• 제목/요약/키워드: Brain tumor, glioma

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뇌경색 환자에서 뇌종양과 유사한 Tc-99m tetrofosmin의 섭취 (Cerebral Infarction Mimicking Brain Tumor on Tc-99m Tetrofosmin Brain SPECT imaging)

  • 김순;전석길;원경숙
    • 대한핵의학회지
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    • 제38권3호
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    • pp.268-271
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    • 2004
  • A 43-year-old man was presented with persistent headache for two weeks. 72 weighted MR imaging showed high signal intensity with surrounding edema in the left frontal lobe. These findings were considered with intracranial tumor such as glioma or metastasis. Tc-99m tetrofosmin SPECT showed focal radiotracer accumulation in the left frontal lobe. The operative specimen contained cerebral infarction with organizing leptomeningeal hematoma by pathologist. Another 73-year-old man was hospitalized for chronic headache. Initial CT showed ill-defined hypodensity with mass effect in the right parietal lobe. Tc-99m tetrofosmin SPECT showed focal radiotracer uptake in the right parietal lobe. These findings were considered with low-grade glioma or infarction. Follow-up CT after 5 months showed slightly decreased in size of low density in the right parietal lobe, and cerebral infarction is more likely than others. Tc-99m tetrofosmin has been proposed as a cardiotracer of myocardial perfusion imaging and an oncotropic radiotracer. Tc-99m tetrofosmin SPECT image provides a better attractive alternative agent than T1-201 as a tumor-imaging agent, with characteristics such as high-energy flux, short half-life, favorable biodistribution, dosimetry and lower background radioactivity. We have keep in mind on the analysis of Tc-99m tetrofomin imaging when cerebral infarction is being differentiated from brain tumor.

Pediatric Glioma at the Optic Pathway and Thalamus

  • Park, Eun Suk;Park, Jun Bum;Ra, Young-Shin
    • Journal of Korean Neurosurgical Society
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    • 제61권3호
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    • pp.352-362
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    • 2018
  • Gliomas are the most common pediatric tumors of the central nervous system. In this review, we discuss the clinical features, treatment paradigms, and evolving concepts related to two types of pediatric gliomas affecting two main locations: the optic pathway and thalamus. In particular, we discuss recently revised pathologic classification, which adopting molecular parameter. We believe that our review contribute to the readers' better understanding of pediatric glioma because pediatric glioma differs in many ways from adult glioma according to the newest advances in molecular characterization of this tumor. A better understanding of current and evolving issues in pediatric glioma is needed to ensure effective management decision.

FoxD2-AS1 is a prognostic factor in glioma and promotes temozolomide resistance in a O6-methylguanine-DNA methyltransferase-dependent manner

  • Shangguan, Wenbing;Lv, Xuyang;Tian, Nan
    • The Korean Journal of Physiology and Pharmacology
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    • 제23권6호
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    • pp.475-482
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    • 2019
  • Glioma is the most common brain tumor with a dismal prognosis. While temozolomide (TMZ) based chemotherapy significantly improves survival in glioma patients, resistance against this compound commonly leads to glioma treatment failure. Overexpression of long-noncoding RNA (LncRNA) FoxD2 adjacent opposite strand RNA 1 (FoxD2-AS1) was identified to promote glioma development, but the role in TMZ resistance remains unclear. In this paper, we found that FoxD2-AS1 was overexpressed in recurrent glioma, high FoxD2-AS1 expression was significantly correlated with poor patient outcome. Methylation of $O^6$-methylguanine-DNA methyltransferase (MGMT) is significantly less frequent in high FoxD2-AS1 expression patients. Knockdown of FoxD2-AS1 decreased the proliferation, metastatic ability of glioma cells and promote the sensitivity to TMZ in glioma cells. Furthermore, knockdown of FoxD2-AS1 induced hypermethylation of the promoter region of MGMT. Our data suggested that FoxD2-AS1 is a clinical relevance LncRNA and mediates TMZ resistance by regulating the methylation status of the MGMT promoter region.

