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Nationwide Population-Based Incidence and Survival Rates of Malignant Central Nervous System Germ Cell Tumors in Korea, 2005-2012
Seung Hoon Lee, Kyu-Won Jung, Johyun Ha, Chang-Mo Oh, Hyeseon Kim, Hyeon Jin Park, Heon Yoo, Young-Joo Won
Cancer Res Treat. 2017;49(2):494-501. Published online August 24, 2016
DOI: https://doi.org/10.4143/crt.2016.129
AbstractCancer Research and Treatment (2)PDFPubReaderePub
Purpose
Malignant central nervous system (CNS) germ cell tumors (GCTs), although rare, are thought to occur more frequently among Asians. However, a recent population-based study revealed no differences in GCT incidence between Asians and Caucasians. Therefore, this study was conducted to determine the incidence and survival rates of CNS GCTs using the national cancer incidence database, and to compare these rates to those in the United States and Japan.
Materials and Methods
We extracted CNS GCT patients diagnosed between 2005 and 2012 from the Korea Central Cancer Registry database. Age-standardized rates (ASRs), annual percentage change, and the male-female incidence rate ratios (IRRs) were calculated. To estimate the survival rate, we used data for patients diagnosed between 2005 and 2010 and followed their cases until December 31, 2013.
Results
The ASR for CNS GCT between 2005 and 2012 was 0.179 per 100,000 (95% confidence interval, 0.166 to 0.193), with an overall male-to-female (M:F) IRR of 2.95:1. However, when stratified by site, the M:F IRR was 13.62:1 for tumors of the pineal region and 1.87:1 for those located in nonpineal regions. The most frequent histologic type was germinoma (76.0%), and the most frequent location was the suprasellar region (48.5%). The 5-year survival rate of germinoma patients was 95.3%.
Conclusion
The incidence rate of CNS GCTs in Korea during 2005-2012 was 0.179 per 100,000, which was similar to that of the Asian/Pacific Islander subpopulation in the United States. Moreover, the CNS GCT survival rate in Korea was similar to rates in Japan and the United States.

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Population-based Incidence and Survival for Primary Central Nervous System Lymphoma in Korea, 1999-2009
Sang-Hoon Shin, Kyu-Won Jung, Johyun Ha, Seung Hoon Lee, Young-Joo Won, Heon Yoo
Cancer Res Treat. 2015;47(4):569-574. Published online February 12, 2015
DOI: https://doi.org/10.4143/crt.2014.085
AbstractCancer Research and Treatment (9)PDFPubReaderePub
Purpose
Primary central nervous system lymphoma (PCNSL) is an uncommon brain tumor accounting for 2%-5% of all primary brain tumors. Few population-based analyses of survival for patients with PCNSL have been conducted, particularly in Asian countries. Materials and Methods Using the Korea National Cancer Incidence Database, 1,062 cases of PCNSL newly diagnosed from 1999 to 2009 were analyzed. The crude rate, age-standardized rate (ASR), and annual percent change were calculated. To estimate the observed survival, we restricted the data to between 1999 and 2007 and followed the cases until December 2010. The overall survival was estimated using the Kaplan-Meier method, and piecewise Poisson regression model.
Results
The ASR for PCNSL between 1999 and 2009 was 0.17 per 100,000, and the annual percent change from 1999 to 2009 was 8.8% (p < 0.001). The ASR of males was higher than that of females, and the older groups (60s or over) showed the largest increase in incidence rates. For all ages, the five-year survival from PCNSL was 29.9% between 1999 and 2007. Survival from PCNSL is known to show strong association with age at diagnosis. Conclusion These results are similar to those of previous studies. Our findings may be helpful to clinicians and patients in determining long-term prognoses for PCNSL.

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Radiation-Induced Autophagy Contributes to Cell Death and Induces Apoptosis Partly in Malignant Glioma Cells
Guk Heui Jo, Oliver Bögler, Yong-Joon Chwae, Heon Yoo, Seung Hoon Lee, Jong Bae Park, Youn-Jae Kim, Jong Heon Kim, Ho-Shin Gwak
Cancer Res Treat. 2015;47(2):221-241. Published online August 29, 2014
DOI: https://doi.org/10.4143/crt.2013.159
AbstractCancer Research and Treatment (17)PDFPubReaderePub
Purpose
Radiation-induced autophagy has been shown to play two different roles, in malignant glioma (MG) cells, cytocidal or cytoprotective. However, neither the role of radiation-induced autophagy for cell death nor the existence of autophagy-induced apoptosis, a well-known cell-death pathway after irradiation, has been verified yet. Materials and Methods We observed both temporal and dose-dependent response patterns of autophagy and apoptosis to radiation in MG cell lines. Additionally, we investigated the role of autophagy in apoptosis through knockdown of autophagy-related proteins. Results Autophagic activity measured by staining of acidic vesicle organelles and Western blotting of LC-3 protein increased in proportion to radiation dose from day 1 to 5 after irradiation. Apoptosis measured by annexin-V staining and Western blotting of cleaved poly(ADP-ribose) polymerase demonstrated relatively late appearance 3 days after irradiation that increased for up to 7 days. Blocking of pan-caspase (Z-VAD-FMK) did not affect apoptosis after irradiation, but silencing of Atg5 effectively reduced radiation-induced autophagy, which decreased apoptosis significantly. Inhibition of autophagy in Atg5 knockdown cells was shown to be beneficial for cell survival. Stable transfection of GFP-LC3 cells was observed after irradiation. Annexin-V was localized in cells bearing GFP-LC3 punctuated spots, indicating autophagy in immunofluorescence. Some of these punctuated GFP-LC3 bearing cells formed conglomerated spots and died in final phase. Conclusion These findings suggest that autophagy appears earlier than apoptosis after irradiation and that a portion of the apoptotic population that appears later is autophagy-dependent. Thus, autophagy is a pathway to cell death after irradiation of MG cells.

