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Cancer Research and Treatment

2001  to  Present  ISSN: 1598-2998

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Long-term Survival after Surgical Resection for Liver Metastasis from Gastric Cancer: Two Case Reports.

Jong Keun LIM ; Joong Bae AHN ; Sung Ha CHEON ; Hyun CHANG ; Jong Yul JUNG ; Sun Young RHA ; Jae Kyung ROH ; Sung Hoon NOH ; Ho Geun KIM ; Hyun Cheol CHUNG ; Hei Cheul JEUNG

Cancer Research and Treatment.2006;38(3):184-188.

Surgical resection of colorectal cancer metastasis to the liver results in a 5-year survival rate of around 40%. Liver metastasis from other cancers such as neuroendocrine carcinoma and genitourinary tumors are also treated effectively with combined liver resection. However, hepatic metastasectomy for liver tumor from gastric cancer hasn't been considered as a standard treatment, and the benefit for this treatment has not been established. We report here on two cases of gastrectomy and combined liver resection for synchronous liver metastasis without any evidence of other metastatic lesions, and these two patients have survived for more than 7 years without evidence of disease recurrence. In conclusion, for patients with hepatic metastasis from gastric cancer, combined surgical resection of the liver metastasis should be considered as a treatment option when metastasis to other sites can be excluded.
Carcinoma, Neuroendocrine ; Colorectal Neoplasms ; Gastrectomy ; Humans ; Liver* ; Metastasectomy ; Neoplasm Metastasis* ; Recurrence ; Stomach Neoplasms* ; Survival Rate

Carcinoma, Neuroendocrine ; Colorectal Neoplasms ; Gastrectomy ; Humans ; Liver* ; Metastasectomy ; Neoplasm Metastasis* ; Recurrence ; Stomach Neoplasms* ; Survival Rate

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Neoadjuvant Imatinib in Locally Advanced Gastrointestinal Stromal Tumors of the Stomach: Report of Three Cases.

Ji Seon OH ; Jae Lyun LEE ; Mi Jung KIM ; Min Hee RYU ; Heung Moon CHANG ; Tae Won KIM ; Se Jin JANG ; Jeong Hwan YOOK ; Sung Tae OH ; Byung Sik KIM ; Yoon Koo KANG

Cancer Research and Treatment.2006;38(3):178-183.

Neoadjuvant imatinib therapy used to treat locally advanced or metastatic gastrointestinal stromal tumors (GI ST) remains under active investigation. We studied three cases of locally advanced gastric GISTs treated with imatinib on a neoadjuvant basis, followed by a complete surgical resection. Three patients were diagnosed with locally advanced unresectable GIST of the stomach and were started on imatinib 400 mg/day. After the imatinib treatment, partial responses were achieved in all patients and the tumors were considered resectable. Surgical resection was done after 7, 11, and 8 months of imatinib therapy, respectively. In one case, a metastatic liver lesion was detected during the imatinib treatment using computed tomography scans, so the imatinib therapy was maintained for 11 months postoperatively. In the other two patients without distant metastasis, imatinib treatment was not restarted after surgery. Mutational analysis revealed a mutation in exon 11 of the c-kit gene in two patients, and wild-type c-kit and PDGFRA in one patient. During pathology review of all three cases, we noted several features common to imatinib treatment. There was no evidence of tumor recurrence in all three patients at respective follow-up visits of 22, 15, and 7 months. These results suggest that the neoadjuvant imatinib therapy is a potentially curative approach for selected patients with locally advanced GIST.
Exons ; Follow-Up Studies ; Gastrointestinal Stromal Tumors* ; Humans ; Liver ; Neoadjuvant Therapy ; Neoplasm Metastasis ; Pathology ; Recurrence ; Stomach* ; Imatinib Mesylate

Exons ; Follow-Up Studies ; Gastrointestinal Stromal Tumors* ; Humans ; Liver ; Neoadjuvant Therapy ; Neoplasm Metastasis ; Pathology ; Recurrence ; Stomach* ; Imatinib Mesylate

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Cell Cycle Regulatory Protein Expression Profiles by Adenovirus p53 Infection in Human Papilloma Virus-associated Cervical Cancer Cells.