A Deep Learning Method for Brain Tumor Classification Based on Image Gradient

  • Long, Hoang;Lee, Suk-Hwan;Kwon, Seong-Geun;Kwon, Ki-Ryong
    • 한국멀티미디어학회논문지
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    • 제25권8호
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    • pp.1233-1241
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    • 2022
  • Tumors of the brain are the deadliest, with a life expectancy of only a few years for those with the most advanced forms. Diagnosing a brain tumor is critical to developing a treatment plan to help patients with the disease live longer. A misdiagnosis of brain tumors will lead to incorrect medical treatment, decreasing a patient's chance of survival. Radiologists classify brain tumors via biopsy, which takes a long time. As a result, the doctor will need an automatic classification system to identify brain tumors. Image classification is one application of the deep learning method in computer vision. One of the deep learning's most powerful algorithms is the convolutional neural network (CNN). This paper will introduce a novel deep learning structure and image gradient to classify brain tumors. Meningioma, glioma, and pituitary tumors are the three most popular forms of brain cancer represented in the Figshare dataset, which contains 3,064 T1-weighted brain images from 233 patients. According to the numerical results, our method is more accurate than other approaches.

실험관 및 생체내에서 U-87 교모세포종 세포주의 광역학 치료 효과에 대한 연구 (in vitro and in vivo Photodynamic Activity Study of U-87 Human Glioma Cell with Photofrin)

  • 조우진;조경근;지철;박성찬;박해관;강준기;최창락
    • Journal of Korean Neurosurgical Society
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    • 제30권5호
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    • pp.553-560
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    • 2001
  • Objective : The objective of this study was to determine the photodynamic therapeutic response of U-87 human glioma cell in vitro as well as in the nude rat xenograft model using photofrin as photosensitizer. Material and Method : U-87 cells were cultured on 96-well culture plates, photofrin(Quadralogic Technologies Inc., Vancouver, Canada) was added into the cell culture medium at concentration of $1{\mu}g/ml$, $2.5{\mu}g/ml$, $5{\mu}g/ml$, $10{\mu}g/ml$ and $20{\mu}g/ml$. 24 hour after drug treatment, cells were treated with optical(632nm) irradiation of $100mJ/cm^2$, $200mJ/cm^2$ and $400mJ/cm^2$. Photofrin(12.5mg/kg, i.p.) was administered to 28 nude rats containing intracerebral U-87 human glioma as well as 26 normal nude rats. 48 hours after administration, animals were treated with optical irradiation(632nm) of $35J/cm^2$, $140J/cm^2$ and $280J/cm^2$ to exposed tumor and normal brain. The photofrin concentration was measured in tumor and normal brain in a separate population of animals. Results : By MTT assay, there was 100% cytotoxicity at any dose of photofrin with optical irradiation of $200mJ/cm^2$ and $400mJ/cm^2$. But at the optical irradiation of $100mJ/cm^2$ cells were killed in dose dependent manner 28.5%, 49.1%, 54.4%, 78.2%, and 84.6% at concentration of $1{\mu}g/ml$, $2.5{\mu}g/ml$, $5{\mu}g/ml$, $10{\mu}g/ml$ and $20{\mu}g/ml$, respectively. Dose dependent PDT lesions in both tumor and normal brain were observed. In the tumor lesion, only superficial tissue damage was found with optical irradiation of $35J/cm^2$. However, in the optical irradiation group of $140J/cm^2$ and $280J/cm^2$ the volume of lesions was measured of $7.2mm^3$ and $14.0mm^3$ for treatment at $140J/cm^2$ and $280J/cm^2$, respectively. The U-87 bearing rats showed a photofrin concentration in tumor tissue of $6.53{\pm}2.16{\mu}g/g$, 23 times higher than that found in the contralateral hemisphere of $0.28{\pm}0.15{\mu}g/g$. Conclusion : Our data indicate that the U-87 human glioma in vitro and in the xenografted rats is responsive to PDT. At these doses, a reproducible injury can be delivered to human glioma in this model. Strategies to spare the normal brain collateral damage are being studied.

