start-ver=1.4
cd-journal=joma
no-vol=7
cd-vols=
no-issue=4
article-no=
start-page=e33544
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2012
dt-pub=20120412
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=A Model of Cancer Stem Cells Derived from Mouse Induced Pluripotent Stem Cells
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Cancer stem cells (CSCs) are capable of continuous proliferation and self-renewal and are proposed to play significant roles in oncogenesis, tumor growth, metastasis and cancer recurrence. CSCs are considered derived from normal stem cells affected by the tumor microenvironment although the mechanism of development is not clear yet. In 2007, Yamanaka's group succeeded in generating Nanog mouse induced pluripotent stem (miPS) cells, in which green fluorescent protein (GFP) has been inserted into the 5'-untranslated region of the Nanog gene. Usually, iPS cells, just like embryonic stem cells, are considered to be induced into progenitor cells, which differentiate into various normal phenotypes depending on the normal niche. We hypothesized that CSCs could be derived from Nanog miPS cells in the conditioned culture medium of cancer cell lines, which is a mimic of carcinoma microenvironment. As a result, the Nanog miPS cells treated with the conditioned medium of mouse Lewis lung carcinoma acquired characteristics of CSCs, in that they formed spheroids expressing GFP in suspension culture, and had a high tumorigenicity in Balb/c nude mice exhibiting angiogenesis in vivo. In addition, these iPS-derived CSCs had a capacity of self-renewal and expressed the marker genes, Nanog, Rex1, Eras, Esg1 and Cripto, associated with stem cell properties and an undifferentiated state. Thus we concluded that a model of CSCs was originally developed from miPS cells and proposed the conditioned culture medium of cancer cell lines might perform as niche for producing CSCs. The model of CSCs and the procedure of their establishment will help study the genetic alterations and the secreted factors in the tumor microenvironment which convert miPS cells to CSCs. Furthermore, the identification of potentially bona fide markers of CSCs, which will help the development of novel anti-cancer therapies, might be possible though the CSC model.
en-copyright=
kn-copyright=
en-aut-name=ChenLing
en-aut-sei=Chen
en-aut-mei=Ling
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=
en-aut-name=KasaiTomonari
en-aut-sei=Kasai
en-aut-mei=Tomonari
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=
en-aut-name=LiYueguang
en-aut-sei=Li
en-aut-mei=Yueguang
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=
en-aut-name=SugiiYuh
en-aut-sei=Sugii
en-aut-mei=Yuh
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=
en-aut-name=JinGuoliang
en-aut-sei=Jin
en-aut-mei=Guoliang
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=
en-aut-name=OkadaMasashi
en-aut-sei=Okada
en-aut-mei=Masashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=
en-aut-name=VaidyanathArun
en-aut-sei=Vaidyanath
en-aut-mei=Arun
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=
en-aut-name=MizutaniAkifumi
en-aut-sei=Mizutani
en-aut-mei=Akifumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=
en-aut-name=SatohAyano
en-aut-sei=Satoh
en-aut-mei=Ayano
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=
en-aut-name=KudohTakayuki
en-aut-sei=Kudoh
en-aut-mei=Takayuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=
en-aut-name=HendrixMary J. C.
en-aut-sei=Hendrix
en-aut-mei=Mary J. C.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=
en-aut-name=SalomonDavid S
en-aut-sei=Salomon
en-aut-mei=David S
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=
en-aut-name=FuLi
en-aut-sei=Fu
en-aut-mei=Li
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=
en-aut-name=SenoMasaharu
en-aut-sei=Seno
en-aut-mei=Masaharu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=
affil-num=1
en-affil=
kn-affil=Okayama Univ
affil-num=2
en-affil=
kn-affil=Okayama Univ
affil-num=3
en-affil=
kn-affil=Tianjin 4th Ctr Hosp
affil-num=4
en-affil=
kn-affil=Okayama Univ
affil-num=5
en-affil=
kn-affil=Okayama Univ
affil-num=6
en-affil=
kn-affil=Okayama Univ
affil-num=7
en-affil=
kn-affil=Okayama Univ
affil-num=8
en-affil=
kn-affil=Okayama Univ
affil-num=9
en-affil=
kn-affil=Okayama Univ
affil-num=10
en-affil=
kn-affil=Okayama Univ
affil-num=11
en-affil=
kn-affil=Northwestern Univ
affil-num=12
en-affil=
kn-affil=NCI
affil-num=13
en-affil=
kn-affil=Tianjin Med Univ
affil-num=14
en-affil=
kn-affil=Okayama Univ
END
start-ver=1.4
cd-journal=joma
no-vol=73
cd-vols=
no-issue=4
article-no=
start-page=1049
end-page=1054
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2009
dt-pub=20090315
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Analysis of Factors Associated With Radiation-Induced Bronchiolitis Obliterans Organizing Pneumonia Syndrome After Breast-Conserving Therapy
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Purpose: To evaluate factors associated with radiation-induced bronchiolitis obliterans organizing pneumonia (BOOP) syndrome after breast-conserving therapy.
