• 대한핵의학회:학술대회논문집
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• 1989.06a
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• pp.141.1-141.1
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• 1989

• Journal of the Korean Association of Oral and Maxillofacial Surgeons
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• v.35 no.4
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• pp.213-220
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• 2009

Purpose: The present study was aimed to examine the usefulness of 18F-FDG PET/CT in the evaluation of cervical lymph node metastasis in patients with oral cancer. Materials and methods: Twenty-two patients who underwent neck dissection to treat oral cancer were subjected for examination. The cervical node metastasis was evaluated by means of clinical examination, CT scan, PET, and histologic examination. By comparing the results of each examination modality with those of histologic examination, it's sensitivity, specificity, positive predictive value, and negative predictive value were determined. Results: The oral cancer was more frequent in males with a ratio of 2.14:1. The sixth decade showed the highest incidence in age distribution with mean of $56{\pm}16$. Histologic findings showed that squamous cell carcinoma was the most common (15 patients), and mucoepidermoid carcinoma (3), malignant melanoma (2), and adenoid cystic carcinoma and ghost cell odontogenic carcinoma (1 each), in order. In most cases, wide surgical excision of the primary cancer and neck dissection was performed, followed by reconstruction with free flaps when necessary. When comparing the results of each examination modality with those of the histologic examination, clinical examination showed sensitivity, specificity, positive predictive value, and negative predictive value at 11%, 85%, 33%, and 58%, respectively. CT scans showed at 67%, 77%, 67%, and 77%, while $^{18}F$-FDG PET/CT at 78%, 77%, 70%, and 83%, respectively. Conclusions: These results suggest that PET is more useful, compared with clinical examination and CT scans, in the evaluation of cervical lymph node metastasis in patients with oral cancer.

• Asian Pacific Journal of Cancer Prevention
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• v.14 no.12
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• pp.7569-7576
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• 2013

Background: The purpose of this article is to present preliminary results of simultaneous boost irradiation radiotherapy for locally advanced nasopharyngeal carcinoma (NPC). Methods: Fifty-eight patients who underwent simultaneous boost irradiation radiotherapy for NPC in Cancer Center of Sun Yat-sen University between September 2004 and December 2009 were eligible. Acute and late toxicities were scored weekly according to the Radiation Therapy Oncology Group (RTOG) acute and late radiation morbidity scoring schemes. An especial focus was on evidence of post-radiation brain injury. Also quality of life was analysed according to the EORTC (European Organisation for Research and Treatment of Cancer) recommendations. Discrete variables were compared by ${\chi}^2$ test. The Kaplan-Meier method was used to calculate the survival rates and generate survival curves. Results: A total of 58 patients with a mean follow-up time of 36 months completed clinical trials.Fifty-seven patients (98.3) achieved complete remission in the primary sites and cervical lymph nodes, with only one patient (1.7%) showing partial remission.The most frequently observed acute toxicities during the concurrent chemoradiotherapy were mucositis and leucopenia. Four patients (6.9%) had RTOG grade 3 mucositis, whereas four patients (6.9%) had grade 3 leucopenia. No patient had grade 4 acute toxicity. Three (5.17%) of the patients exhibited injury to the brain on routine MRI examination, with a median observation of 32 months (range, 25-42months). All of them were RTOG grade 0. The 3-year overall, regional-free and distant metastasis-free survival rates were 85%, 94% and 91%, respectively. Conclusion: Simultaneous boost irradiation radiotherapy is feasible in patients with locally advanced nasopharyngeal carcinoma. The results showed excellent local control and overall survival, with no significant increase the incidence of radiation brain injury or the extent of damage. A larger population of patients and a longer follow-up period are needed to evaluate ultimate tumor control and late toxicity.

• Proceedings of the Korean Society of Toxicology Conference
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• 2001.05a
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• pp.145-145
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• 2001

Xanthorrhizol is a sesquiterpenoid isolated from Curcuma xanthorrhiza Roxb. (Zingiberaceae) that has been traditionally used in Indonesia for dietary and medicinal purposes. In our studies to evaluate the cancer chemopreventive potential, xanthorrhizol inhibited the mutagenesis induced by reactive oxygen species in Sa;monella typhimurium TA 102 in a dose-related manner and decreased significantly the incidence and the multiplicity of skin tumors initiated by 7, 12-dimethylbenz[$\alpha$]anthracene and promoted by 12-Ο-tetradecanoylphorbol-13-acetate at 19 weeks.(omitted)