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Inhibitory Effects of Phylligenin on the Proliferation of Cultured Rat Neural Progenitor Cells

  • Lee, Sung-Hoon;Go, Hyo-Sang;Choi, Chang-Soon;Cheong, Jae-Hoon;Han, Sun-Young;Bae, Ki-Hwan;Ko, Kwang-Ho;Park, Seung-Hwa
    • Biomolecules & Therapeutics
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    • 제18권1호
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    • pp.48-55
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    • 2010
  • Neural progenitor cells (NPCs) differentiate into astrocytes, neurons and oligodendrocytes, which is controlled by various factors in brain. Recent evidences suggest that small molecules modulating the proliferation and differentiation of NPCs may have therapeutic value as well as the potential use as chemical probes. Phylligenin is a lignan with anti-inflammatory activity that is isolated from the fruits of Forsythia koreana. We investigated effects of phylligenin on proliferation and differentiation of NPCs. Treatment of phylligenin decreased the number of proliferating NPCs in culture without effects on the differentiation and survival of neural cells such as neurons and astrocytes. To examine the mechanism of the decreased NPCs number, we performed cell cycle analysis. Proliferation of NPCs was decreased via G1-S transition block by phylligenin treatment, and it was mediated by the increase of p21 level. However, phylligenin did not induce apoptosis of NPCs as determined by TUNEL assay and PARP cleavage. We also found that viability of glioma cell lines such as C6 and U87MG glioma cells, but not that of primary neuron and astrocyte, was inhibited by phylligenin. These results suggest that phylligenin selectively inhibits proliferation of rapidly growing cells such as neural stem cells and glioma cells. Given that the possible role of brain tumor stem cells in the pathology of brain cancers, the inhibitory effects of phylligenin might be useful in the development of new therapeutic agents against brain cancers.

CXCR4-STAT3 Axis Plays a Role in Tumor Cell Infiltration in an Orthotopic Mouse Glioblastoma Model

  • Han, Ji-hun;Yoon, Jeong Seon;Chang, Da-Young;Cho, Kyung Gi;Lim, Jaejoon;Kim, Sung-Soo;Suh-Kim, Haeyoung
    • Molecules and Cells
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    • 제43권6호
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    • pp.539-550
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    • 2020
  • Glioblastoma multiforme (GBM) is a fatal malignant tumor that is characterized by diffusive growth of tumor cells into the surrounding brain parenchyma. However, the diffusive nature of GBM and its relationship with the tumor microenvironment (TME) is still unknown. Here, we investigated the interactions of GBM with the surrounding microenvironment in orthotopic xenograft animal models using two human glioma cell lines, U87 and LN229. The GBM cells in our model showed different features on the aspects of cell growth rate during their development, dispersive nature of glioma tumor cells along blood vessels, and invasion into the brain parenchyma. Our results indicated that these differences in the two models are in part due to differences in the expression of CXCR4 and STAT3, both of which play an important role in tumor progression. In addition, the GBM shows considerable accumulation of resident microglia and peripheral macrophages, but polarizes differently into tumor-supporting cells. These results suggest that the intrinsic factors of GBM and their interaction with the TME determine the diffusive nature and probably the responsiveness to non-cancer cells in the TME.

Software Implementation for 3D visualization of brain fiber tractography and high-resolution anatomical data

  • Oh, Jung-Su;Song, In-Chan;Ikhwan Cho;Kim, Jong-Hyo;Chang, Kee-Hyun;Park, Kwang-Suk
    • 대한자기공명의과학회:학술대회논문집
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    • 대한자기공명의과학회 2003년도 제8차 학술대회 초록집
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    • pp.83-83
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    • 2003
  • Purpose: The purpose of paper is to implement a PC-based software for 3D visualization of brain fiber tractography and high-resolution anatomical data introduction: DTI (Diffusion tensor imaging) is a very useful noninvasive MRI technique for providing the direction and connectivity information of brain fiber tracts. Especially in patients with glioma, fiber tracts on the lesion side in the brain had varying degrees of displacement or disruption as a result of the tumor. Tract disruption resulted from direct tumor involvement, compression on the tract, and vasogenic edema surrounding the tumor. To combine information on fiber tracts surrounding tumor with a high-resolution anatomical 3D image may be clinically useful for surgical planning. Therefore we implemented a software for visualizing both brain fiber tractography and anatomical data.