Yong Seok LEE ; Su Mi BAE ; Sun Young KWAK ; Dong Chun PARK ; Yong Wook KIM ; Soo Young HUR ; Eun Kyung PARK ; Byoung Don HAN ; Young Joo LEE ; Chong Kook KIM ; Do Kang KIM ; Woong Shick AHN

Cancer Research and Treatment.2006;38(3):168-177.

PURPOSE: The tumor suppressor gene, p53, has been established as an essential component for the suppression of tumor cell growth. In this study, we investigated the time-course anticancer effects of adenoviral p53 (Adp53) infection on human ovarian cancer cells to provide insight into the molecular-level understanding of the growth suppression mechanisms involved in Adp53-mediated apoptosis and cell cycle arrest. MATERIALS AND METHODS: Three human cervical cancer cell lines (SiHa, CaSki, HeLa and HT3) were used. The effect of Adp53 infection was studied via cell count assay, cell cycle analysis, FACS, Western blot and macroarray assay. RESULTS: Adp53 exerts a significant role in suppressing cervical cancer cell growth. Adp53 also showed growth inhibitory effects in each cell line, and it induced apoptosis and cell cycle arrest. Adp53 differentially regulated the expression of genes and proteins, and the gene expression profiles in the SiHa cells revealed that the p21, p53 and mdm2 expressions were significantly up-regulated at 24 and 48 hr. Western blot shows that the p21 and p53 expressionlevels were significantly increased after Adp53 infection. In addition, in all cell lines, both the CDK4 and PCNA protein expression levels were decreased 48 h after Adp53 infection. Cell cycle arrest at the G1 phase was induced only in the SiHa and HeLa cells, suggesting that exogenous infection of Adp53 in cancer cells was significantly different from the other HPV-associated cervical cancer cells. CONCLUSION: Adp53 can inhibit cervical cancer cell growth through induction of apoptosis and cell cycle arrest, as well as through the regulation of the cell cycle-related proteins. The Adp53-mediated apoptosis can be employed as an advanced strategy for developing preferential tumor cell-specific delivery.
Adenoviridae* ; Apoptosis ; Blotting, Western ; Cell Count ; Cell Cycle Checkpoints ; Cell Cycle* ; Cell Line ; G1 Phase ; Genes, Tumor Suppressor ; Genetic Therapy ; HeLa Cells ; Humans* ; Ovarian Neoplasms ; Papilloma* ; Proliferating Cell Nuclear Antigen ; Transcriptome ; Uterine Cervical Neoplasms*

Adenoviridae* ; Apoptosis ; Blotting, Western ; Cell Count ; Cell Cycle Checkpoints ; Cell Cycle* ; Cell Line ; G1 Phase ; Genes, Tumor Suppressor ; Genetic Therapy ; HeLa Cells ; Humans* ; Ovarian Neoplasms ; Papilloma* ; Proliferating Cell Nuclear Antigen ; Transcriptome ; Uterine Cervical Neoplasms*

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The Synergism between Belotecan and Cisplatin in Gastric Cancer.

Joo Young JUNG ; Sang Hyun SONG ; Tae Young KIM ; Jung Hyun PARK ; Hyun Soon JONG ; Seock Ah IM ; Tae You KIM ; Yung Jue BANG ; Noe Kyoung KIM

Cancer Research and Treatment.2006;38(3):159-167.

