Faculty Profiles - TOYOOKA Shinichi

Papers - TOYOOKA Shinichi

Division display 881 - 900 of about 940 ／ All the affair displays >>

肺高血圧症の治療の現状と移植適応両側生体部分肺移植後に肺リンパ脈管筋腫症再発を来たした一例

杉本龍士郎, 伊達洋至, 杉本誠一郎, 青江基, 豊岡伸一, 岡部和倫, 岡崎恵, 佐野由文

移植 41 ( 1 ) 57 - 58 2006.2

Mutational and epigenetic evidence for independent pathways for lung adenocarcinomas arising in smokers and never smokers. Reviewed

Toyooka S, Tokumo M, Shigematsu H, Matsuo K, Asano H, Tomii K, Ichihara S, Suzuki M, Aoe M, Date H, Gazdar AF, Shimizu N

Cancer research 66 ( 3 ) 1371 - 1375 2006.2

切除肺癌における再発と腫瘍マーカーの検討

増田紘子, 豊岡伸一, 宗淳一, 原田昌明, 末久弘, 青江基, 佐野由文, 岡部和倫, 伊達洋至, 清水信義

岡山医学会雑誌 117 ( 3 ) 258 - 258 2006.1

LTC-1 Bilateral phrenic nerve paralysis after livingdonor lobar lung transplantation : A case report(Lung Transplant Conference)

Sano Yoshifumi, Aoe Motoi, Toyooka Shinichi, Shigematsu Hisayuki, Okazaki Megumi, Date Hiroshi

The Journal of the Japanese Association for Chest Surgery 20 ( 3 ) 981 - 981 2006

P-501 原発性肺癌の孤立性転移性副腎腫瘍に対する腹腔鏡下副腎摘出術4例の検討(一般示説71 症例(2),世界をリードする呼吸器外科医に!,第23回日本呼吸器外科学会総会)

青江基, 井野川英利, 佐藤仁, 重松久之, 豊岡伸一, 佐野由文, 岡部和倫, 伊達洋至, 清水信義

日本呼吸器外科学会雑誌 20 ( 3 ) 966 - 966 2006

P-530 特発性喉頭・気管狭窄の2例(一般示説75 気道疾患,世界をリードする呼吸器外科医に!,第23回日本呼吸器外科学会総会)

脇直久, 豊岡伸一, 青江基, 伊達洋至, 清水信義

日本呼吸器外科学会雑誌 20 ( 3 ) 973 - 973 2006

OP20-2 Matched Pair Analysisを用いた原発性肺癌における開胸下肺葉切除術と胸腔鏡下肺葉切除術との比較(一般口演20 胸腔鏡,世界をリードする呼吸器外科医に!,第23回日本呼吸器外科学会総会)

重松久之, 豊岡伸一, 青江基, 岡部和倫, 佐野由文, 伊達洋至

日本呼吸器外科学会雑誌 20 ( 3 ) 828 - 828 2006

RP-022 肺転移性腫瘍の手術適応を考える : 多発例と単発例の臨床的比較(要望口演05 胚細胞性腫瘍・多発肺転移,世界をリードする呼吸器外科医に!,第23回日本呼吸器外科学会総会)

佐野由文, 重松久之, 豊岡伸一, 青江基, 岡部和倫, 伊達洋至

日本呼吸器外科学会雑誌 20 ( 3 ) 798 - 798 2006

多発肺癌におけるEGFR遺伝子の変異と増幅

市原周治, 豊岡伸一, 徳毛誠樹, 宗淳一, 末久弘, 浅野博昭, 富井邦年, 青江基, 佐野由文, 岡部和倫, 伊達洋至, 清水信義

肺癌 45 ( 5 ) 527 - 527 2005.11

原発性肺癌手術症例における術後気管支断端瘻発生症例の検討

青江基, 重松久之, 佐藤仁, 市原周治, 宗淳一, 豊岡伸一, 佐野由文, 岡部和倫, 伊達洋至, 清水信義

肺癌 45 ( 5 ) 640 - 640 2005.11

EGFR遺伝子変異と臨床病理学的因子の検討

原田昌明, 豊岡伸一, 市村浩一, 徳毛誠樹, 宗淳一, 末久弘, 青江基, 岡部和倫, 佐野由文, 伊達洋至, 清水信義

The Japanese Journal of THORACIC AND CARDIOVASCULAR SURGERY 53 ( Suppl.II ) 410 - 410 2005.9

EGFR遺伝子L858R変異を有するGefitinib非感受性肺癌の2例

豊岡伸一, 徳毛誠樹, 木浦勝行, 市原周治, 細川忍, 青江基, 佐野由文, 岡部和倫, 大橋圭明, 田端雅弘, 伊達洋至, 清水信義

日本癌治療学会誌 40 ( 2 ) 347 - 347 2005.9

切除肺癌における再発と腫瘍マーカーの検討

増田紘子, 豊岡伸一, 宗淳一, 原田昌明, 末久弘, 青江基, 佐野由文, 岡部和倫, 伊達洋至, 清水信義

The Japanese Journal of THORACIC AND CARDIOVASCULAR SURGERY 53 ( Suppl.II ) 544 - 544 2005.9

肺癌における病期とリンパ節郭清術前リンパ節転移の評価

豊岡伸一, 宗淳一, 末久弘, 青江基, 岡部和倫, 佐野由文, 伊達洋至, 清水信義

The Japanese Journal of THORACIC AND CARDIOVASCULAR SURGERY 53 ( Suppl.II ) 211 - 211 2005.9

当科における季節別に見た肺癌手術成績

宗淳一, 豊岡伸一, 末久弘, 青江基, 岡部和倫, 佐野由文, 伊達洋至, 清水信義

The Japanese Journal of THORACIC AND CARDIOVASCULAR SURGERY 53 ( Suppl.II ) 540 - 540 2005.9

