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PURPOSE: There are no specific clinical and histopathologic characteristics of malignant pheochromocytoma and the optimal treatment modality has not been established yet. We analyzed the clinical and histopathologic features of malignant pheochromocytoma and treatment results. MATERIALS AND METHODS: We reviewed the clinical records of 10 patients with malignant pheochromocytoma diagnosed at Seoul National University Hospital from March 1987 to June 1998. RESULTS: Nine of 10 (90%) patients had functional tumors. The biochemical laboratory findings showed elevated 24-hour urine VMA level in nine patients available. The median size of the tumors was 11x11 cm. Six of 10 (60%) patients were initially diagnosed as malignant tumors because of direct invasions to adjacent tissues or distant metastases. On the other hand, remaining 4 patients were initially diagnosed as benign, but the distant metastases developed metachronously after resection of the primary lesion. The median duration between the initial operation and the detection of metastases was 57 months (range: 47~72 months) in these patients. The liver was the most common site of metastases (60%). With regards to the histopathological features, most of the tumors (87.5%) showed capsulation, necrosis and hemorrhage. The findings of lymphatic invasion, angio-invasion, and mitosis were found in 62.5% of the cases. All but 2 patients were initially treated with radical operation for the primary lesions. The disease recurrences or metastases occurred in 7 out of 10 patients. Of these, 4 patients were treated with chemotherapy or interferon- a after recurrences. Overall, the median survival for all patients was 82 months (range: 37~143 months). Two patients is alive and only one patient is alive without recurrence. CONCLUSION: The careful follow-up for at least 5 years and the aggressive multi-disciplinary therapy may be needed for the diagnosis and the management of malignant pheochromocytoma.
Diagnosis ; Drug Therapy ; Follow-Up Studies ; Hand ; Hemorrhage ; Humans ; Liver ; Mitosis ; Necrosis ; Neoplasm Metastasis ; Pheochromocytoma* ; Recurrence ; Seoul

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Intracavitary 166 Holmium - chitosan Complex Therapy in Patients with Malignant Peritoneal or Pleural Effusions.

Do Yeun CHO ; Hyun Soo KIM ; Joon Seong PARK ; Cheol Kweon JEONG ; Jin Hyuk CHOI ; Ho Yeong LIM ; Chan Hee PARK ; Mi Son CHUN ; Young Mi KIM ; Kyung Bae PARK ; Hugh Chul KIM

Journal of the Korean Cancer Association.1999;31(6):1297-1306.

PURPOSE: Most malignant peritoneal or pleural effusions caused by advanced malignancy are unresponsive to systemic chemotherapy except for chemotherapy sensitive tumors, and they are equally ineffective to regional therapy or radiotherapy. Thus, for the purpose of palliating the symptoms related to malignant effusion and to reduce fluid reaccumulations, we evaluated the therapeutic feasibility and efficacy of intracavitary ' Ho-CHICO (chito- san complex) instillation for intractable malignant effusions. MATERIALS AND METHODS: Thirty one patients with cytologically or pathologically proven malignant effusions underwent intracavitary 166Ho-CHICO therapy from May 1996 to March 1998 at Ajou University Hospital. The subjective and objective responses were evaluated 4 weeks after the treatment, including the changes of symptoms, weight, abdominal girth, doses of diuretics, frequencies and amounts of repeat aspirations for fluid reaccumulations, and imaging studies of chest radiograph and ultrasounds. RESULTS: The response rates treated with Ho-CHICO were 50% in patients with peritoneal effusion and 46% in patients with pleural effusion (overall 49%). The response rates between 166Ho-CHICO doses of 50-80 mCi and 90-100 mCi were similar (50% vs 47%). Response rate of 70% was noted in patients with even distribution of radioisotope on the post-therapy scan, but, the response rate was lower in cases with focal (44%) and uneven (29%) distribution pattern. There was no difference in response by the effusion sites. All patients tolerated intracavitary 166Ho-CHICO instillation well, although the majority of patients experienced Grade I/II side effects such as pain, fever, weakness and dyspnea. But, no serious complications of Grade lII or IV degree were observed with 166Ho-CHICO therapy. CONCLUSION: Intracavitary 166Ho-CHICO instillation was clinically efficacious in controlling malignant effusions without a significant toxicity seen with conventional sclerotic therapy. The therapeutic modality appeared to offer similar benefits obtained with the conventional intracavitary therapy.
Ascitic Fluid ; Aspirations (Psychology) ; Chitosan* ; Diuretics ; Drug Therapy ; Dyspnea ; Fever ; Holmium* ; Humans ; Pleural Effusion* ; Radiography, Thoracic ; Radiotherapy ; Ultrasonography

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Somatic Mutations of APC Presenting Polymorphisms in the Hamartomatous Polyps of the Colon.

