scholarly journals Histology of human glioblastoma transplanted on chicken chorioallantoic membrane

Medicina ◽  
2009 ◽  
Vol 45 (2) ◽  
pp. 123 ◽  
Author(s):  
Neringa Balčiūnienė ◽  
Arimantas Tamašauskas ◽  
Angelija Valančiūtė ◽  
Vytenis Deltuva ◽  
Gintautas Vaitiekaitis ◽  
...  
Keyword(s):  
T Cells ◽  
S100 Protein ◽  
Chorioallantoic Membrane ◽  
Experimental Models ◽  
Transplanted Tumors ◽  
Chicken Tissue ◽  
Cytological Features ◽  
Astrocytic Gliomas ◽  
Chicken Erythrocytes ◽  
Chicken Chorioallantoic Membrane

Glioblastoma is the most malignant tumor in the range of cerebral astrocytic gliomas. A lot of experimental models are used to evaluate various properties of glioblastoma. Chicken chorioallantoic membrane model is one of them. Objective. To evaluate histology and survival of glioblastoma tumors taken immediately from operating theatre and transplanted on chicken chorioallantoic membrane. Materials and methods. Glioblastoma samples obtained from 10 patients were transplanted onto 200 eggs. Overall, we used 15 tumors; only 5 of them were not glioblastomas as it was revealed later. Results. The transplanted tumors survive up to 6 days. Transplants do not survive longer because during embryo’s development the nourishing membrane dries. Transplanted glioblastomas exhibited the same features as original glioblastomas – necrosis, endothelium proliferation, cellular polymorphism – while transplanted glioblastomas also showed glial fibrillary acidic protein (GFAP), vimentin, Ki67, S100 protein, neurofilament immunoreactivity, and infiltration of macrophages (CD68) and T cells (CD3+, CD8+). Transplanted glioblastomas did not show any immunoreactivity of p53. Invasion of vessels from the chicken into transplanted tumor is not observed. Chicken erythrocytes did not appear within the transplants, and tumor cells invade chicken tissue at the minimum. Conclusion. Our data show that transplanted pieces of glioblastoma survive with all cytological features. The presence of macrophages (marker CD68) and T cells (markers CD3+ and CD8+) can be registered in the transplant. The data revealed that transplanted glioblastoma remains as insulated unit, which survives from nourishment of the chorioallantoic membrane apparently only by diffusion. The features of original tumor-host reaction of the patient remained too.

scholarly journals Distinct Roles of Vav Family Members in Adaptive and Innate Immune Models of Arthritis

Biomedicines ◽  
2021 ◽  
Vol 9 (6) ◽  
pp. 695
Author(s):  
Javier Conde ◽  
Isabel Fernández-Pisonero ◽  
Myriam Cuadrado ◽  
Antonio Abad ◽  
Javier Robles-Valero ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
T Cells ◽  
Family Members ◽  
Experimental Models ◽  
Innate Immune ◽  
Main Role ◽  
Zymosan A ◽  
Proliferation And Differentiation ◽  
Signal Transduction Proteins ◽  
Selection Of

Genetic evidence suggests that three members of the VAV family (VAV1, VAV2 and VAV3) of signal transduction proteins could play important roles in rheumatoid arthritis. However, it is not known currently whether the inhibition of these proteins protects against this disease and, if so, the number of family members that must be eliminated to get a therapeutic impact. To address this issue, we have used a collection of single and compound Vav family knockout mice in experimental models for antigen-dependent (methylated bovine serum albumin injections) and neutrophil-dependent (Zymosan A injections) rheumatoid arthritis in mice. We show here that the specific elimination of Vav1 is sufficient to block the development of antigen-induced arthritis. This protection is likely associated with the roles of this Vav family member in the development and selection of immature T cells within the thymus as well as in the subsequent proliferation and differentiation of effector T cells. By contrast, we have found that depletion of Vav2 reduces the number of neutrophils present in the joints of Zymosan A-treated mice. Despite this, the elimination of Vav2 does not protect against the joint degeneration triggered by this experimental model. These findings indicate that Vav1 is the most important pharmacological target within this family, although its main role is limited to the protection against antigen-induced rheumatoid arthritis. They also indicate that the three Vav family proteins do not play redundant roles in these pathobiological processes.

