• Journal of the Korean Association of Oral and Maxillofacial Surgeons
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• v.34 no.5
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• pp.509-517
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• 2008

DNA damage accumulates in cells as a result of exposure to exogenous agents such as benzopyrene, cigarette smoke, ultraviolet light, X-ray, and endogenous chemicals including reactive oxygen species produced from normal metabolic byproducts. DNA damage can also occur during aberrant DNA processing reactions such as DNA replication, recombination, and repair. The major of DNA damage affects the primary structure of the double helix; that is, the bases are chemically modified. These modification can disrupt the molecules'regular helical structure by introducing non-native chemical bonds or bulky adducts that do not fit in the standard double helix. DNA repair genes and proteins scan the global genome to detect and remove DNA damage and damage to single nucleotides. Direct reversal of DNA damage, base excision repair, double strand break. DNA repair are known relevant DNA repair mechanisms. Four different mechanisms are distinguished within excision repair: direct reversal, base excision repair, nucleotide excision repair, and mismatch repair. Genetic variation in DNA repair genes can modulate DNA repair capacity and alter cancer risk. The instability of a cell to properly regulate its proliferation in the presence of DNA damage increase risk of gene mutation and carcinogenesis. This article aimed to review mechanism of excision repair and to understand the relationship between genetic variation of excision repair genes and head and neck cancer.

• Journal of Korean Neurosurgical Society
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• v.42 no.1
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• pp.27-34
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• 2007

Objective : On the magnetic resonance image (MRI) of the infiltrating brain tumor, enhancement is usually higher in malignant tumor than in benign tumor, and tumor cells can invade into the peritumoral area without definite enhancement. In various pathological conditions, the blood brain barrier (BBB) becomes changed to pathological condition, allowing various materials extravasating into the interstitial space, and degree of enhancement is depend on the pathology. Authors performed dynamic MRI on enhancing and surrounding edematous area in order to evaluate the degrees of opening of BBB, to differentiate tumor from non-tumorous condition, and to determine its relationship with the recurrence of the tumor. Methods : Dynamic MRI was performed in 25 patients. Dynamic scans were done every 15 seconds after administration of Gd-DTPA on the enhancing and surrounding area for maximum 300 seconds, and the patterns of enhancement were ana lysed. The enhancement curve with initial steep increase followed by slow decrease was defined as "N pattern", those with initial steep increase followed by additional slow increase as "T pattern", and those with initial steep increase followed by plateau as "E pattern". Histopathological findings were compared with the dynamic scan. Results : The graphs taken from enhancing area showed "T pattern" regardless of pathology. In the surrounding area, "T pattern" was noticed in the malignant tumors, but "E pattern" or "N pattern" was noted in low-grade or benign tumors and non-tumorous condition. "T pattern" in the surrounding area was related to the malignant with tumor cell infiltration and recurrence. Conclusion : The results suggest that the malignant tumor infiltration changes the condition of BBB enough to extravasate the Gd-DTPA. Enhancement pattern in the surrounding edematous area may be a useful information to differentiate the malignant glioma with the low-grade and benign tumors or other non-tumorous conditions.

• The Korean Journal of Nuclear Medicine
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• v.32 no.3
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• pp.290-297
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• 1998

Purpose : The aim of this study was to evaluate the feasibility of 3-[$^{131}I$]iodo-O-methyl-L-${\alpha}$-methyltyrosine ([$^{131}I$]OMIMT) as an agent for tumor image. Materials and Methods : After synthesis of 4-O-methyl-L-${\alpha}$-methyltyrosine (OMAMT), OMAMT was labeled with [$^{131}I$] using Iodogen method. In vitro cellular uptake study was performed using 9 L gliosarcoma cells at various time points upto 4 hr. The biodistribution (five rats implanted with the 9 L gliosar-coma cells per group) was evaluated at 30 min, 2 hr, 24 hr after iv injection of 3.7 MBq [$^{131}I$]OMIMT or L-3-[$^{131}I$]iodo-${\alpha}$-methyltyrosine [$^{131}I$]IMT). Gamma camera images were obtained at 30 min, 2 hr and 24 hr. Results: [$^{131}I$]OMIMT uptake was 3.3 times and 2.5 times higher than [$^{131}I$]IMT uptake at 30 min and 60 min, respectively and same after 2 hr in in vitro study using 9L gliosarcoma cells. Maximum accumulation in tumor occurred at 30 min for both [$^{131}I$]OMIMT and [$^{131}I$]IMT in tumor bearing rats. The tumor uptake of [$^{131}I$]OMIMT was significantly higher than that of [$^{131}I$]IMT at early time point studied ($3.74{\pm}0.48$ vs $0.38{\pm}0.17%$ ID/g at 30 min and $2.40{\pm}0.17$ vs $0.24{\pm}0.03%$ ID/g at 2 hr, respectively, p<0.01). However, the tumor uptake of both radiolabels were not significantly different at 24 hr ($0.04{\pm}0.01$ vs $0.05{\pm}0.01%$ ID/g). Tumor was visualized as early as at 30 min in gamma camera images. Conclusion: These data suggested that [$^{131}I$]OMIMT might be a useful tumor imaging agent and has more advantage for the tumor imaging compared to [$^{131}I$]IMT