Jin Cheon KIM ; Seon Ae ROH ; Hee Cheol KIM ; Chang Sik YU ; Nichoias E BECK ; Walter F BODMER

Journal of the Korean Cancer Association.1999;31(6):1288-1296.

No abstract available.
Colon* ; Polyps*

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Role of ATF on Transcriptional Regulation of DNA Topoisomerase II a Gene in HL - 60 Arrested to G2 / M and M Phase.

Kyu LIM ; Mee Young SON ; Byung Ik CHOI ; Kyung Ah YUN ; Meizi ZHENG ; Tae Wook KANG ; Young Chul LEE ; Jong II PARK ; Wan Hee YOON ; Byung Doo HWANG

Journal of the Korean Cancer Association.1999;31(6):1279-1287.

PURPOSE: To gain insight on transcriptional repression of Topo II a in HL-60 cells arrested to G2/M and M phase, the levels of Topo IIa mRNA and the binding activity of ATF have been investigated with Northern blot hybridization and DNA mobility shift assay, respectively. MATERIALS AND METHODS: HL-60 cells were grown in RPMI 1640 medium supplemented with 10% heat-mactivated fetal bovine serum and antibiotics in a humidified 5% CO2 at 37C degree. Total RNA was prepared by a modification of the method of Karlinsey et al. Northern blot hybridization was performed by the method of Virca et al. A Xho I-Mlu I fragment of phTOP2 was used as probe for Northern blot analysis of Topo II a mRNA. DNA mobility shift assay was performed by the method of Lim et al. End labeled DNA oligomer (upper strand, 5-TCTCCGCTATGACGCCGAGTGGTG-3) for ATF binding activity was mixed with nuclear extracts in a 20 pl reaction volume containing 60 mM KC1, 12 mM HEPES, pH 7.9, 5 mM MgCl2, 0.2 mM EDTA, 0.2 mM DTT, 12% glycerol, and 2 ug of poly [dI-dC]. RESULTS: HL-60 cells were arrested at G2/M phase and M phase after taxol or nocodazole treatment. The levels of Topo II a mRNA were reduced at 24 hours after exposure with nocodazole or taxol but the unknotting activities were not changed. DNA mobility shift assay using oligonucleotide containing the ATF binding site showed that ATF binding activity was reduced after pretreatment of nododazole or taxol. CONCLUSIONS: These results suggest that the reduction of ATF binding activity may be important to transcriptional repression of Topo II a gene by nocodazole and taxol in HL- 60 cells.
Anti-Bacterial Agents ; Binding Sites ; Blotting, Northern ; Cell Division* ; DNA Topoisomerases, Type I* ; DNA Topoisomerases, Type II* ; DNA* ; Edetic Acid ; Electrophoretic Mobility Shift Assay ; Genes, vif ; Glycerol ; HEPES ; HL-60 Cells ; Humans ; Hydrogen-Ion Concentration ; Magnesium Chloride ; Nocodazole ; Paclitaxel ; Repression, Psychology ; RNA ; RNA, Messenger

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Adaptive Change of AP DNA Endonuclease Against Genotoxic Agents in Normal and Transformed Cells.

Young Hee LEE ; In Cheol JEONG ; Sang Hwan OH ; Moo Youn CHO

Journal of the Korean Cancer Association.1999;31(6):1271-1278.

