1998 Fiscal Year Final Research Report Summary
Basic study for ascites formation in terminal stage gynecologic cancer patients
| Project/Area Number |
08671935
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Obstetrics and gynecology
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| Research Institution | Nihon University |
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Principal Investigator |
SAKAMOTO Hideki Nihon University, School of Medicine, Associate Professor, 医学部, 助教授 (80158922)
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| Co-Investigator(Kenkyū-buntansha) |
TAKAMI Takeshi Nihon University School of Medicie, Research Assistant, 医学部, 助手 (90297812)
OHTANI Kaori Nihon University School of Medicine, Research Assistant, 医学部, 助手 (40246872)
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| Project Period (FY) |
1996 – 1998
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| Keywords | ascites / c-erbB-2 |
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| Research Abstract |
Thymidinc phosphorylase (dThdPase) expression was studied in well differentiated endometrial carcinomas. The expression was exclusively observed in the stromal macrophges (Mphi)of the cancerous portion of the endometrial stroma and not in benign lesions. The dThdPase expression colocalized with a area of high neovascularization. These observation suggest that cancer may produce paracrine factor(s) to induce dThdPase in stromal Mphi and induce neovascular formation by a dThdPase dependent manner. 4x104 HL-60 cells were cultured in (i) Nunc tissue culture inserts (Inter Med, Denmark), placed in culture dishes of Ishikawa or mEIIL (a metastatic subclone of Ishikawa) endometrial cancer cells or with (ii) ascitic fluid from endometrial cancer patients (n=l0) or nonmalignant tumors (n=20) for 48 hours. Terminal differentiation was monitored by an attachment assay or phagocytotic phenomenon. The dThdPase induction was examined by (i) RT-PCR and (ii) Western blot (antibody kindly provided by Nippon Roch). HL-60 cells were negative for dThdPase mRNA or protein whereas Ishikawa and mEIIL were both very weakly positive. HL-60 cells being exposed to the conditioned medium of lshikawa or mEIIL showed positive transcription and translation. The expression of dThdPase was approximately 1,000 fold higher in HL-60 cells exposed to mEIIL.Also ascitic fluid from cancer patients but not benign tumors, showed concentration dependent induction of dThdPase and differentiation of HL-60 cells. The factor(s) is heat labile and has molecular size of less than 15 Kd.
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