MECHANISM OF ANTITUMORAL ACTIVITY OF MEDROXYPROGESTERONE ACETATE FOR ENDOMETRIAL CANCER
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概要
- 論文の詳細を見る
高分化型子宮内膜腺癌由来で, progestogen receptor (PR)を有するIshikawa株細胞のcolony 形成能は, 高濃度(μM)のmedroxyprogesterone acetate (MPA)によつて抑制された. しかしながら, 黄体hormoneの一つであるnorethindrone (ENT)や抗progestogenである17β-hydroxy-11β-(4-dimethylaminophenyl-1)-17α(prop-1-ynyl)-estra-4,9-dien-3-one (RU-486)では, そのcolony形成の抑制はできなかつた. MPA単独でもMPAとENTもしくはMPAとRU-486の2剤併用でも, この細胞のcolony形成の抑制に有意差がなかつた. ENTやRU-486はMPAと同様にPRに高い親和性がある. もし, MPAによるこのcolony形成の抑制が, PRを介する機構で起こるとすれば, この抑制は競合的にENTやRU-486で阻害できるはずであるが, そうではなかつた. したがつて, 高濃度のMPAは, この細胞のcolony形成抑制においていわゆるPRを介さない機構で作用すると考えられ, 子宮内膜癌症例においてもこの考えがあてはまるかもしれない.
- 社団法人日本産科婦人科学会の論文
- 1989-11-01
著者
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FUJITA Hiroyuki
Department of Rheumatology/Hematology/Infectious Disease, Yokohama City University Hospital
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藤本 次良
Department Of Obstctrics And Gynecology Kyoto Prefectural University Of Medicine
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HOSODA Shuji
Department of Obstctrics and Gynecology, Kyoto Prefectural University of Medicine
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Fujita Hiroyuki
Department Of Environmental Immuno-dermatology Yokohama City University Graduate School Of Medicine
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Hosoda Shuji
Department Of Obstctrics And Gynecology Kyoto Prefectural University Of Medicine
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Fujita Hiroyuki
Department Of Obstctrics And Gynecology Kyoto Prefectural University Of Medicine
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