expression and proliferation index were found. The results indicated that survivin is commonly expressed in canine lymphomas. Nuclear labelling together with the relation of its expression and proliferative activity in highly proliferative areas of neoplastic tissue suggest a potential role of survivin in cell cycle activation in canine lymphoma cells. However, further studies of the relation between expression of survivin and other proteins involved in cell cycle regulation are needed. Moreover, the results suggest that survivin may pose the therapeutic target in canine lymphomas.