• Asian Pacific Journal of Cancer Prevention
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• v.15 no.8
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• pp.3607-3612
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• 2014

Background: In recent years, numerous studies have been performed to investigate the CCND1 G870A gene polymorphism impact on brain tumors susceptibility. Unfortunately, the results of previous studies were inconsistent. Therefore, we performed a meta-analysis to derive a more precise estimation of any association. Materials and Methods: We conducted a search in PubMed, Embase and CNKI covering all published papers up to November, 2013. Odds ratios (ORs) and their 95% confidence intervals (95%CIs) were applied to assess associations. Results: A total of 6 publications including 9 case-control studies met the inclusion criteria. The pooled ORs for the total included studies showed significant association among comparison A vs G (OR= 1.246, 95%CI= 1.092-1.423, p= 0.001), homozygote comparison AA vs GG (OR= 1.566, 95%CI= 1.194-2.054, p= 0.001), heterozygote comparison AG vs GG (OR= 1.290, 95%CI= 0.934-1.782, p= 0.122), dominant model AA/GA vs GG (OR= 1.381, 95%CI= 1.048-1.821, p= 0.022) and recessive model AA vs GA/GG (OR= 1.323, 95%CI= 1.057-1.657, p= 0.015) especially in glioma. Conclusions: CCND1 G870A polymorphism may increase brain tumor risk, especially for gliomas. However, more primary large scale and well-designed studies are still required to evaluate the interaction of CCND1 G870A polymorphism with brain tumor risk.

• Biomolecules & Therapeutics
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• v.27 no.6
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• pp.530-539
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• 2019

Brain aging is an inevitable process characterized by structural and functional changes and is a major risk factor for neurodegenerative diseases. Most brain aging studies are focused on neurons and less on astrocytes which are the most abundant cells in the brain known to be in charge of various functions including the maintenance of brain physical formation, ion homeostasis, and secretion of various extracellular matrix proteins. Altered mitochondrial dynamics, defective mitophagy or mitochondrial damages are causative factors of mitochondrial dysfunction, which is linked to age-related disorders. Etoposide is an anti-cancer reagent which can induce DNA stress and cellular senescence of cancer cell lines. In this study, we investigated whether etoposide induces senescence and functional alterations in cultured rat astrocytes. Senescence-associated ${\beta}$-galactosidase (SA-${\beta}$-gal) activity was used as a cellular senescence marker. The results indicated that etoposide-treated astrocytes showed cellular senescence phenotypes including increased SA-${\beta}$-gal-positive cells number, increased nuclear size and increased senescence-associated secretory phenotypes (SASP) such as IL-6. We also observed a decreased expression of cell cycle markers, including PhosphoHistone H3/Histone H3 and CDK2, and dysregulation of cellular functions based on wound-healing, neuronal protection, and phagocytosis assays. Finally, mitochondrial dysfunction was noted through the determination of mitochondrial membrane potential using tetramethylrhodamine methyl ester (TMRM) and the measurement of mitochondrial oxygen consumption rate (OCR). These data suggest that etoposide can induce cellular senescence and mitochondrial dysfunction in astrocytes which may have implications in brain aging and neurodegenerative conditions.

• The Journal of Internal Korean Medicine
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• v.25 no.2
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• pp.202-213
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• 2004

Object : Objective: This study was conducted to investigate the anti-cancer effects of Mylabris phalerata (반모) in some kinds of cancer cells. Materials and Methods: Some kinds of cancer cells lines were treated. We used nine kinds of cancer cell lines, such as stomach cancer cells (Kato), lung cancer cells (Calu-1, NCI-H 1395), urinary bladder cancer cells (HS789T), bone cancer cells (Saos-2), brain cancer cells (SK-N-MC), liver cancer cells (Hep-G2), skin cancer cells (Mo-1) and prostate cancer cells (PC-3) with the water decoction of Mylabris phalerata. The histological changes of all cell lines in the media (RPMI-1640) containing the decoction of Mylabris phalerata were observed and we examined cell death assay by trypan blue exclusion testing was examined. Finally, the change of mitochondrial membrane potential was measurd and the inhibitory effect of Mylabris phalerata on cell increase was examined by analyzing the cell cycle. Results: In histologic change all cancer cell lines showed withdrawn and floating appearance that is typical in cellular impairment. Most of the cell lines showed over 50% death rate after 24 hours in trypan blue exclusion tests. Especially the stomach, urinary bladder. brain and liver cell lines showed over 30% death rate after 12 hours. All cell lines treated with Mylabris phalerata were less stained than the control group and the mitochondrial membrane potential in the Mylabris phalerata treated cell lines was markedly lower than that in the control group. The measurement of DNA quantity in all cell lines showed the disappearance of the peak and the thickened left axis, which suggests that all cellular DNA degraded. Conclusion: Mylabris phalerata had cytotoxicity on various kinds of cancer cell lines and the mechanism of that was the impairment of mitochondria by the breakdown of the mitochondrial cell membrane. We propose that this is in part attributable to the destruction of DNA in cancer cells.

