Masao Omata
University of Tokyo
1054 Papers
11.9K Citations
Masao Omata is an academic researcher from University of Tokyo. The author has contributed to research in topics: Medicine & Hepatocellular carcinoma. The author has an hindex of 111, co-authored 990 publications. Previous affiliations of Masao Omata include St. Marianna University School of Medicine & Dokkyo University.
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Papers
Pseudo-Meigs’ syndrome due to ovarian metastases from colon cancer: a case report and review of the literature
Atsushi Yamamoto,Yoshiaki Miyasaka,Kazushige Furuya,Hideki Watanabe,Masahiro Maruyama,Haruka Nakada,Atsushi Takano,Masao Hada,Hiroshi Nakagomi,Masao Omata,Toshio Oyama +10 more
TL;DR: The patient developed both synchronous and metachronous ovarian metastases and achieved a 7-year disease-free survival after the operation and the pathogenesis of pseudo-Meigs’ syndrome should be distinguished from carcinomatous peritonitis and/or pleuritis of malignant disease.
A Randomized, Controlled Trial of Interferon-β Treatment for Acute Hepatitis C
Masao Omata,Susumu Takano +1 more
- 01 Jan 1994
TL;DR: Serum hepatitis C virus (HCV)-RNA fell below detectable concentrations in 10 of 11 treated and in only 1 of 12 control patients, which suggests that interferon prevents the progression of acute non-A, non-B hepatitis to chronicity by eradicating HCV.
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De novo synthesis of phospholipase A2 and prostacyclin production by proliferating rat smooth muscle cells.
Yoshio Uehara,Yukari Kawabata,Taiji Nagata,Tokuichiro Sugimoto,Masao Omata,H. Hara,Ichiro Kudo,Keizo Inoue,Satoru Takada,Atsushi Numabe,Toshio Ikeda,N. Hirawa +11 more
TL;DR: Ex vivo PGI2 generation is mainly increased during the G0/G1 period and this event is secondary to de novo synthesis of PLA2 and probably, at least in part, to cyclooxygenase induction, which provides a negative feedback regulating VSMC proliferation.
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Elucidation of radiation-resistant clones by a serial study of intratumor heterogeneity before and after stereotactic radiotherapy in lung cancer.
Takahiro Nakagomi,Taichiro Goto,Yosuke Hirotsu,Daichi Shikata,Kenji Amemiya,Toshio Oyama,Hitoshi Mochizuki,Masao Omata +7 more
TL;DR: The number of mutations decreased after SRT, suggesting that it induced mutation selection, and analyses of the statistical inference of clonal population structure showed that this evolving heterogeneous genomic landscape may be caused by heterogeneous responsiveness to SRT.