Degree 【 display / non-display 】

Degree 【 display / non-display 】

• Ph.D.(1999)

Affiliation 【 display / non-display 】

Affiliation 【 display / non-display 】

• Sapporo Medical University   School of Medicine, Dept.of Obstetrics and Gynecology   Assistant Professor  

Misc 【 display / non-display 】

Misc 【 display / non-display 】

• Ultrastructural study of benign, low-malignant potential (LMP), and malignant ovarian tumors

  Shin-Ichi Ishioka, Satoru Sagae, Eiki Ito, Ryuichi Kado

  Medical Electron Microscopy   37 ( 1 ) 37 - 44  2004.03

  Book review, literature introduction, etc.  

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  Ultrastructural characteristics of benign, low-malignant potential (LMP), and malignant ovarian tumors were investigated, considering the aspects of histologic subtypes and histologic grading. In addition, the histogenesis of ovarian cancer was histologically investigated in an attempt to elucidate whether malignant tumor was generated from benign or LMP tumor, or whether it was generated de novo from normal tissues. Although all the benign, LMP, and malignant tumors appeared to be derived from Mullerian duct in serous tumors, the origin of endometrioid or mucinous tumor could not be ultrastructurally clarified. However, there was ultrastructural similarity between benign and malignant tumors among serous, endometrioid, and mucinous tumors, and it was suggested that benign adenoma may be the developmental origin of malignant tumors regardless of the histologic subtype. In addition, the investigation of endometrioid tumors revealed that the differences of histologic grading in malignant tumors reflected the ultrastructural differences, and that G1 tumor had an ultrastructure that was more similar to that of benign and LMP tumors than to that of G2 tumor.

  DOI PubMed CiNii

• Preoperative diagnosis and treatment results in 106 patients with uterine sarcoma in Hokkaido, Japan

  S Sagae, K Yamashita, S Ishioka, Y Nishioka, K Terasawa, M Mori, K Yamashiro, T Kanemoto, R Kudo

  ONCOLOGY ( KARGER )  67 ( 1 ) 33 - 39  2004

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  Objective: The aim of this study was to evaluate the clinicopathological features of uterine sarcoma in Hokkaido, Japan, between 1990 and 1999, and to identify prognostic factors of patients with such malignancies in this area and period. Methods: One hundred and six patients with histologically proven uterine sarcoma were evaluated retrospectively. Results: 93.5% of the patients with carcinosarcoma ( CS) were diagnosed as having malignant disease preoperatively, while 65% of those with leiomyosarcoma (LMS) and 75% of those with endometrial stromal sarcoma (ESS) were preoperatively diagnosed as benign leiomyoma. When patients had no residual disease postoperatively, 5-year survival rates in patients with CS and LMS were 78.8 and 73.0%, respectively. ESS cases had a better prognosis (94.7% for stage I cases). In patients with early-stage sarcoma, pelvic lymphadenectomy and adjuvant chemotherapy, with or without cis-diamminedichloroplatinum, failed to show a survival benefit in both CS and LMS cases. Distant metastasis, myometrial invasion, and no residual disease at surgery were significantly associated with risk of death or recurrence in CS and LMS cases. Conclusion: Accurate preoperative diagnosis of uterine sarcoma was difficult, and no residual disease at surgery was the most important prognostic factor in patients with this disease. Postoperative adjuvant therapy had little effect on survival, especially in early-stage disease. Copyright (C) 2004 S. Karger AG, Basel.

  DOI

• [A pilot study of combined chemotherapy with paclitaxel, doxorubicin and cisplatin for endometrial cancer]

  Gan To Kagaku Ryoho   31   549 - 53  2004

• [Surgical treatment of ovarian cancer]

  Nippon Rinsho   62   522 - 6  2004

• Mechanisms of paclitaxel-induced apoptosis in an ovarian cancer cell line and its paclitaxel-resistant clone

  M Sugimura, S Sagae, S Ishioka, Y Nishioka, K Tsukada, R Kudo

  ONCOLOGY ( KARGER )  66 ( 1 ) 53 - 61  2004

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  Background: To understand the complicated network of paclitaxel ( PTX)- induced apoptosis pathways and to elucidate mechanisms of drug resistance in ovarian cancer, we looked at PTX- induced apoptosis by using cDNA microarray. We also quantitated the changes in apoptosis-related proteins in the process of apoptosis. Methods: An ovarian cancer cell line KF, and its PTX- resistant clone KFTX, were treated with PTX or carboplatin ( CBDCA). After exposure to PTX or CBDCA, the induction of apoptosis was examined by internucleosomal DNA fragmentation. Changes in mRNA expression after 12 h of exposure to PTX were studied using cDNA microarray and RT- PCR. Changes in P53 and Bcl- 2 levels were also measured over 24 h by ELISA. Results: With increased doses of PTX or CBDCA, an increase in apoptosis was noted in both cell lines. cDNA microarray revealed that PTX treatment upregulated expression of caspase 1, 2, 3, 4, 6, 9, 10, their activator apaf- 1, and stress reaction- related genes, gadd34, gadd153 in KF, although most of them were unchanged or downregulated in KFTX. bag- 1 and hsc70 were markedly upregulated in KFTX. p53 and bcl- 2 were not upregulated in either cell line. Results from protein studies also supported the cDNA microarray data. Conclusion: p53- independent mitochondrial pathways and stress- reaction- induced pathways play critical roles in PTX- induced apoptosis in ovarian cancer cells. Suppression of those pathways and upregulation of bag- 1 and hsp- 70 played an important role in acquiring resistance to PTX. Copyright (C) 2004 S. Karger AG, Basel.

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