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Cancer Research and Treatment (22)

Cancer Research and Treatment (23)

Incidence of Primary Spinal Cord, Spinal Meninges, and Cauda Equina Tumors in Korea, 2006-2010
Kyu-Won Jung, Kwang Hyon Park, Johyun Ha, Seung Hoon Lee, Young-Joo Won, Heon Yoo
Cancer Res Treat. 2015;47(2):166-172. Published online October 30, 2014
DOI: https://doi.org/10.4143/crt.2014.017
AbstractCancer Research and Treatment (25)PDFPubReaderePub
Purpose
Primary spinal cord and appendage tumors (PSCAT) originating from the spinal cord, spinal meninges, and cauda equina are uncommon. Worldwide, population-based cancer registry data are mostly based on malignant tumors only, which means few data are available on PSCATs, including non-malignant tumors. Therefore, the objective of this study was to provide information regarding the incidence of both non-malignant and malignant PSCATs in Korea on a national level. Materials and Methods Incidence of PSCATs was estimated from cases diagnosed between 2006 and 2010 using the National Cancer Incidence Database in Korea. Age-adjusted rates were calculated using the world standard population, and male-to-female rate ratios were calculated by histology type. Results Of all PSCATs registered (n=3,312), 86.6% were non-malignant. The overall age-adjusted incidence of PSCATs was 1.08 per 100,000 person-years, with an incidence of 0.99 per 100,000 in females and 1.15 in males. The most common site of PSCATs was the spinal cord (83.4%), followed by spinal meninges (16.1%) and cauda equina (0.5%). The most common histological type was neurilemmoma (41.3%), followed by meningiomas (20.1%) and ependymomas (7.6%). Men had significantly higher rates than women for ependymomas and lymphomas but had lower rates for meningiomas. Conclusion This study provides the first population-based analysis of PSCATs in Korea.

Citations

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Cancer Research and Treatment (30)
Surgical Outcomes of Hemorrhagic Metastatic Brain Tumors
Heon Yoo, Eugene Jung, Ho Shin Gwak, Sang Hoon Shin, Seung Hoon Lee
Cancer Res Treat. 2011;43(2):102-107. Published online June 30, 2011
DOI: https://doi.org/10.4143/crt.2011.43.2.102
AbstractCancer Research and Treatment (32)PDFPubReaderePub
PURPOSE
Hemorrhagic metastatic brain tumors are not rare, but little is known about the surgical outcome following treatment. We conducted this study to determine the result of the surgical outcome of hemorrhagic metastatic brain tumors.
MATERIALS AND METHODS
From July 2001 to December 2008, 21 patients underwent surgery for hemorrhagic metastatic brain tumors at our institution. 15 patients had lung cancer, 3 had hepatocellular carcinoma, and the rest had rectal cancer, renal cell carcinoma, and sarcoma. 20 patients had macroscopic hemorrhage in the tumors, and one patient had intracerebral hemorrhage surrounding the tumor. A retrospective clinical review was conducted focusing on the patterns of presenting symptoms and signs, as well as local recurrence following surgery.
RESULTS
Among 21 hemorrhagic brain metastases, local recurrence developed in two patients. The 12 month progression free survival rate was 86.1%. Mean time to progression was 20.8 months and median survival time after surgery was 11.7 months.
CONCLUSION
The results of our study showed that hemorrhagic metastatic brain tumors rarely recurred after surgery.Surgery should be considered as a good treatment option for hemorrhagic brain metastasis, especially in cases with increased intracranial pressure or severe neurologic deficits.

