• The Korean Journal of Nuclear Medicine
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• v.30 no.4
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• pp.476-483
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• 1996

Following radiation therapy for brain tumors, patients often have clinical deterioration due to either radiation necrosis or recurrent tumor progression in the treatment field. The distinction between these entities is important but difficult clinically or even with CT or MRI. T1-201 has been known to accumulate in various tumors and be useful to grade, predict prognosis or detect recurrence of glioma. The aim of this study was to evaluate the usefulness of T1-201 SPECT in the differentiation of recurrent tumor from radiation necrosis. Of 67 patients who did T1-201 brain SPECT imaging with clinically suspected recurrent tumor or radiation necrosis, 20 patients underwent histopathological examination and constituted the study population. T1-201 uptake indices on T1-201 brain SPECT imaging rrere calculated and correlated with histopathological diagnosis. Of 20 patients, 15 were histopathologically confirmed as recurrent original tumor or malignant transformation of benign tumor and 5 were diagnosed as radiation necrosis. On T1-201 SPECT, 18 of 20 had T1-201 index above 2.5 which was regarded as positive indicator for the presence of tumor. Seventeen cases showed concordance, which consisted of 15 true positive and 2 true negative. Discordant 3 cases were all false positive. There was no case of false negative. The sensitivity, specificity, positive and negative predictive value of T1-201 SPECT were 100%, 40%, 83% and 100%. In conclusion, T1-201 brain SPECT is a sensitive diagnostic test in the detection of recurrent tumor following radiation therapy and is useful in the differentiation of recurrent tumor from radiation necrosis. Relatively low specificity should be evaluated further in larger number of patients in consideration of sampling error and referral bias for pathologic examination.

• Journal of Yeungnam Medical Science
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• v.22 no.2
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• pp.166-182
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• 2005

Background: Cyclin-dependent kinase (CDK) inhibitors are family of molecules that regulate the cell cycle. The CDKN2, a CDK4 inhibitor, also called p16, has been implicated in human tumorigenesis. The CDKN2 inhibits the cyclin/CDK complexes which regulate the transition from G1 to S phase of cell cycle. There is a previous report that homozygous deletion of CDKN2 region on chromosome 9p21 was detected frequently in astrocytoma, glioma and osteosarcoma, less frequently in lung cancer, leukemia and ovarian cancer, but not detected in colon cancer and neuroblastoma. However, little is known about the relationship between CDKN2 and laryngeal cancer. Therefore this study was initiated to investigate the role of CDKN2 in human laryngeal squamous cell carcinoma development.1) Materials and methods: We used 5 human laryngeal carcinoma cell lines whether they have deletions or losses of CDKN2 gene expression by DNA-PCR or RT-PCR, respectively. We examined 8 fresh frozen human laryngeal cancer tissues to detect the loss of heterozygosity (LOH) of CDKN2. PCR was performed by using microsatellite markers of short arm of human chromosome 9 (D9S126, D9S144, D9S156, D9S161, D9S162, D9S166, D9S171, D9S200 and D9SIFNA). For informative cases, allelic loss was scored if the signal of one allele was significantly decreased in tumor DNA when compared to the same allele in normal DNA. Results: The CDKN2 DNA deletion was observed in 3 cell lines. The CDKN2 mRNA expression was observed in only one cell line, which was very weak. LOH was detected in 7 cases (87.5%). Conclusion: These results suggest that CDKN2 plays a role in the carcinogenesis of human laryngeal squamous cell carcinoma.

• 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