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45 results on '"Koshikawa, Katsumi"'

2. Expression of CD109 in human cancer

Author

Hashimoto, Mizuo, Ichihara, Masatoshi, Watanabe, Tsuyoshi, Kawai, Kumi, Koshikawa, Katsumi, Yuasa, Norihiro, Takahashi, Takashi, Yatabe, Yasushi, Murakumo, Yoshiki, Zhang, Jing-min, Nimura, Yuji, and Takahashi, Masahide

Published
2004
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21. PELVIC CASTLEMAN DISEASE

Author

KAMATA, Tsugumasa, primary, HATTORI, Norifumi, additional, KOSHIKAWA, Katsumi, additional, YOKOYAMA, Hiroyuki, additional, TANIGUCHI, Kenji, additional, and SUENAGA, Hiroyuki, additional

Published
2008
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40. Frequent promoter methylation and gene silencing of CDH13in pancreatic cancer

Author

Sakai, Mitsuru, Hibi, Kenji, Koshikawa, Katsumi, Inoue, Soichiro, Takeda, Shin, Kaneko, Tetsuya, and Nakao, Akimasa

Abstract

It has recently been reported that CDH13expression is silenced by aberrant methylation of the promoter region in several cancers. We examined the methylation status of the CDH13gene in pancreatic cancer using methylation‐specific PCR (MSP), and detected aberrant methylation of CDH13in all 6 pancreatic cancer cell lines examined. To confirm the status of the CDH13gene in relation to the methylation pattern, we next examined CDH13expression in these cell lines using reverse transcription (RT)‐PCR. As expected, no CDH13expression was detected in any of the 6 pancreatic cancer cell lines. Moreover, 5‐aza‐2′‐deoxycytidine (5‐aza‐dC) treatment of CDH13‐methylated cell lines led to restoration of CDH13expression. Among primary pancreatic cancers, 19 of 33 (58%) cases exhibited CDH13methylation, while no cases exhibited it in corresponding normal pancreatic tissues. CDH13methylation was detected even in relatively early pancreatic cancers, such as stage II cancers and cancers less than 2 cm in diameter. Our results suggest that the aberrant methylation of CDH13occurs frequently in pancreatic cancer, even at a relatively early stage.

Published
2004
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41. [Suggesting the Significance of Pericardial Fat Pad in Bronchial Stump Fistula].

Author

Fukuoka T, Sano M, Tominaga N, Sanada S, Uno Y, Oya H, Nishi T, and Koshikawa K

Subjects
Bronchi surgery, Humans, Male, Middle Aged, Postoperative Complications, Sigmoid Neoplasms surgery, Adipose Tissue surgery, Bronchial Fistula surgery, Pericardium surgery, Pneumonectomy
Abstract

Bronchial stump fistula is a post-operative complication with poor outcome after pulmonary lobectomy. In order to prevent this complication, the bronchial stump is covered with pericardial fat tissue in our hospital. The case was 58 year old male who received adjuvant chemotherapy after sigmoidectomy for sigmoid colon cancer. As he developed multiple pulmonary metastases, 48 courses of chemotherapy were performed. The lesions had been localized at the right lower lobe, and neither increase in the size of these lesions nor development of other lesions were observed. Hence, an operation was performed. After right lower lobectomy, the bronchial stump was covered with the pericardial fat tissue. Three months after the operation, he developed pneumothorax, and bubbles were detected inside the fat. The pneumothorax was cured conservatively, and the bubbles disappeared spontaneously after 10 months. It is rare that the patient with bubbles in the covering tissue observed for a long time is cured conservatively, suggesting the significance of the stump pad.

Published
2016

42. A phase II study of weekly paclitaxel as second-line chemotherapy for advanced gastric Cancer (CCOG0302 study).

Author

Kodera Y, Ito S, Mochizuki Y, Fujitake S, Koshikawa K, Kanyama Y, Matsui T, Kojima H, Takase T, Ohashi N, Fujiwara M, Sakamoto J, and Akimasa N

Subjects
Aged, Drug Administration Schedule, Female, Humans, Male, Middle Aged, Adenocarcinoma drug therapy, Antineoplastic Agents, Phytogenic administration & dosage, Paclitaxel administration & dosage, Stomach Neoplasms drug therapy
Abstract

Background: Although paclitaxel was given triweekly in phase II trials prior to its approval for gastric cancer in Japan, it is currently more often delivered by a weekly schedule in the second-line setting., Patients and Methods: A phase II trial with response rate as the primary end-point was conducted. Patients with metastatic or unresectable gastric adenocarcinoma who had measurable lesions and had disease progression with the front-line chemotherapy were treated by weekly administration of paclitaxel at a dose of 80 mg/m2., Results: Forty-five patients were accrued and 44 were assessable for response. Partial responses were observed in 7 patients (16%). Stable disease was documented in further 14 patients (48%). Median progression-free survival of all patients enrolled was 2.6 months and median overall survival was 7.8 months. Toxicity was mild and manageable, the most frequent > or = grade 3 toxicity being neutropenia occurring in 16% of the patients., Conclusion: With modest response rate, favorable toxicity profile, and progression-free or overall survival similar to those of more intense combination regimens, weekly paclitaxel remains a rational therapeutic option for gastric cancer refractory to the first-line chemotherapy.