PURPOSE: We wanted to demonstrate the anti-cancer effect and interaction between belotecan and cisplatin on gastric cancer cell line and we evaluated the mechanisms of this synergistic effect in vitro. MATERIALS AND METHODS: The growth inhibitory effect of belotocan and cisplatin against several gastric cancer cell lines (SNU-5, SNU-16 and SNU-601) was estimated by tetrazolium dye assay. The effect of a combination treatment was evaluated by the isobologram method. The biochemical mechanisms for the interaction between the drugs were analyzed by measuring the formation of DNA interstrand cross-links (ICLs) and DNA topo-I activity. RESULTS: Belotecan showed synergism with cisplatin for growth inhibitory effect on the gastric cancer cell lines SNU-5, and SNU-16, but this was subadditive on the SNU-601 cell line. The formation of DNA ICLs in SNU-16 cells by cisplatin was increased by combination with belotecan, but this was not affected in SNU-601 cells. The topo-I inhibition by belotecan was enhanced at high concentrations of cisplatin in SNU-16, but not in SNU-601 cells. CONCLUSION: Belotecan and cisplatin show various combination effect against gastric cancer cells. The synergism between cisplatin and belotecan could be the result of one of the following mechanisms: the modulating effect of belotecan on the repair of cisplatin-induced DNA adducts and the enhancing effect of cisplatin on the belotecan-induced topo-I inhibitory effect.
Cell Line ; Cisplatin* ; DNA ; DNA Adducts ; Stomach Neoplasms*

Cell Line ; Cisplatin* ; DNA ; DNA Adducts ; Stomach Neoplasms*

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Inhibition of Phorbol Ester-induced Mouse Skin Tumor Promotion and COX-2 Expression by Celecoxib: C/EBP as a Potential Molecular Target.

Kyung Soo CHUN ; Joydeb Kumar KUNDU ; Kwang Kyun PARK ; Won Yoon CHUNG ; Young Joon SURH

Cancer Research and Treatment.2006;38(3):152-158.

PURPOSE: Inflammation acts as a driving force for the development of cancer. Multiple lines of evidence suggest that nonsteroidal anti-inflammatory drugs, especially those that specifically target cyclooxygenase-2 (COX-2), are effective in preventing certain cancers. The present study was aimed at investigating the antitumor promoting potential of celecoxib in chemically induced mouse skin tumorigenesis, as well as elucidating the underlying molecular mechanisms. MATERIALS AND METHODS: To study the antitumor promoting effects of celecoxib, we used the classical two-stage mouse skin tumorigenesis model that involves initiation with a single application of 7,12-dimethylbenz[alpha]anthracene (DMBA) followed by promotion with repeated applications of 12-O-tetradecanoylphorbol-13-acetate (TPA). The effects of celecoxib on the expression of COX-2, vascular endothelial growth factor (VEGF), p65 and the different isoforms of CCAAT/enhancer binding protein (C/EBP) were examined by performing Western blot analysis. Electrophoretic mobility gel shift assay was used to examine the effects of celecoxib on the TPA-induced DNA binding activities of various transcription factors. RESULTS: Our study revealed that topical application of celecoxib (10 micromol) significantly reduced the multiplicity of papillomas in DMBA-initiated and TPA-promoted mouse skin. Pretreatment with celecoxib also diminished the expression of COX-2 and VEGF in the mouse skin papillomas. Pretreatment with celecoxib attenuated DNA binding of transcription factor (C/EBP) in the TPA-stimulated mouse skin. Moreover, celecoxib suppressed the TPA-induced nuclear expression of C/EBPdelta, but not C/EBPbeta, in mouse skin in vivo. CONCLUSION: Our study demonstrates the inhibitory effects of celecoxib on mouse skin tumor promotion, which was associated with a decreased expression of COX-2 and VEGF, as well as inhibition of C/EBP activation.
Animals ; Blotting, Western ; Carcinogenesis ; Carrier Proteins ; Chemoprevention ; Cyclooxygenase 2 ; DNA ; Inflammation ; Mice* ; NF-kappa B ; Papilloma ; Protein Isoforms ; Skin* ; Transcription Factors ; Vascular Endothelial Growth Factor A ; Celecoxib

Animals ; Blotting, Western ; Carcinogenesis ; Carrier Proteins ; Chemoprevention ; Cyclooxygenase 2 ; DNA ; Inflammation ; Mice* ; NF-kappa B ; Papilloma ; Protein Isoforms ; Skin* ; Transcription Factors ; Vascular Endothelial Growth Factor A ; Celecoxib

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AKAP12alpha is Associated with Promoter Methylation in Lung Cancer.

