scholarly journals NI-16 * INTRA-OPERATIVE USE OF FLUORESCEIN FOR MALIGNANT GLIOMA RESECTION DIFFERENTIATES TUMOR FROM NORMAL BRAIN TISSUE BASED ON HISTOPATHOLOGIC ANALYSIS

2014 ◽  
Vol 16 (suppl 5) ◽  
pp. v141-v141
Author(s):  
M. Decker ◽  
J. Kresak ◽  
A. Yachnis ◽  
F. Bova ◽  
M. Rahman
2021 ◽  
Author(s):  
Fei Yan ◽  
Lele Du ◽  
Jiatao Lv ◽  
Haitao Zhang ◽  
Jianxin Zhu ◽  
...  

Abstract Background: Yes-associated protein(YAP) plays an important role in signal transduction and gene transcription regulation in 1 normal cells, with elevated and over-expressed YAP levels observed in various malignant tumors. The aim of this study was 2 to investigate the expression of YAP in malignant glioma, and to study the possible relationship of YAP expression with the 3 occurrence and development of malignant glioma. 4 Methods: Immunohistochemical staining was used to assess the expression of YAP and phosphor-YAP in malignant glioma 5 tissue and normal brain tissue, and their protein and mRNA levels were evaluated through Western blotting and reverse 6 transcription-polymerase chain reaction (RT-PCR), respectively. Normal brain tissue obtained from the functional lesion of 7 the epilepsy patients. After transfection of YAPsiRNA oligonucleotides or pcDNA3.1-hYAP plasmid, their effects on glioma 8 cells were investigated using western blot, cell proliferation, cycle, apoptosis and invasion, respectively. We conducted the 9 2 co-Immunoprecipitation to verify the combination of YAP and PPARγ, explore the mechanism of action. 10 Results: YAP-positive expression was found in 9 cases of normal brain and 60 cases of glioma. A significantly higher 11 expression of YAP in glioma tissue as compared with normal brain tissue at both protein and mRNA levels, and YAP proteins 12 mainly expressed and located in the nucleus and only a small percentage in the cytoplasm of glioma tissue. Phosphor-YAP 13 protein expression showed high staining of the cytoplasm, but no staining of the nuclear. While, with the enhancement of 14 the malignant degree, the cytoplasm YAP(p-YAP) expression is lower gradually than normal brain tissues. Further study in 15 glioma cell lines in which YAP was either overexpressed or depleted confirmed that YAP markedly promoted the cell 16 proliferation, cycle, invasion and inhibited the cell apoptosis. Moreover, YAP in company with PPARγ regulates the cell 17 proliferatin and effects the gliomagenesis. 18 Conclusion: These results indicate that YAP plays an important role in glioma and might be a useful therapeutic target of 19 glioma. 20


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Mariano Guardia Clausi ◽  
Alexander M. Stessin ◽  
Zirun Zhao ◽  
Stella E. Tsirka ◽  
Samuel Ryu

AbstractThe efficacy of combining radiation therapy with immune checkpoint inhibitor blockade to treat brain tumors is currently the subject of multiple investigations and holds significant therapeutic promise. However, the long-term effects of this combination therapy on the normal brain tissue are unknown. Here, we examined mice that were intracranially implanted with murine glioma cell line and became long-term survivors after treatment with a combination of 10 Gy cranial irradiation (RT) and anti-PD-1 checkpoint blockade (aPD-1). Post-mortem analysis of the cerebral hemisphere contralateral to tumor implantation showed complete abolishment of hippocampal neurogenesis, but neural stem cells were well preserved in subventricular zone. In addition, we observed a drastic reduction in the number of mature oligodendrocytes in the subcortical white matter. Importantly, this observation was evident specifically in the combined (RT + aPD-1) treatment group but not in the single treatment arm of either RT alone or aPD-1 alone. Elimination of microglia with a small molecule inhibitor of colony stimulated factor-1 receptor (PLX5622) prevented the loss of mature oligodendrocytes. These results identify for the first time a unique pattern of normal tissue changes in the brain secondary to combination treatment with radiotherapy and immunotherapy. The results also suggest a role for microglia as key mediators of the adverse treatment effect.


1989 ◽  
Vol 9 (1) ◽  
pp. 87-95 ◽  
Author(s):  
Michihiro Kirikae ◽  
Mirko Diksic ◽  
Y. Lucas Yamamoto

We examined the rate of glucose utilization and the rate of valine incorporation into proteins using 2-[18F]fluoro-2-deoxyglucose and L-[1-14C]-valine in a rat brain tumor model by quantitative double-tracer autoradiography. We found that in the implanted tumor the rate of valine incorporation into proteins was about 22 times and the rate of glucose utilization was about 1.5 times that in the contralateral cortex. (In the ipsilateral cortex, the tumor had a profound effect on glucose utilization but no effect on the rate of valine incorporation into proteins.) Our findings suggest that it is more useful to measure protein synthesis than glucose utilization to assess the effectiveness of antitumor agents and their toxicity to normal brain tissue. We compared two methods to estimate the rate of valine incorporation: “kinetic” (quantitation done using an operational equation and the average brain rate coefficients) and “washed slices” (unbound labeled valine removed by washing brain slices in 10% thrichloroacetic acid). The results were the same using either method. It would seem that the kinetic method can thus be used for quantitative measurement of protein synthesis in brain tumors and normal brain tissue using [11C]-valine with positron emission tomography.