Published
2007

43. [Two cases of advanced gastric cancer with peritoneal dissemination acquired long-term response three years or more by postoperative treatment with oral anticancer drug TS-1].

Author

Shikano T, Koshikawa K, Kiriyama K, Wada M, Taniguchi K, and Suenaga H

Subjects
Administration, Oral, Aged, Combined Modality Therapy, Drug Administration Schedule, Drug Combinations, Female, Gastrectomy, Humans, Male, Middle Aged, Stomach Neoplasms surgery, Survivors, Adenocarcinoma, Mucinous drug therapy, Adenocarcinoma, Mucinous secondary, Antimetabolites, Antineoplastic administration & dosage, Oxonic Acid administration & dosage, Peritoneal Neoplasms drug therapy, Peritoneal Neoplasms secondary, Pyridines administration & dosage, Stomach Neoplasms pathology, Tegafur administration & dosage
Abstract

The first patient is a 60-year-old man who underwent total gastrectomy and splenectomy for type-3 gastric cancer after neoadjuvant chemotherapy. The second patient is a 69-year-old woman who underwent distal gastrectomy for type-2 gastric cancer and pyloric stenosis after neoadjuvant chemotherapy. Some peritoneal dissemination was observed in these two cases. No re-growth of peritoneal dissemination was seen for three years or more from treatment with the oral anticancer drug TS-1. Treatment on an outpatient basis, therefore, greatly contributed to their quality of life. We consider TS-1 as a first-line anti-cancer drug for advanced gastric cancer.

Published
2006

44. Allelic imbalance at 1p36 in the pathogenesis of human hepatocellular carcinoma.

Author

Koshikawa K, Nomoto S, Yamashita K, Ishigure K, Takeda S, and Nakao A

Subjects
Chromosome Mapping, Humans, Microsatellite Repeats, Allelic Imbalance, Carcinoma, Hepatocellular genetics, Chromosomes, Human, Pair 1 genetics, Liver Neoplasms genetics
Abstract

Background/aims: It has been well accepted that there is an allelic imbalance at a subtelomeric region of chromosome 1p in various human malignancies including hepatocellular carcinoma. We conducted a detailed deletion mapping study at 1p36 loci in 65 hepatocellular carcinomas as an initial step towards positional cloning of the target gene., Methodology: We performed a fine-scale deletion mapping using 10 highly polymorphic microsatellite markers along the telomeric region of 1p (1p32-p36.3) and compared the clinicopathologic features with allelic imbalance of 1p36 loci., Results: Allelic imbalance occurred in at least one locus on 1p in 32 (49.2%) of the 65 cases. Consequently, it was confirmed that a common region of overlaps was restricted to 1p36 and it was further clearly demonstrated that there were at least three independent regions in 1p36 (1p36.1, p36.2'36.3 and p36.3). An apparent trend towards significance has been demonstrated between allelic imbalance at 1p36 loci and tumors with classifcation T1-T2 (p<0.01)., Conclusions: The present study demonstrated that the shortest region of overlap was confined within 1p36 chromosomal sub-band in human hepatocellular carcinoma, which might be involved in an early step of hepatocarcinogenesis, and it encourages future studies to identify the putative tumor suppressor gene(s) at 1p36.

Published
2004

45. Mitochondrial D-loop mutations as clonal markers in multicentric hepatocellular carcinoma and plasma.

Author

Nomoto S, Yamashita K, Koshikawa K, Nakao A, and Sidransky D

Subjects
Adult, Aged, Female, Humans, Male, Middle Aged, Oligonucleotides metabolism, Polymerase Chain Reaction, Biomarkers, Tumor, Carcinoma, Hepatocellular blood, Carcinoma, Hepatocellular genetics, DNA, Mitochondrial, Liver Neoplasms blood, Liver Neoplasms genetics, Mutation
Abstract

Purpose: Hepatocellular carcinoma (HCC) is a highly malignant tumor prone to multicentric occurrence. Differentiation between a true relapse of HCC and a second primary tumor is of clinical importance. We sought to identify mitochondrial mutations in HCC and test their use as clonal markers in this disease., Experimental Design: Primary HCC tissue samples were obtained from 19 patients and analyzed for mutations within the mitochondrial displacement loop (D-loop). The discovered mutations were used to determine tumor clonality and provided the basis for detection of tumor DNA in corresponding plasma samples., Results: Thirteen of 19 HCC cases (68%) were identified as having D-loop mitochondrial DNA (mtDNA) mutations in at least one tumor. In 3 of these 13 cases, the same mutation was observed in multiple tumors, indicating monoclonal origin. Remarkably, in 8 of 13 mutated cases, we detected deletion/insertion mutations in the C-tract, a recently reported hotspot and potential replication start site of the closed, circular mitochondrial genome. In addition, we detected mutant mtDNA in 8 of 10 tested paired plasma DNA samples using a highly sensitivity molecular assay., Conclusions: mtDNA mutations within the D-loop control region are a frequent event in HCC, providing a molecular tool for the determination of clonality. In addition, detection of tumor-specific mtDNA mutations in plasma DNA needs to be explored further for monitoring patients with primary HCC.

Published
2002

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