Ukhyun JO ; Young Mi WHANG ; Han Kyeom KIM ; Yeul Hong KIM

Cancer Research and Treatment.2006;38(3):144-151.

PURPOSE: Promoter methylation is an important mechanism for silencing tumor-suppressor genes in cancer and it is a promising tool for the development of molecular biomarkers. The purpose of the present study was to investigate whether inactivation of the A Kinase Anchoring Protein 12 (AKAP12) gene is associated with promoter methylation in lung cancer. MATERIALS AND METHODS: The AKAP12 expression was examined by reverse transcription-polymerase chain reaction (RT-PCR) in ten lung cancer cell lines. The methylation status of the AKAP12alpha promoter was analyzed by performing bisulfite sequencing analysis in ten lung cancer cell lines, twenty four lung tissues and matched normal tissues. RESULTS: The AKAP12alpha expression was reduced in 6 of 10 (60%) lung cancer cell lines, whereas the AKAP12beta expression was absent in 1 of 10 (10%) lung cancer cell lines. The AKAP12alpha expression was restored after treatment with the demethylating agent 5-aza-2'-deoxycytidine in three lung cancer cell lines. Methylation of CpG island 1 in the AKAP12alpha promoter was detected in 30% of the lung cancer cell lines, whereas methylation of CpG island 2 in the AKAP12alpha promoter was observed in the immortalized bronchial cell line and in all the lung cancer cell lines. In lung tumors, the CpG island 1 in the AKAP12alpha promoter was infrequently methylated. However, CpG island 2 in the AKAP12alpha promoter was highly methylated in lung tumors compared with the surrounding normal tissues, and this was statistically significant (p=0.0001). CONCLUSION: Our results suggest that inactivation of the AKAP12alpha expression is associated with DNA methylation of the promoter region in lung cancer, and that AKAP12alpha may play an important role in lung cancer carcinogenesis.
Biomarkers ; Carcinogenesis ; Cell Line ; CpG Islands ; DNA Methylation ; Lung Neoplasms* ; Lung* ; Methylation* ; Phosphotransferases ; Promoter Regions, Genetic

Biomarkers ; Carcinogenesis ; Cell Line ; CpG Islands ; DNA Methylation ; Lung Neoplasms* ; Lung* ; Methylation* ; Phosphotransferases ; Promoter Regions, Genetic

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Occludin Expression in Brain Tumors and its Relevance to Peritumoral Edema and Survival.

Min Woo PARK ; Choong Hyun KIM ; Jin Hwan CHEONG ; Koang Hum BAK ; Jae Min KIM ; Suck Jun OH

Cancer Research and Treatment.2006;38(3):139-143.

PURPOSE: Peritumoral brain edema (PTBE) is a serious causative factor that contributes the morbidity or mortality of brain tumors. The development of PTBE is influenced by many factors, including such tight junction proteins as occludin. We evaluated the PTBE volume and survival time with respect to the occludin expression in various pathological types of brain tumors. MATERIALS AND METHODS: Fresh-frozen specimens from sixty patients who had brain tumors were obtained during surgery and the tumors were confirmed pathologically. The occludin expression was investigated by Western blot analysis. The PTBE volume was measured by using preoperative magnetic resonance (MR) imaging, and the survival time in each patient was estimated retrospectively. RESULTS: Occludin was detected in 41 (68.3%) of the cases with brain tumors and it was not expressed in the other 19 (31.7%) cases. Although the lowest expression was revealed in high-grade gliomas, its expression was variable according to the pathology of the brain tumors (p>0.05). The difference of PTBE volume between occludin-positive and negative brain tumors was statistically significant (2072.46+/-328.73 mm3 vs. 7452.42+/-1504.19 mm3, respectively, p=0.002). The mean survival time was longer in the occludin-positive tumor group than in the occludin-negative group (38.63+/-1.57 months vs. 26.16+/-3.83 months, respectively; p=0.016). CONCLUSIONS: This study suggests that the occludin expression is highly correlated to the development of PTBE in brain tumors and it might be a prognostic indicator for patient survival.
Blotting, Western ; Brain Edema ; Brain Neoplasms* ; Brain* ; Edema* ; Glioma ; Humans ; Mortality ; Occludin* ; Pathology ; Retrospective Studies ; Survival Rate ; Tight Junction Proteins