PURPOSE: AP DNA endonuclease (APE), an enzyme responsible for the repair of damaged DNAs, is essential for the maintenance of genetic information of cells. Deficiency of APE in certain hereditary skin tumor and senescent cells has been implicated but the regulation of APE activity as well as the expression of APE gene in response to DNA damage has not been well documented. Genotoxic agents including ultimate carcinogens that can damage DNA were treated to cultured normal and transformed human cells and adaptive response of APE gene expression to these treatments was measured in order to evaluate the role of APE in chemical carcinogenesis. MATERIALS AND METHODS: Hydroxyl radical ('OH) generated from H2O2 (60 uM) through Fenton reaction, each 100 uM of N-nitrosomethylurea (NMU), 3-methyl-4-monomethyl- aminoazobenzene (3'-MeMAB) and N-acetoxy-2-acetaminofluorene (AAAF) were treated to umbilical cord blood cells (UCBC), HepG2 cells and HL-60 cells. APEX mRNA and APEX protein contents expressed in these cells exposed to each of these agents were measured by Northern blot hybridization and Western blot immunodetection analysis. The changes of APE activity in cells exposed to these genetoxic agents were measured. RESULTS: Treatment of H2O2 (60 uM) to UCBC, HepG2, and HL-60 cells increased APE activity significantly and pretreatment of a catalytic agent for OH, FeSO4 (60 pM) to the cells prior to H2O2 exposure did not further increase the APE activity in cells. Adaptive response to H2O2 in HL-60 cells increased in proportion to the concentration of H2O2 up to 60 pM. However, further increase in H2O2 concentration had no effect on the enzyme activity. Treatment of NMU (100 pM), 3-MeMAB (100 pM) and AAAF (100 pM) to these cells brought about a slight increase in the APE activity. APEX mRNA expression in UCBC and HepG2 cells exposed to H2O2, NMU, 3-MeMAB was markedly increased in APEX mRNA expression. APEX mRNA expression was also increased in HL-60 cells exposed to H2O2 (60 pM) and 3-MeMAB (100 uM) but NMU (100 pM) exposure to the cells resulted in a slight increase of it (Fig. 2). APEX protein expression was increased in all UCBC, HepG2 and HL-60 cells exposed to these genotoxic agents (Fig. 3). CONCLUSION: These results implicate that exposure of genotoxic agents to the cultured cells may cause DNA damage and lead to adaptive increase in APE activity as well as APE gene expression. It is probable that APE gene is transcriptionally regulated in response to the exposure of H2O2 or 3-MeMAB in cultured human cells as a consequence of activation of DNA repair system for the adaptation to the crisis.
Blotting, Northern ; Blotting, Western ; Carcinogenesis ; Carcinogens ; Cells, Cultured ; Deoxyribonuclease I* ; DNA Damage ; DNA Repair ; DNA* ; Fetal Blood ; Gene Expression ; Hep G2 Cells ; HL-60 Cells ; Hominidae ; Humans ; Hydroxyl Radical ; RNA, Messenger ; Skin

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The Clinical Values of Metaplasia, p 53, c - erbB2 and CEA Expression in Gallbladder Carcinoma.

Seok Mo KIM ; Seong Hwan KIM ; Jeong Hwan CHANG ; Sung chul LIM ; Chae Hong SUH

Journal of the Korean Cancer Association.1999;31(6):1261-1270.

PURPOSE: We evaluated the correlation between the carcinogenesis of gallbladder and the expression of lysozyme, p53, c-erbB2 and CEA in gallbladder lesions. MATERIALS AND METHODS: Thirty cases of gallbladder lesions (containing 17 cases of GB carcinoma) were examined. We analyzed the clinicopathologic findings of the early (stage I & II) and advanced carcinoma (stage III, IV & V) and those of carcinoma with or without metaplasia in the tumor. We performed p53, c-erbB2 and CEA immunohistochemical staining and compared their findings with those of normal mucosa and preneoplastic lesions. We also performed lysozyme immunohistochemical staining and compared its finding with metaplastic and non-metaplastic lesions. RESULTS: There are two distinct genetic pathways in gallbladder cacinogenesis and metaplastic carcinoma was more frequent than non-metaplastic carcinoma. Metaplasia of gallbladder did not reveal any difference of the clinicopathologic findings and depth of invasion (Nevin stage). Lysozyme expression was found in all metaplastic lesions but non-expression did not indicate non-metaplastic lesions. p53 mutations and c-erbB2 alterations may have a role in the carcinogenesis of gallbladder carcinomas, especially, in a late event, and in an early and late events, respectively. The correlation of p53 and c-erbB2 expressions was found but which did not indicate that the co-expression was needed in the carcinogenesis. CEA immunohistochemical staining may be helpful in the differential diagnosis of benign lesions and precancerous and cancerous lesions of the gallbladder. CONCLUSION: These results suggest that p53 mutations and c-erbB2 alterations may have a role in the carcinogenesis of gallbladder carcinomas, especially, in a late event, and in an early and late events, respectively.
Carcinogenesis ; Diagnosis, Differential ; Gallbladder* ; Metaplasia* ; Mucous Membrane ; Muramidase

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