EGFR mutation陽性肺非小細胞癌におけるgefitinibの有害反応に関する検討

藤原義朗, 豊岡伸一, 瀧川奈義夫, 田端雅弘, 徳毛誠樹, 青江基, 木浦勝行, 谷本光音

日本癌治療学会誌 40 ( 2 ) 522 - 522 2005.9

Antitumor effect of gefitinib ('Iressa') on esophageal squamous cell carcinoma cell lines in vitro and in vivo Reviewed

F Hara, M Aoe, H Doihara, N Taira, T Shien, H Takahashi, S Yoshitomi, K Tsukuda, S Toyooka, T Ohta, N Shimizu

CANCER LETTERS 226 ( 1 ) 37 - 47 2005.8

Language：English Publishing type：Research paper (scientific journal) Publisher：ELSEVIER IRELAND LTD

High expression of epidermal growth factor receptor (EGFR) is thought to be correlated with cell proliferation, invasion, metastasis, resistance to chemoradiotherapy, and poor prognosis in Various kinds of human cancers. Blockade of EGFR signal transduction can be a promising strategy for cancer therapy. Approximately 40-70% of esophageal squamous cell carcinomas (ESCCs) show high expression of EGFR. In this study, we examined the antitumor effect of gefitinib, an EGFR tyrosine kinase inhibitor, against ESCC cells in vitro and in vivo. In three ESCC cell lines (TE8, T.T and T.Tn), cell proliferation had been inhibited in a dose-dependent manner and IC(50) Values (respectively, 8.49, 18.9 and 17.3 mu M). Gefitinib inhibited EGF-induced autophosphorylation of EGFR and its downstream signaling pathways, Ras/Raf/MAPK and PI3K/Akt, and caused G(1) arrest of cell cycle and apoptosis confirmed with flow cytometry. We examined the effect of gefitinib on nude mice bearing established TE8 and T.T xenografts. Gefitimb (100 or 200 mg/kg once-daily, p.o.) showed antitumor activity in a dose-dependent manner, resulting in a significantly improved survival of treated mice as compared with untreated mice. Immunohistochemical examination of the harvested tumor was performed to examine the status of phosphorylated EGFR, PCNA, Factor VIII and apoptosis. We found inhibition of EGFR phosphorylation, cell cycle arrest (by PCNA staining), decrease of microvessel density (Factor VIII) and induction of apoptosis by TUNEL staining. In conclusion, our findings demonstrate that gefitinib is effective for growth inhibition of ESCC cell lines in vitro and in vivo and suggest that gefitinib may be one of the new therapeutic options for ESSC. (c) 2005 Elsevier Ireland Ltd. All rights reserved.

DOI： 10.1016/j.canlet.2004.12.025

Web of Science

researchmap

Promoter hypermethylation profile of ovarian epithelial neoplasms Reviewed

PB Makarla, MH Saboorian, R Ashfaq, KO Toyooka, S Toyooka, JD Minna, AF Gazdar, JO Schorge

CLINICAL CANCER RESEARCH 11 ( 15 ) 5365 - 5369 2005.8

Language：English Publishing type：Research paper (scientific journal) Publisher：AMER ASSOC CANCER RESEARCH

Purpose: Ovarian carcinomas are believed to arise de novo from surface epithelium, but the actual molecular pathogenesis is unknown. The aim of this study was to compare the promoter hypermethylation profiles of ovarian epithelial neoplasms to better understand the role of epigenetic silencing in carcinogenesis.
Experimental Design: We analyzed the DNA promoter methylation status of eight tumor suppressor and cancer-related genes (p16, RAR beta, E-cadherin H-cadherin, APC, GSTP1, MGMT, RASSF1A) in 23 benign cystadenomas, 23 low malignant potential (LMP) tumors, and 23 invasive carcinomas by methylation-specific PCR.
Results: Benign cystadenomas exhibited promoter hypermethylation in only two genes, p16 (13%) and E-cadherin (13%). LMP tumors also showed p16 (22%) and E-cadherin (17%) methylation, in addition to RAR beta (9%) and H-cadherin (4%). All eight genes were hypermethylated in invasive cancers at a frequency of 9% to 30%. The mean methylation index was highest in invasive tumors [0.20 versus 0.065 (LMP) and 0,033 (cystadenomas); P = 0.001]. Promoter methylation of at least one gene was most commonly observed among invasive cancers [78% versus 44% (LMP; P = 0.03) and 26% (cystadenomas; P = 0.0009)]. Three genes exhibited higher methylation frequencies in invasive tumors: RASSF1A (30% versus 0%; P = 0.0002), H-cadherin (22% versus 2%; P = 0.013), and APC (22% versus 0%; P = 0.003).
Conclusions: Promoter hypermethylation is a frequent epigenetic event that occurs most commonly in invasive epithelial ovarian carcinomas. The profile of aberrant methylation suggests that an accumulation of events at specific genes may trigger malignant transformation of some benign cystaclenomas and LMP tumors.

Web of Science

researchmap

EGFR mutation and response of lung cancer to gefitinib. Reviewed

Toyooka S, Kiura K, Mitsudomi T

The New England journal of medicine 352 ( 20 ) 2136; author reply 2136 2005.5

primary pericardial synovial sarcomaの1手術例

宗淳一, 青江基, 豊岡伸一, 岡部和倫, 佐野由文, 伊達洋至, 清水信義

日本呼吸器外科学会雑誌 19 ( 3 ) 373 - 373 2005.5

　 PREV - NEXT 　

< TOYOOKA Shinichi >

Papers - TOYOOKA Shinichi