Blotting, Western ; Brain Edema ; Brain Neoplasms* ; Brain* ; Edema* ; Glioma ; Humans ; Mortality ; Occludin* ; Pathology ; Retrospective Studies ; Survival Rate ; Tight Junction Proteins

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Patterns of Failure after Postoperative Radiation Therapy for Endometrial Carcinoma.

Suzy KIM ; Hong Gyun WU ; Hyo Pyo LEE ; Soon Beom KANG ; Yong Sang SONG ; Noh Hyun PARK ; Sung Whan HA

Cancer Research and Treatment.2006;38(3):133-138.

PURPOSE: We tried to investigate the outcome and patterns of failure of endometrial cancer patients who were treated with surgery and postoperative radiation therapy (RT). MATERIALS AND METHODS: Eighty-three patients with endometrial cancer who received postoperative RT between May 1979 and August 2000 were included in this retrospective study. Forty-one patients received total abdominal hysterectomy, 41 patients received Wertheim's operation and 1 underwent vaginal hysterectomy. Pelvic lymph node dissection or pelvic lymph node sampling was done in 56 patients and peritoneal cytology was done in 35. All the patients were staged according to 1988 FIGO (International Federation of Gynecology and Obstetrics) staging system; 2 were stage IA, 23 were stage IB, 20 were stage IC, 4 were stage IIA, 5 were stage IIB, 9 were stage IIIA, 2 were stage IIIB and 18 were stage IIIC. The histologic diagnoses were adenocarcinoma in seventy-four patients (89%). The histologic grades were Grade 1, 2 and 3 in 21 (25%), 43 (52%) and 10 (12%) patients, respectively. All the patients received external beam RT (EBRT) with a median dose of 5,040 cGy (range: 4,500~5,075 cGy) to the whole pelvis. Five patients with pathologically confirmed paraaortic lymph node metastasis received 4500 cGy to the paraaortic lymph nodes. Fifteen patients received low-dose intracavitary brachytherapy after their EBRT. A total dose of 7,500~9,540 cGy (median dose: 8511) was prescribed to the vaginal surface. RESULTS: Overall, 11 patients (13%) experienced disease relapse: 4 with initial stage I or II disease and 7 with initial stage III disease. Among the 54 stage I or II patients, 1 (2%) relapsed in the pelvis only, 2 (4%) relapsed in the vagina and distant organs, and 1 (2%) relapsed in the paraaortic lymph nodes (PANs). Among the 29 stage III patients, 1 (3%) relapsed in the vagina. The most common sites of failure for the stage III patients were the peritoneum (3 patients, 10%), PANs (2 patients, 7%), and lung (2 patients, 7%). With a median follow-up period of 86 months, the overall survival (OS) and disease-free survival (DFS) rates at 5 years were 87% for both. The five-year DFS rate was 93%, 100% and 74% for the stage I, II and III patients, respectively. Three patients experienced severe radiation-related late complications: RTOG (Radiation Therapy Oncology Group) grade 3 radiation cystitis was seen in one patient, and grade 3 bowel obstruction was seen in two patients. CONCLUSIONS: Postoperative RT was useful for controlling pelvic disease. The major patterns of failure for stage III patients were peritoneal seeding and distant metastasis. Selective use of whole abdominal radiotherapy or adjuvant chemotherapy may improve the therapeutic outcome of these patients.
Adenocarcinoma ; Brachytherapy ; Chemotherapy, Adjuvant ; Cystitis ; Diagnosis ; Disease-Free Survival ; Endometrial Neoplasms* ; Female ; Follow-Up Studies ; Gynecology ; Humans ; Hysterectomy ; Hysterectomy, Vaginal ; Lung ; Lymph Node Excision ; Lymph Nodes ; Neoplasm Metastasis ; Pelvis ; Peritoneum ; Radiotherapy ; Recurrence ; Retrospective Studies ; Vagina