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EID3 Promotes Glioma Cell Proliferation and Survival by Inactivating AMPKα1

  • Xiang, Yaoxian;Zhu, Lei;He, Zijian;Xu, Lei;Mao, Yuhang;Jiang, Junjian;Xu, Jianguang
    • Journal of Korean Neurosurgical Society
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    • 제65권6호
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    • pp.790-800
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    • 2022
  • Objective : EID3 (EP300-interacting inhibitor of differentiation) was identified as a novel member of EID family and plays a pivotal role in colorectal cancer development. However, its role in glioma remained elusive. In current study, we identified EID3 as a novel oncogenic molecule in human glioma and is critical for glioma cell survival, proliferation and invasion. Methods : A total of five patients with glioma were recruited in present study and fresh glioma samples were removed from patients. Four weeks old male non-obese diabetic severe combined immune deficiency (NOD/SCID) mice were used as transplant recipient models. The subcutaneous tumor size was calculated and recorded every week with vernier caliper. EID3 and AMP-activated protein kinase α1 (AMPKα1) expression levels were confirmed by real-time polymerase chain reaction and Western blot assays. Colony formation assays were performed to evaluate cell proliferation. Methyl thiazolyl tetrazolium (MTT) assays were performed for cell viability assessment. Trypan blue staining approach was applied for cell death assessment. Cell Apoptosis DNA ELISA Detection Kit was used for apoptosis assessment. Results : EID3 was preferentially expressed in glioma tissues/cells, while undetectable in astrocytes, neuronal cells, or normal brain tissues. EID3 knocking down significantly hindered glioma cell proliferation and invasion, as well as induced reduction of cell viability, apoptosis and cell death. EID3 knocking down also greatly inhibited tumor growth in SCID mice. Knocking down of AMPKα1 could effectively rescue glioma cells from apoptosis and cell death caused by EID3 absence, indicating that AMPKα1 acted as a key downstream regulator of EID3 and mediated suppression effects caused by EID3 knocking down inhibition. These findings were confirmed in glioma cells generated patient-derived xenograft models. AMPKα1 protein levels were affected by MG132 treatment in glioma, which suggested EID3 might down regulate AMPKα1 through protein degradation. Conclusion : Collectively, our study demonstrated that EID3 promoted glioma cell proliferation and survival by inhibiting AMPKα1 expression. Targeting EID3 might represent a promising strategy for treating glioma.

Effects of Hydroxychloroquine Co-administered with Chemotherapeutic Agents on Malignant Glioma Cell Lines : in vitro Study

  • Park, Yong-Sook;Choi, Jae-Young;Chang, Jong-Hee;Park, Yong-Gou;Chang, Jin-Woo
    • Journal of Korean Neurosurgical Society
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    • 제38권1호
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    • pp.47-53
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    • 2005
  • Objective : Anti-malaria drugs may modulate tumor resistance to chemotherapeutic agents, but it has not been proven effective in the treatment of malignant gliomas. The aim of this study was to determine whether adequate pre-clinical data on co-administration of chemotherapeutic agents with anti-malaria drugs on malignant cell lines could be obtained that would warrant its further potential consideration for use in a clinical trial for malignant gliomas. Methods : Two malignant glioma cell lines [U87MG, T98G] were treated with chemotherapeutic agents alone or with anti-malaria drugs. Cells were incubated with drugs for 4 days. Following the 4-day incubation, drug sensitivity assays were performed using 3-[4,5-dimethyl-2-thiazol-2-yl] 2,5-diphenyltetrazolium bromide [MTT] assay following optimization of experimental conditions for each cell lines and cell viability was calculated. Results : In all of four chemotherapeutic agents[doxorubicin. vincrisitne, nimustine, and cisplatin], the cell viability was found to be markedly decreased when hydroxychloroquine was co-administered on both U87MG and T98G cell lines. The two way analysis of variance[ANOVA] yielded a statistically significant two-sided p-value of 0.0033[doxorubicin], 0.0005[vincrisitne], 0.0007[nimustine], and 0.0003[cisplatin] on U87MG cell lines and 0.0006[doxorubicin], 0.0421[vincrisitne], 0.0317[nimustine], and 0.0001[cisplatin] on T98G cell lines, respectively. However, treatment with chloroquine and primaquine did not induce a decrease in cell viability on both U87MG and T98G cell lines. Conclusion : Our data support further consideration of the use of hydroxychloroquine prior to systemic chemotherapy to maximize its tumoricidal effect for patients with malignant gliomas.