• Asian Pacific Journal of Cancer Prevention
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• v.17 no.6
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• pp.2767-2773
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• 2016

Human glioma, arising from glial cells of the central nervous system, accounts for almost 30%of all brain tumours, neoplasms with a poor prognosis and high mortality rates worldwide. In the present study we assessed tissue architectural modifications associated with macrophage lineage cells, controversial major immune effector cells within the brain, in human glioma tissue samples from eastern India. Ethically cleared post-operative human glioma samples from our collaborative neurosurgery unit with respective CT/MRI and patient history were collected from the Nodal Centre of Neurosciences in Kolkata, over 9 months. Along with conventional histopathology, samples were subjected to silver-gold staining and fluorescence tagged immunophenotyping for the detection of electron dense brain macrophage/microglia cells in glioma tissue, followed by immune-phenotyping of cells. With higher grades, CD11b+/Iba-1+ macrophage/microglia architecture with de-structured boundaries of glioma lesions indicated malfunction and invasive effector state. Present study documented a contribution of microglia to glioma progression in Eastern India.

• Radiation Oncology Journal
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• v.19 no.2
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• pp.146-152
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• 2001

Purpose : To investigate the regulation of apoptosis and cell cycle in mouse brain irradiation. Materials and Methods : 8-week old male mice, C57B1/6J were given whole body $\gamma-radiation$ with a single dose of 25 Gy using Cobalt 60 irradiator. At different times 1, 2, 4, 8 and 24hr after irradiation, mice were killed and brain tissues were collected. Apoptotic cells were scored by TUNEL assay. Expression of p53, Bcl-2, and Bax and cell cycle regulating molecules; cyclins Bl, Dl, E and cdk2, cdk4, $p34^{cdc2}$ were analysed by Western blotting. Cell cycle was analysed by Flow cytometry. Results : The peak of radiation induced apoptosis is shown at 8 hour after radiation. With a single 25 Gy irradiation, the peak of apoptotic index in C57B1/6J is $24.0{\pm}0.25$ (p<0.05) at 8 hour after radiation. Radiation upregulated the expression of p53/tubulin, Bax/tubulin, and Bcl-2/tubulin with 1.3, 1.1 and 1.45 fold increase, respectively were shown at the peak level at 8 hour after radiation. The levels of cell cycle regulating molecules after radiation are not changed significantly except cyclin D1 with 1.3 fold increase. Fractions of Go-Gl, G2-M and S phase in the cell cycle does not specific changes by time. Conclusion : In mouse brain tissue, radiation induced apoptosis is particularly shown in a specific area, subependyma. These results and lack of radiation induced changes in cell cycle ofter better understanding of radiation response of noraml brain tissue.

• Journal of the Korean Association of Oral and Maxillofacial Surgeons
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• v.35 no.5
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• pp.376-379
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• 2009

Likely to be the most common oral cancer, squamous cell carcinoma(SCC) of the tongue accounts for about 20% of all oral and pharyngeal cancers. SCC of the tongue frequently arises in the lateral border, and if it metastasize, it occurs on submandibular gland and neck lymph nodes. Location of the primary lesions and neck lymph node metastasis affect the prognosis and decrease survival rate of patients with carcinoma of the tongue. The authors experienced the patient with contralateral neck lymph node metastasis of SCC of the tongue. The patient came to our department with chief complaint of elevated lesion on left lateral border of the tongue. The mass was diagnosed as $T_2N_0M_0$, Stage II invasive SCC of oral tongue. Computed tomography(CT) & magnetic resonance imaging(MRI) which were taken before the operation showed no significant finding of metastasis. Surgical mass removal and preventive neck dissection on the left side were done. While follow up PET/CT, contralateral neck lymph node metastasis(right side, level II) was detected, and re-operation(Rt. side RND) was done. There are few studies concerning the contralateral neck lymph node metastasis related with SCC of the tongue. The purpose of this report is to introduce the uncommon case of contralateral neck lymph node metastasis occurred in the $T_2$-stage of SCC of the tongue treated by surgical resection.