Adenocarcinoma ; Brachytherapy ; Chemotherapy, Adjuvant ; Cystitis ; Diagnosis ; Disease-Free Survival ; Endometrial Neoplasms* ; Female ; Follow-Up Studies ; Gynecology ; Humans ; Hysterectomy ; Hysterectomy, Vaginal ; Lung ; Lymph Node Excision ; Lymph Nodes ; Neoplasm Metastasis ; Pelvis ; Peritoneum ; Radiotherapy ; Recurrence ; Retrospective Studies ; Vagina

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Effects of the Expression of Leptin and Leptin Receptor (OBR) on the Prognosis of Early-stage Breast Cancers.

Yongnam KIM ; Si Young KIM ; Jae Jin LEE ; Jeongho SEO ; Youn Wha KIM ; Suck Hwan KOH ; Hwi Joong YOON ; Kyung Sam CHO

Cancer Research and Treatment.2006;38(3):126-132.

PURPOSE: Obesity-related leptin and leptin receptor (OBR) have a relation to the development of cancer and metastasis and also the low survival rate for breast cancer patients. Leptin has been associated with increased aromatase activity and it displays functional cross-talk with estrogen. This study was designed to determine the relationship between the expression of leptin and OBR in breast cancer tissue and the prognosis of early-stage breast cancer patients, and especially for the tamoxifen-treated patients. MATERIALS AND METHODS: Ninety-five patients with early-stage breast cancer and who had undergone surgical treatment at Kyung Hee University Hospital between January 1994 and June 2004 were analyzed. The surgical specimens underwent immunohistochemical analysis for leptin and OBR. The patients' survival and clinical characteristics were obtained from the medical records. RESULTS: Of the 95 patients, 79 (83%) and 32 (33.7%) showed the expression of leptin and OBR in breast cancer tissue, respectively. The expression of leptin and OBR in breast cancer tissue was not significantly related to the clinicopathological characteristics, including obesity, the expression of hormonal receptor, the HER-2/neu expression, menopause, stage and the nuclear grade. The expression of leptin and OBR was not significantly related to the overall disease-free survival (DFS). For the tamoxifen-treated postmenopausal obese patients, the DFS of the leptin-positive group was higher than that of the leptin-negative group (p=0.017). CONCLUSION: The expression of leptin and OBR in breast cancer tissue may be not a prognostic factor for disease-free survival of breast cancer patients. In the future, further studies are needed to determine whether leptin expression could be a predictive factor for tamoxifen therapy in the postmenopausal obese subgroup among the early breast cancer patients.
Aromatase ; Breast Neoplasms ; Breast* ; Disease-Free Survival ; Estrogens ; Female ; Humans ; Leptin* ; Medical Records ; Menopause ; Neoplasm Metastasis ; Obesity ; Postmenopause ; Prognosis* ; Receptors, Leptin* ; Survival Rate ; Tamoxifen

Aromatase ; Breast Neoplasms ; Breast* ; Disease-Free Survival ; Estrogens ; Female ; Humans ; Leptin* ; Medical Records ; Menopause ; Neoplasm Metastasis ; Obesity ; Postmenopause ; Prognosis* ; Receptors, Leptin* ; Survival Rate ; Tamoxifen

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A Pilot Study of Cisplatin, Irinotecan, Leucovorin and 5-fluorouracil (PILF) Combination Chemotherapy for Advanced Gastric Cancer.