Methods and materials: A total of 702 women with breast cancer who received radiotherapy after breast-conserving surgery at seven institutions between July 1995 and December 2006 were analyzed. In all patients, the whole breast was irradiated with two tangential photon beams. The criteria used for the diagnosis of radiation-induced BOOP syndrome were as follows: (1) radiotherapy to the breast within 12 months, (2) general and/or respiratory symptoms lasting for >or=2 weeks, (3) radiographs showing lung infiltration outside the radiation port, and (4) no evidence of a specific cause.
Results: Radiation-induced BOOP syndrome was seen in 16 patients (2.3%). Eleven patients (68.8%) were administered steroids. The duration of steroid administration ranged from 1 week to 3.7 years (median, 1.1 years). Multivariate analysis revealed that age (>or=50 years; odds ratio [OR] 8.88; 95% confidence interval [CI] 1.16-67.76; p = 0.04) and concurrent endocrine therapy (OR 3.05; 95% CI 1.09-8.54; p = 0.03) were significantly associated with BOOP syndrome. Of the 161 patients whose age was >or=50 years and who received concurrent endocrine therapy, 10 (6.2%) developed BOOP syndrome.
Conclusions: Age (>or=50 years) and concurrent endocrine therapy can promote the development of radiation-induced BOOP syndrome after breast-conserving therapy. Physicians should carefully follow patients who received breast-conserving therapy, especially those who are older than 50 years and received concurrent endocrine therapy during radiotherapy.
en-copyright=
kn-copyright=
en-aut-name=KatayamaNorihisa
en-aut-sei=Katayama
en-aut-mei=Norihisa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=
en-aut-name=SatoShuhei
en-aut-sei=Sato
en-aut-mei=Shuhei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=
en-aut-name=KatsuiKuniaki
en-aut-sei=Katsui
en-aut-mei=Kuniaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=
en-aut-name=TakemotoMitsuhiro
en-aut-sei=Takemoto
en-aut-mei=Mitsuhiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=
en-aut-name=TsudaToshihide
en-aut-sei=Tsuda
en-aut-mei=Toshihide
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=
en-aut-name=YoshidaAtsushi
en-aut-sei=Yoshida
en-aut-mei=Atsushi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=
en-aut-name=MoritoTsuneharu
en-aut-sei=Morito
en-aut-mei=Tsuneharu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=
en-aut-name=NakagawaTomio
en-aut-sei=Nakagawa
en-aut-mei=Tomio
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=
en-aut-name=MizutaniAkifumi
en-aut-sei=Mizutani
en-aut-mei=Akifumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=
en-aut-name=WakiTakahiro
en-aut-sei=Waki
en-aut-mei=Takahiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=
en-aut-name=NiiyaHarutaka
en-aut-sei=Niiya
en-aut-mei=Harutaka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=
en-aut-name=KanazawaSusumu
en-aut-sei=Kanazawa
en-aut-mei=Susumu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=
affil-num=1
en-affil=Department of Radiology, Okayama University Hospital
kn-affil=
affil-num=2
en-affil=Department of Radiology, Okayama University Hospital
kn-affil=
affil-num=3
en-affil=Department of Radiology, Okayama University Hospital
kn-affil=
affil-num=4
en-affil=Department of Radiology, Okayama University Hospital
kn-affil=
affil-num=5
en-affil=Department of Radiology, Okayama University Hospital
kn-affil=
affil-num=6
en-affil=Department of Radiology, Okayama University Hospital
kn-affil=
affil-num=7
en-affil=Department of Radiology, Okayama University Hospital
kn-affil=
affil-num=8
en-affil=Department of Radiology, Okayama University Hospital
kn-affil=
affil-num=9
en-affil=Department of Radiology, Okayama University Hospital
kn-affil=
affil-num=10
en-affil=Department of Radiology, Okayama University Hospital
kn-affil=
affil-num=11
en-affil=Department of Radiology, Okayama University Hospital
kn-affil=
affil-num=12
en-affil=Department of Radiology, Okayama University Hospital
kn-affil=
en-keyword=Breast cancer
kn-keyword=Breast cancer
en-keyword=Breast-conserving surgery
kn-keyword=Breast-conserving surgery
en-keyword=Radiotherapy
kn-keyword=Radiotherapy
en-keyword=Radiation-induced BOOP syndrome
kn-keyword=Radiation-induced BOOP syndrome
en-keyword=Endocrine therapy
kn-keyword=Endocrine therapy
END
start-ver=1.4
cd-journal=joma
no-vol=9
cd-vols=
no-issue=9
article-no=
start-page=e107976
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2014
dt-pub=20140929
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Efficient Drug Delivery of Paclitaxel Glycoside: A Novel Solubility Gradient Encapsulation into Liposomes Coupled with Immunoliposomes Preparation
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Although the encapsulation of paclitaxel into liposomes has been extensively studied, its significant hydrophobic and uncharged character has generated substantial difficulties concerning its efficient encapsulation into the inner water core of liposomes. We found that a more hydrophilic paclitaxel molecule, 7-glucosyloxyacetylpaclitaxel, retained tubulin polymerization stabilization activity. The hydrophilic nature of 7-glucosyloxyacetylpaclitaxel allowed its efficient encapsulation into the inner water core of liposomes, which was successfully accomplished using a remote loading method with a solubility gradient between 40% ethylene glycol and Cremophor EL/ethanol in PBS. Trastuzumab was then conjugated onto the surface of liposomes as immunoliposomes to selectively target human epidermal growth factor receptor-2 (HER2)-overexpressing cancer cells. In vitro cytotoxicity assays revealed that the immunoliposomes enhanced the toxicity of 7-glucosyloxyacetylpaclitaxel in HER2-overexpressing cancer cells and showed more rapid suppression of cell growth. The immunoliposomes strongly inhibited the tumor growth of HT-29 cells xenografted in nude mice. Notably, mice survived when treated with the immunoliposomes formulation, even when administered at a lethal dose of 7-glucosyloxyacetylpaclitaxel in vivo. This data successfully demonstrates immunoliposomes as a promising candidate for the efficient delivery of paclitaxel glycoside.
en-copyright=
kn-copyright=
en-aut-name=ShigehiroTsukasa
en-aut-sei=Shigehiro
en-aut-mei=Tsukasa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=
en-aut-name=KasaiTomonari
en-aut-sei=Kasai
en-aut-mei=Tomonari
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=
en-aut-name=MurakamiMasaharu
en-aut-sei=Murakami
en-aut-mei=Masaharu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=
en-aut-name=SekharSreeja C.
en-aut-sei=Sekhar
en-aut-mei=Sreeja C.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=
en-aut-name=TominagaYuki
en-aut-sei=Tominaga
en-aut-mei=Yuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=
en-aut-name=OkadaMasashi
en-aut-sei=Okada
en-aut-mei=Masashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=
en-aut-name=KudohTakayuki
en-aut-sei=Kudoh
en-aut-mei=Takayuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=
en-aut-name=MizutaniAkifumi
en-aut-sei=Mizutani
en-aut-mei=Akifumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=
en-aut-name=MurakamiHiroshi
en-aut-sei=Murakami
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=
en-aut-name=SalomonDavid S.
en-aut-sei=Salomon
en-aut-mei=David S.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=
en-aut-name=MikuniKatsuhiko
en-aut-sei=Mikuni
en-aut-mei=Katsuhiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=
en-aut-name=MandaiTadakatsu
en-aut-sei=Mandai
en-aut-mei=Tadakatsu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=
en-aut-name=HamadaHiroki
en-aut-sei=Hamada
en-aut-mei=Hiroki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=
en-aut-name=SenoMasaharu
en-aut-sei=Seno
en-aut-mei=Masaharu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=
affil-num=1
en-affil=
kn-affil=Department of Biotechnology, Graduate School of Natural Science and Technology, Okayama University
affil-num=2
en-affil=
kn-affil=Department of Biotechnology, Graduate School of Natural Science and Technology, Okayama University
affil-num=3
en-affil=
kn-affil=Department of Biotechnology, Graduate School of Natural Science and Technology, Okayama University
affil-num=4
en-affil=
kn-affil=Department of Biotechnology, Graduate School of Natural Science and Technology, Okayama University
affil-num=5
en-affil=
kn-affil=Department of Biotechnology, Graduate School of Natural Science and Technology, Okayama University
affil-num=6
en-affil=
kn-affil=Department of Biotechnology, Graduate School of Natural Science and Technology, Okayama University
affil-num=7
en-affil=
kn-affil=Department of Biotechnology, Graduate School of Natural Science and Technology, Okayama University
affil-num=8
en-affil=
kn-affil=Department of Biotechnology, Graduate School of Natural Science and Technology, Okayama University
affil-num=9
en-affil=
kn-affil=Department of Biotechnology, Graduate School of Natural Science and Technology, Okayama University
affil-num=10
en-affil=
kn-affil=Mouse Cancer Genetics Program, Center for Cancer Research, National Cancer Institute
affil-num=11
en-affil=
kn-affil=Ensuiko Sugar Refining Co., Ltd.
affil-num=12
en-affil=
kn-affil=Faculty of Life Science, Kurashiki University of Science and the Arts
affil-num=13
en-affil=
kn-affil=Faculty of Science, