• Title/Summary/Keyword: glioblastoma (GBM)

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A Case Report on the Therapeutic Effect of Integrated Cancer Therapy for Glioblastoma Multiforme (교모세포종에 대한 통합암치료의 치료 효과 증례보고)

  • Yang, Jin-sung;Jang, Hyuk-jun;Song, Si-yeon;Park, Ji-hye;Park, So-jung;Yoo, Hwa-seung
    • The Journal of Internal Korean Medicine
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    • v.43 no.2
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    • pp.320-325
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    • 2022
  • Objective: The purpose of this report is to present the effects of integrative cancer treatment (ICT) on a patient diagnosed with glioblastoma multiforme (GBM). Methods: A 71-year-old male GBM patient received ICT from May 14 to October 12, 2021 and concurrently received temozolomide and radiotherapy. The effect on symptoms was evaluated using a visual analog scale (VAS), and changes in tumor size were assessed using magnetic resonance imaging. Results: After treatment, the VAS score for nausea decreased from 5 to 1, and the tumor size also reduced. Conclusion: ICT could be effective in treating GBM patients by reducing the size of the tumor as well as alleviating the side effects.

Continuous Low-Dose Temozolomide Chemotherapy and Microvessel Density in Recurrent Glioblastoma

  • Woo, Jong-Yun;Yang, Seung Ho;Lee, Youn Soo;Lee, Su Youn;Kim, Jeana;Hong, Yong Kil
    • Journal of Korean Neurosurgical Society
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    • v.58 no.5
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    • pp.426-431
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    • 2015
  • Objective : The purpose of this study was to evaluate the clinical efficacy of continuous low-dose temozolomide (TMZ) chemotherapy for recurrent and TMZ-refractory glioblastoma multiforme (GBM) and to study the relationship between its efficacy and microvessel density within the tumor. Methods : Thirty patients who had recurrent GBM following Stupp's regimen received TMZ daily at $50mg/m^2/day$ until tumor progression between 2007 and 2013. The median duration of continuous low-dose TMZ administration was 8 weeks (range, 2-64). Results : The median progression-free survival (PFS) of continuous low-dose TMZ therapy was 2 months (range, 0.5-16). At 6 months, PFS was 20%. The median overall survival (OS) from the start of this therapy to death was 6 months (95% CI : 5.1-6.9). Microvessel density of recurrent tumor tissues obtained by reoperation of 17 patients was $22.7{\pm}24.1/mm^2$ (mean${\pm}$standard deviation), and this was lower than that of the initial tumor ($61.4{\pm}32.7/mm^2$) (p-value=0.001). It suggests that standard TMZ-chemoradiotherapy reduces the microvessel density within GBM and that recurrences develop in tumor cells with low metabolic burden. The efficacy of continuous low-dose TMZ could not be expected in recurrent GBM cells in poor angiogenic environments. Conclusion : The efficacy of continuous low-dose TMZ chemotherapy is marginal. This study suggests the need to develop further treatment strategies for recurrent and TMZ-refractory GBM.

Specificity Protein 1 Expression Contributes to Bcl-w-Induced Aggressiveness in Glioblastoma Multiforme

  • Lee, Woo Sang;Kwon, Junhye;Yun, Dong Ho;Lee, Young Nam;Woo, Eun Young;Park, Myung-Jin;Lee, Jae-Seon;Han, Young-Hoon;Bae, In Hwa
    • Molecules and Cells
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    • v.37 no.1
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    • pp.17-23
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    • 2014
  • We already had reported that Bcl-w promotes invasion or migration in gastric cancer cells and glioblastoma multiforme (GBM) by activating matrix metalloproteinase-2 (MMP-2) via specificity protein 1 (Sp1) or ${\beta}$-cateinin, respectively. High expression of Bcl-w also has been reported in GBM which is the most common malignant brain tumor and exhibits aggressive and invasive behavior. These reports propose that Bcl-w-induced signaling is strongly associated with aggressive characteristic of GBM. We demonstrated that Sp1 protein or mRNA expression is induced by Bcl-w using Western blotting or RT-PCR, respectively, and markedly elevated in high-grade glioma specimens compared with low-grade glioma tissues using tissue array. However, relationship between Bcl-w-related signaling and aggressive characteristic of GBM is poorly characterized. This study suggested that Bcl-w-induced Sp1 activation promoted expression of glioma stem-like cell markers, such as Musashi, Nanog, Oct4 and sox-2, as well as neurosphere formation and invasiveness, using western blotting, neurosphere formation assay, or invasion assay, culminating in their aggressive behavior. Therefore, Bcl-w-induced Sp1 activation is proposed as a putative marker for aggressiveness of GBM.

Glioblastoma Multiforme in the Pineal Region with Leptomeningeal Dissemination and Lumbar Metastasis

  • Matsuda, Ryosuke;Hironaka, Yasuo;Suigimoto, Tadashi;Nakase, Hiroyuki
    • Journal of Korean Neurosurgical Society
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    • v.58 no.5
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    • pp.479-482
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    • 2015
  • We report a case of a 31-year-old woman with glioblastoma multiforme (GBM) in the pineal region with associated leptomeningeal dissemination and lumbar metastasis. The patient presented with severe headache and vomiting. Magnetic resonance imaging (MRI) of the brain showed a heterogeneously enhanced tumor in the pineal region with obstructive hydrocephalus. After an urgent ventricular-peritoneal shunt, she was treated by subtotal resection and chemotherapy concomitant with radiotherapy. Two months after surgery, MRI showed no changes in the residual tumor but leptomeningeal dissemination surrounding the brainstem. One month later, she exhibited severe lumbago and bilateral leg pain. Thoracico-lumbar MRI showed drop like metastasis in the lumbar region. Finally she died five months after the initial diagnosis. Neurosurgeons should pay attention to GBM in the pineal region, not only as an important differential diagnosis among the pineal tumors, but due to the aggressive features of leptomeningeal dissemination and spinal metastasis.

Radiation-Induced Glioblastoma Multiforme in a Remitted Acute Lymphocytic Leukemia Patient

  • Joh, Dae-Won;Park, Bong-Jin;Lim, Young-Jin
    • Journal of Korean Neurosurgical Society
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    • v.50 no.3
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    • pp.235-239
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    • 2011
  • Radiation therapy has been widely applied for cancer treatment. Childhood acute lymphocytic leukemia (ALL), characterized by frequent central nervous system involvement, is a well documented disease for the effect of prophylactic cranio-spinal irradiation. Irradiation, however, acts as an oncogenic factor as a delayed effect and it is rare that glioblastoma multiforme develops during the remission period of ALL. We experienced a pediatric radiation-induced GBM patient which developed during the remission period of ALL, who were primarily treated with chemotherapeutic agents and brain radiation therapy for the prevention of central nervous system (CNS) relapse. Additionally, we reviewed the related literature regarding on the effects of brain irradiation in childhood and on the prognosis of radiation induced GBM.

Should Adjuvant Radiotherapy Be Recommended for Pediatric Craniopharyngiomas?

  • Dadlani, Ravi;Ghosal, Nandita;Hegde, Alangar Sathya
    • Journal of Korean Neurosurgical Society
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    • v.55 no.1
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    • pp.54-56
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    • 2014
  • Intracranial tumors secondary to radiotherapy are rare. In this group gliomas are the rarest. Only 6 cases of glioblastoma multiforme (GBM) have been reported in patients undergoing radiotherapy (RT) for craniopharyngiomas of which only 4 have been in children less than 18 years of age. In recent years RT has become a mainstay of adjuvant therapy for recurrent or partially excised craniopharyngiomas. We report a child of 12 years who had previously undergone RT for a suprasellar craniopharyngioma and presented 10 years later with a GBM. This is the 5th pediatric case in literature demonstrating a GBM after RT for a craniopharyngioma. The implications of subjecting the pediatric population to RT for a benign lesion versus the outcome of gross total removal and management of RT induced tumors is discussed and the need to avail of safer alternatives such as stereotactic radiosurgery is stressed.

Chemotherapeutic Drug Resistant Cancer Stem-like Cells of Glioma (다형성 교모세포종의 항생제 내성 종양 줄기세포)

  • Kang, Mi-Kyung;Kang, Soo-Kyung
    • Journal of Life Science
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    • v.17 no.8 s.88
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    • pp.1039-1045
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    • 2007
  • Glioblastoma multiforme (GBM) is the most frequently occurring brain cancer. Although the existence of cancer stem cells (CSCs) in GBM has been established, there is little evidence to explain the link between CSCs and chemoresistance. In this study, we investigated that only a few cells of A172 and established GBM2 survived after 1,3-bis(2chloroethyl)-1-nitrosourea (BiCNU) exposures and these sur-vived cells resist the subsequent BiCNU treatment. In addition, these BiCNU-resistant small pop-ulations derived from GBM cells increased the phosphorylations of Erk and Akt and highly expressed CD133 stem cell surface marker. Furthermore, we observed that the BiCNU-resistant cancer cells de-rived from GBM have grown tumors when transplanted into severe combined immuno-deficient (SCID) mouse brain. These results demonstrate that BiCNU-resistant subpopulation cells derived from GBM have cancer stem-like cell properties. Therefore, it may provide provide further evidence that CSCs in GBM have chemotherapeutic drug resistance.

Epigenetic Regulation of miR-129-2 Leads to Overexpression of PDGFRa and FoxP1 in Glioma Cells

  • Tian, Xiang-Yang;Zhang, Ling;Sun, Lai-Guang;Li, Ming
    • Asian Pacific Journal of Cancer Prevention
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    • v.16 no.14
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    • pp.6129-6133
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    • 2015
  • miR-129-2 is frequently downregulated in multiple cancers. However, how it is silenced in cancers remains unclear. Here we investigated the expression profile and potential biological function of miR-129-2 in glioblastoma (GBM), the most common and lethal form of brain tumors in adults. We showed that miR-129-2 is lost in GBM patient specimens and cultured cell lines. miR-129-2 expression could be restored upon treatment with a histone deadetylase inhibitor (trichostatin A) but not a DNA methylation inhibitor (5-Aza-2'-deoxycytidine), and more profound effect was observed with the treatment of these two drugs in combination. Furthermore, forced expression of miR-129-2 repressed the expression of major oncogenic genes such as PDGFRa and Foxp1 in GBMs. Consistently, expression of miR-129-2 significantly inhibits GBM cell proliferation in vitro. These results reveal that miR-129-2 is epigenetically regulated and functions as a tumor suppressor gene in GBMs, suggesting it may serve as a potential therapeutic target for GBM treatment.

Anti-Cancer Effect of Ginsenoside F2 against Glioblastoma Multiforme in Xenograft Model in SD Rats

  • Shin, Ji-Yon;Lee, Jung-Min;Shin, Heon-Sub;Park, Sang-Yong;Yang, Jung-Eun;KimCho, So-Mi;Yi, Tae-Hoo
    • Journal of Ginseng Research
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    • v.36 no.1
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    • pp.86-92
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    • 2012
  • The glioblastoma multiforme (GBM) is the most common malignant brain tumor in adults. Despite combination treatments of radiation and chemotherapy, the survival periods are very short. Therefore, this study was conducted to assess the potential of ginsenoside $F_2$ (F2) to treat GBM. In in vitro experiments with glioblastoma cells U373MG, F2 showed the cytotoxic effect with $IC_{50}$ of 50 ${\mu}g/mL$ through apoptosis, confirmed by DNA condensation and fragmentation. The cell population of cell cycle sub-G1 as indicative of apoptosis was also increased. In xenograft model in SD rats, F2 at dosage of 35 mg/kg weight was intravenously injected every two days. This reduced the tumor growth in magnetic resonance imaging images. The immunohistochemistry revealed that the anticancer activity might be mediated through inhibition of proliferation judged by Ki67 and apoptosis induced by activation of caspase-3 and -8. And the lowered expression of CD31 showed the reduction in blood vessel densities. The expression of matrix metalloproteinase-9 for invasion of cancer was also inhibited. The cell populations with cancer stem cell markers of CD133 and nestin were reduced. The results of this study suggested that F2 could be a new potential chemotherapeutic drug for GBM treatment by inhibiting the growth and invasion of cancer.

Glioblastoma Cellular Origin and the Firework Pattern of Cancer Genesis from the Subventricular Zone

  • Yoon, Seon-Jin;Park, Junseong;Jang, Dong-Su;Kim, Hyun Jung;Lee, Joo Ho;Jo, Euna;Choi, Ran Joo;Shim, Jin-Kyung;Moon, Ju Hyung;Kim, Eui-Hyun;Chang, Jong Hee;Lee, Jeong Ho;Kang, Seok-Gu
    • Journal of Korean Neurosurgical Society
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    • v.63 no.1
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    • pp.26-33
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    • 2020
  • Glioblastoma (GBM) is a disease without any definite cure. Numerous approaches have been tested in efforts to conquer this brain disease, but patients invariably experience recurrence or develop resistance to treatment. New surgical tools, carefully chosen samples, and experimental methods are enabling discoveries at single-cell resolution. The present article reviews the cell-of-origin of isocitrate dehydrogenase (IDH)-wildtype GBM, beginning with the historical background for focusing on cellular origin and introducing the cancer genesis patterned on firework. The authors also review mutations associated with the senescence process in cells of the subventricular zone (SVZ), and biological validation of somatic mutations in a mouse SVZ model. Understanding GBM would facilitate research on the origin of other cancers and may catalyze the development of new management approaches or treatments against IDH-wildtype GBM.