Se Hoon PARK ; Soo Yeon JEON ; Kwang Il KO ; Eunmi NAM ; Soo Mee BANG ; Eun Kyung CHO ; Dong Bok SHIN ; Jae Hoon LEE ; Woon Ki LEE ; Min CHUNG

Cancer Research and Treatment.2006;38(3):121-125.

PURPOSE: Irinotecan, in combination with leucovorin/ 5-fluorouracil (FU) or with cisplatin, is known to be active for treating advanced gastric cancer (AGC). This pilot study evaluated a novel three-drug combination of irinotecan, leucovorin/FU and cisplatin as a first-line treatment of AGC. The primary endpoint was to assess the feasibility in anticipation of conducting a larger phase II study. MATERIALS AND METHODS: Chemotherapy-naive AGC patients received irinotecan 150 mg/m2 on day 1, and leucovorin 200 mg/m2 and a 22-h infusion of FU 1000 mg/m2 on days 1 and 2. Cisplatin 30 mg/m2 was administered on day 2. Treatment was repeated every 2 weeks until disease progression or unacceptable toxicity. RESULTS: Of the 17 eligible patients, two patients had an ECOG performance status of 2 and their median age was 48 years (range: 31 to 69). A total of 117 chemotherapy cycles were delivered (median: 6, range: 1 to 12). The causes of treatment discontinuation were disease progression in 9 patients (53%), refusal (35%) and toxicity (12%). Although grade 3 or 4 neutropenia (41% of patients) was the major toxicity that required dose adjustments, only one episode of febrile neutropenia occurred. Grade 3 or 4 nausea and vomiting, diarrhea and fatigue were observed in 35%, 35% and 29% of patients, respectively. None of the patients died of toxicity during treatment. Of the 16 patients who were evaluable for response, 7 (44%) experienced a partial response. CONCLUSION: This novel multi-drug combination was tolerated well in patients with AGC. Based on the encouraging efficacy and tolerability, a randomized phase II study is ongoing in this disease setting.
Cisplatin* ; Diarrhea ; Disease Progression ; Disulfiram ; Drug Therapy ; Drug Therapy, Combination* ; Fatigue ; Febrile Neutropenia ; Fluorouracil* ; Humans ; Leucovorin* ; Nausea ; Neutropenia ; Pilot Projects* ; Stomach Neoplasms* ; Vomiting

Cisplatin* ; Diarrhea ; Disease Progression ; Disulfiram ; Drug Therapy ; Drug Therapy, Combination* ; Fatigue ; Febrile Neutropenia ; Fluorouracil* ; Humans ; Leucovorin* ; Nausea ; Neutropenia ; Pilot Projects* ; Stomach Neoplasms* ; Vomiting

Country

Republic of Korea

Publisher

Korean Cancer Association

ElectronicLinks

http://e-crt.org

Editor-in-chief

Seung Hoon Lee

E-mail

journal@cancer.or.kr

Abbreviation

Cancer Res Treat

Vernacular Journal Title

Journal of the Korean Cancer Association, 대한암학회지

ISSN

1598-2998

EISSN

2005-9256

Year Approved

2007

Current Indexing Status

Currently Indexed

Start Year

2001

Description

(New name) Cancer Research and Treatment: 2001 (v33 n3) to Present pISSN 1598-2998 eISSN 2005-9256 (Old name) Journal of the Korean Cancer Association: 1966 (v1 n1) to 2001 (v33 n2) pISSN 0496-6872 Cancer Research and Treatment is a peer-reviewed open access publication of the Korean Cancer Association. It is published quarterly, one volume per year. Abbreviated title is Cancer Res Treat. It accepts manuscripts relevant to experimental and clinical cancer research. Subjects include carcinogenesis, tumor biology, molecular oncology, cancer genetics, tumor immunology, epidemiology, predictive markers and cancer prevention, pathology, cancer diagnosis, screening and therapies including chemotherapy, surgery, radiation therapy, immunotherapy, gene therapy, multimodality treatment and palliative care.

Previous Title

Journal of the Korean Cancer Association

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