1987 ◽  
Vol 11 (2) ◽  
pp. 208-213 ◽  
Author(s):  
Mats Bergström ◽  
Kaj Ericson ◽  
Lars Hagenfeldt ◽  
Mikael Mosskin ◽  
Hans von Holst ◽  
...  

2021 ◽  
Vol Publish Ahead of Print ◽  
Author(s):  
Kazuaki Sugawara ◽  
Tosiaki Miyati ◽  
Ryo Ueda ◽  
Daisuke Yoshimaru ◽  
Masanobu Nakamura ◽  
...  

2018 ◽  
Vol 28 (1) ◽  
pp. 56-62
Author(s):  
Cahit Kural ◽  
Arzu Kaya Kocdogan ◽  
Gulcin Güler Şimşek ◽  
Serpil Oğuztüzün ◽  
Pınar Kaygın ◽  
...  

Objective: Intracranial tumors are one of the most frightening and difficult-to-treat tumor types. In addition to surgery, protocols such as chemotherapy and radiotherapy also take place in the treatment. Glutathione S-transferase (GST) and cytochrome P450 (CYP) enzymes are prominent drug-metabolizing enzymes in the human body. The aim of this study is to show the expression of GSTP1, GSTM1, CYP1A1, and CYP1B1 in different types of brain tumors and compare our results with those in the literature. Subjects and Methods: The expression of GSTP1, GSTM1, CYP1A1, and CYP1B1 was analyzed using immunostaining in 55 patients with intracranial tumors in 2016–2017. For GST and CYP expression in normal brain tissue, samples of a portion of surrounding normal brain tissue as well as a matched far neighbor of tumor tissue were used. The demographic features of the patients were documented and the expression results compared. Results: The mean age of the patients was 46.72 years; 29 patients were female and 26 were male. Fifty-seven specimens were obtained from 55 patients. Among them, meningioma was diagnosed in 12, metastases in 12, glioblastoma in 9, and pituitary adenoma in 5. The highest GSTP1, GSTM1, and CYP­1A1 expressions were observed in pituitary adenomas. The lowest GSTP1 expression was detected in glioblastomas and the lowest CYP1B1 expression in pituitary adenomas. Conclusion: GSTP1 and CYP expression is increased in intracranial tumors. These results should be confirmed with a larger series and different enzyme subtypes.


1935 ◽  
Vol 31 (1) ◽  
pp. 137-137
Author(s):  
Н. Reichner

Thanks to the work of Vitebsky and Behrens, it became known that within the neuroectoderm itself it is possible to detect immunospecific structural differences that indicate a certain organ, possibly a functionally specific imprint of individual parts of the tissue of the central nervous system.


Stroke ◽  
2020 ◽  
Vol 51 (Suppl_1) ◽  
Author(s):  
Dongdong Zhang ◽  
Abhinav Srinath ◽  
Andrew J Kinloch ◽  
Robert Shenkar ◽  
Le Shen ◽  
...  

Introduction: Previous studies have reported robust inflammatory cell infiltration, selective synthesis of IgG, B-cell clonal expansion, and deposition of immune complexes and complement within Cerebral Cavernous Malformation (CCM) lesions. Furthermore,B-cell depletion has been shown to reduce the maturation of CCM in murine models. We hypothesize that specific autoantigen(s) within the lesional milieu trigger the pathogenetic immune responses in CCMs. This study aims to identify those putative autoantigen(s) using recombinant antibodies (rAbs) derived from plasma cells found in surgical human CCM lesions. Methods: CD138 + plasma cells were laser captured from fresh frozen surgically resected human CCM lesions. Clonally expanded immunoglobulin heavy- and light-chain variable region pairs were cloned into IgG expression vectors and expressed as monoclonal antibodies. Purified rAbs were assayed by immunofluorescence with CCM lesion tissue and normal brain tissue sections. rAbs assayed by immunocytochemistry with human primary cell line were used to further define the staining pattern. The cell lysates were immunoprecipitated with rAb, after protein purification by SDS-PAGE, and analyzed by Mass spectrometry. Results: In normal brain tissue, rAbs stained endothelial cells with limited staining of glial cells. In CCM lesional tissue, rAbs stained endothelial cells, glial cells as well as structures in the acellular matrix adjacent to caverns. In cultured Human Brain Microvascular Endothelial Cells (HBMECs) and Human Astrocytes (HAs), rAbs co-localized with cytoplasmic components. After HBMEC and HA cell lysates were immunoprecipitated with rAb, a Coomassie Stain detected bands of approximately 50 kDa. Conclusions: Our results suggest that autoantigen(s) in human CCM lesions are cytoplasmic components present in lesional tissue as well as in normal brain tissue. Molecular level identification of the triggering antigen is still ongoing by mass spectrometry. Identification of the autoantigen(s) in the lesional milieu might explain the propensity of lesion development from leaky endothelium in the neuroglial parenchyma. Characterization of the autoantigen triggers will open new venues for therapy or vaccine in this disease.


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