Inhibition by doxycycline of angiogenesis in the chicken chorioallantoic membrane (CAM)

2005 ◽  
Vol 56 (1) ◽  
pp. 1-9 ◽  
Author(s):  
Mary Richardson ◽  
David Wong ◽  
Samantha Lacroix ◽  
Jolanta Stanisz ◽  
Gurmit Singh
Keyword(s):  
Chorioallantoic Membrane ◽  
Chicken Chorioallantoic Membrane

scholarly journals Angiotropism of Human Melanoma: Studies Involving In Transit and Other Cutaneous Metastases and the Chicken Chorioallantoic Membrane

2006 ◽  
Vol 28 (3) ◽  
pp. 187-193 ◽  
Author(s):  
Claire Lugassy ◽  
Stephen E. Vernon ◽  
Klaus Busam ◽  
Jean A. Engbring ◽  
Danny R. Welch ◽  
...  
Keyword(s):  
Chorioallantoic Membrane ◽  
Human Melanoma ◽  
Cutaneous Metastases ◽  
In Transit ◽  
Chicken Chorioallantoic Membrane

scholarly journals An antagonist of integrin alpha v beta 3 prevents maturation of blood vessels during embryonic neovascularization

1995 ◽  
Vol 108 (7) ◽  
pp. 2655-2661 ◽  
Author(s):  
C.J. Drake ◽  
D.A. Cheresh ◽  
C.D. Little
Keyword(s):  
Experimental Data ◽  
Monoclonal Antibody ◽  
Blood Vessels ◽  
Chorioallantoic Membrane ◽  
Normal Pattern ◽  
Basal Surface ◽  
Lumen Formation ◽  
Vessel Development ◽  
Alpha V Beta 3 ◽  
Chicken Chorioallantoic Membrane

Experimental data in this study demonstrate that integrin alpha v beta 3 is fundamentally involved in the maturation of blood vessels during embryonic neovascularization (vasculogenesis). Integrin alpha v beta 3 was specifically expressed on the surface of angioblasts during vessel development in quail embryos and vitronectin, a ligand for alpha v beta 3, localized to the basal surface of these cells. More importantly, microinjection of the anti-alpha v beta 3 monoclonal antibody, LM609, disrupted the normal pattern of vascular development. After exposure to LM609 the angioblasts in experimental embryos appeared as clusters of rounded cells lacking normal cellular protrusions. This led to disruption of lumen formation and abnormal vessel patterning. These findings demonstrate that during vasculogenesis ligation of integrin alpha v beta 3 on the surface of primordial endothelial cells is critical for the differentiation and maturation of blood vessels. Similar studies on chicken chorioallantoic membrane showed that LM609 blocks angiogenesis. Together the two studies suggest that integrin alpha v beta 3 plays a role in neovascularization of tissues.

scholarly journals STAT3/5 Inhibitors Suppress Proliferation in Bladder Cancer and Enhance Oncolytic Adenovirus Therapy

2020 ◽  
Vol 21 (3) ◽  
pp. 1106 ◽  
Author(s):  
Sruthi V. Hindupur ◽  
Sebastian C. Schmid ◽  
Jana Annika Koch ◽  
Ahmed Youssef ◽  
Eva-Maria Baur ◽  
...  
Keyword(s):  
Bladder Cancer ◽  
Cell Cycle Progression ◽  
Chorioallantoic Membrane ◽  
Oncolytic Adenovirus ◽  
Cycle Progression ◽  
Cellular Processes ◽  
Division Cell ◽  
Chicken Chorioallantoic Membrane ◽  
Cam Model ◽  
Phosphorylated Stat3

The JAK-STAT signalling pathway regulates cellular processes like cell division, cell death and immune regulation. Dysregulation has been identified in solid tumours and STAT3 activation is a marker for poor outcome. The aim of this study was to explore potential therapeutic strategies by targeting this pathway in bladder cancer (BC). High STAT3 expression was detected in 51.3% from 149 patient specimens with invasive bladder cancer by immunohistochemistry. Protein expression of JAK, STAT and downstream targets were confirmed in 10 cell lines. Effects of the JAK inhibitors Ruxolitinib and BSK-805, and STAT3/5 inhibitors Stattic, Nifuroxazide and SH-4-54 were analysed by cell viability assays, immunoblotting, apoptosis and cell cycle progression. Treatment with STAT3/5 but not JAK1/2 inhibitors reduced survival, levels of phosphorylated STAT3 and Cyclin-D1 and increased apoptosis. Tumour xenografts, using the chicken chorioallantoic membrane (CAM) model responded to Stattic monotherapy. Combination of Stattic with Cisplatin, Docetaxel, Gemcitabine, Paclitaxel and CDK4/6 inhibitors showed additive effects. The combination of Stattic with the oncolytic adenovirus XVir-N-31 increased viral replication and cell lysis. Our results provide evidence that inhibitors against STAT3/5 are promising as novel mono- and combination therapy in bladder cancer.

scholarly journals Tumor Size Matters—Understanding Concomitant Tumor Immunity in the Context of Hypofractionated Radiotherapy with Immunotherapy

Cancers ◽  
2020 ◽  
Vol 12 (3) ◽  
pp. 714
Author(s):  
Jean Philippe Nesseler ◽  
Mi-Heon Lee ◽  
Christine Nguyen ◽  
Anusha Kalbasi ◽  
James W. Sayre ◽  
...  
Keyword(s):  
T Cells ◽  
Cd8 T Cells ◽  
Immune Cell ◽  
Tumor Regression ◽  
Experimental Models ◽  
Tumor Burden ◽  
Local Regression ◽  
Cell Content ◽  
Primary Tumors ◽  
The Impact

The purpose of this study was to determine the dynamic contributions of different immune cell subsets to primary and abscopal tumor regression after hypofractionated radiation therapy (hRT) and the impact of anti-PD-1 therapy. A bilateral syngeneic FSA1 fibrosarcoma model was used in immunocompetent C3H mice, with delayed inoculation to mimic primary and microscopic disease. The effect of tumor burden on intratumoral and splenic immune cell content was delineated as a prelude to hRT on macroscopic T1 tumors with 3 fractions of 8 Gy while microscopic T2 tumors were left untreated. This was performed with and without systemic anti-PD-1. Immune profiles within T1 and T2 tumors and in spleen changed drastically with tumor burden in untreated mice with infiltrating CD4+ content declining, while the proportion of CD4+ Tregs rose. Myeloid cell representation escalated in larger tumors, resulting in major decreases in the lymphoid:myeloid ratios. In general, activation of Tregs and myeloid-derived suppressor cells allow immunogenic tumors to grow, although their relative contributions change with time. The evidence suggests that primary T1 tumors self-regulate their immune content depending on their size and this can influence the lymphoid compartment of T2 tumors, especially with respect to Tregs. Tumor burden is a major confounding factor in immune analysis that has to be taken into consideration in experimental models and in the clinic. hRT caused complete local regression of primary tumors, which was accompanied by heavy infiltration of CD8+ T cells activated to express IFN-γ and PD-1; while certain myeloid populations diminished. In spite of this active infiltrate, primary hRT failed to generate the systemic conditions required to cause abscopal regression of unirradiated microscopic tumors unless PD-1 blockade, which on its own was ineffective, was added to the RT regimen. The combination further increased local and systemically activated CD8+ T cells, but few other changes. This study emphasizes the subtle interplay between the immune system and tumors as they grow and how difficult it is for local RT, which can generate a local immune response that may help with primary tumor regression, to overcome the systemic barriers that are generated so as to effect immune regression of even small abscopal lesions.

scholarly journals ­Active AKT signaling triggers CLL towards Richter's transformation via over-activation of Notch1

Blood ◽  
2020 ◽  
Author(s):  
Vivien Kohlhaas ◽  
Stuart James Blakemore ◽  
Mona Al-Maarri ◽  
Nadine Nickel ◽  
Martin Pal ◽  
...  
Keyword(s):  
T Cells ◽  
S100 Protein ◽  
Significant Proportion ◽  
Lymphocytic Leukemia ◽  
Aggressive Lymphoma ◽  
Akt Phosphorylation ◽  
Recurrent Mutations ◽  
Genomic Aberrations ◽  
Richter’S Transformation ◽  
Richter's Transformation

Richter's transformation (RT) is an aggressive lymphoma which occurs upon progression from chronic lymphocytic leukemia (CLL). Transformation has been associated with genetic aberrations in the CLL-phase involving TP53, CDKN2A, MYC, and NOTCH1, however a significant proportion of RT cases lack CLL-phase associated events. Here, we report that high levels of AKT phosphorylation occurs both in high-risk CLL patients harboring TP53 and NOTCH1 mutations as well as in RT patients. Genetic over-activation of Akt in the murine Eµ-TCL1 CLL mouse model resulted in CLL to RT with significantly reduced survival and an aggressive lymphoma phenotype. In the absence of recurrent mutations, we identified a profile of genomic aberrations intermediate between CLL and DLBCL. Multi-omics assessment by phosphoproteomic/proteomic and single-cell transcriptomic profiles of this Akt-induced murine RT revealed a S100-protein-defined subcluster of highly aggressive lymphoma cells, which developed from CLL cells, through activation of Notch via Notch ligand expressed by T cells. Constitutively active Notch1 similarly induced RT of murine CLL. We identify Akt activation as an initiator of CLL transformation towards aggressive lymphoma by inducing Notch signaling between RT cells and microenvironmental T cells.

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