Citations

Citations to this article as recorded byCancer Research and Treatment (35)

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Cancer Research and Treatment (37)
Radiation-induced Necrosis Deteriorating Neurological Symptoms and Mimicking Progression of Brain Metastasis after Stereotactic-guided Radiotherapy
Young Zoon Kim, Dae Yong Kim, Heon Yoo, Hee Seok Yang, Sang Hoon Shin, Eun Kyung Hong, Kwan Ho Cho, Seung Hoon Lee
Cancer Res Treat. 2007;39(1):16-21. Published online March 31, 2007
DOI: https://doi.org/10.4143/crt.2007.39.1.16
AbstractCancer Research and Treatment (39)PDFPubReaderePub
Purpose

Although radiation-induced necrosis (RIN) is not a tumor in itself, the lesion progressively enlarges with mass effects and diffuse peritumoral edema in a way that resembles neoplasm. To identify the RIN that mimics progression of brain metastasis, we performed surgical resections of symptomatic RIN lesions.

Meterials and Methods

From June 2003 to December 2005, 7 patients received stereotactic-guided radiotherapy (SRT) for metastatic brain tumor, and they later underwent craniotomy and tumor resection due to the progressive mass effects and the peritumoral edema that caused focal neurological deficit. On MR imaging, a ring-like enhanced single lesion with massive peritumoral edema could not be distinguished from progression of brain metastasis.

Results

Four patients had non-small cell lung cancer, 2 patients had colorectal cancer and 1 patient had renal cell carcinoma. The mean tumor volume was 8.7 ml (range: 3.0~20.7 ml). The prescribed dose of SRT was 30 Gy with 4 fractions for one patient, 18 Gy for two patients and 20 Gy for the other four patients. The four patients who received SRT with a dose of 20 Gy had RIN with or without microscopic residual tumor cells.

Conclusions

Early detection of recurrent disease after radiotherapy and identifying radiation-induced tissue damage are important for delivering adequate treatment. Therefore, specific diagnostic tools that can distinguish RIN from progression of metastatic brain tumor need to be developed.

Citations

Citations to this article as recorded byCancer Research and Treatment (42)

  • Salvage craniotomy for treatment-refractory symptomatic cerebral radiation necrosis
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    Alireza M. Mohammadi, Jason L. Schroeder, Lilyana Angelov, Samuel T. Chao, Erin S. Murphy, Jennifer S. Yu, Gennady Neyman, Xuefei Jia, John H. Suh, Gene H. Barnett, Michael A. Vogelbaum
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Cancer Research and Treatment (44)
Adenovirus - Mediated gene Transfer of Wild - Type p53 Results in Restoration of Tumor - Suppressor Function in Glioma Cell Lines
Mi Sook Kim, Hee Chung Kwon, Seok Il Hong, Choon Taek Lee, Seung Hoon Lee
J Korean Cancer Assoc. 1998;30(5):1026-1033.
AbstractCancer Research and Treatment (46)PDF
PURPOSE
The replacement of functional genes into cells that lack genes or mutant genes is the basis of gene therapy. In cancer, where cells often have multiple genetic defects, the replacement of critical genes may suffice to suppress cell growth or induce cell death. In malignant brain tumors, p53 mutation are among the most frequently observed genetic findings and inactivation p53 suggests that p53 plays a critical role in carcinogenesis and tumor progression.Therefore, we study the successful transfer of the wild-type p53 gene using a replicative deficient adenovirus vector into human glioma and medulloblastoma c~ell lines. Meterials and Methods: The human glioma cell line T-98G, U-87MG, U-373MG were used. To determine the efficiency of the adenovirus vector, cell lines were transfected with the Ad-p gal and analysed with X-Gal staining. Cell viability was determined by trypan blue exclusion every day after infection and Westem blot analysis was used to conform the expression of the exogenous p53 protein.
RESULTS
Cell growth of the Ad-CMV-p53 infected U-373MG, and U-87MG was significantly suppressed. It appeared that exogenous p53 protein expression had an earlier ad more profound suppressive effect on U-373MG having a mutated p53 gene than on U-87MG having a wild-type p53. The expression of the exogenous p53 was more than 10 times higher than the expression of the endogenous p53. To examine the decreased viability, U-373MG was stained with Hochest 33258 and detected nuclear condensation and apoptic body. Staining results suggest that cells undergo apoptosis.
CONCLUSION
The replicative deficient adenoviral vector can transfer and express p53 in human glioma cell lines in vitro, restoring wild-type p53 tumor suppressor functions.The restoration of normal p53-encoded protein in the mutant ceil lines induced cell death. The high expression of the newly transduced protein had different effects on the growth rate of the infected cell lines depending on the p53 status of the cells.
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Cancer Research and Treatment (47)

Cancer Research and Treatment (48)
Molecular genetic study of primary malignant brain tumors:loss of heterozygosity on chromosome 10, 13q, 17q and 22q
Seung Hoon Lee, Jong Hyun Kim, Chang Hoon Lee, Young Soon Kang, Je Ho Lee
J Korean Cancer Assoc. 1993;25(5):717-724.
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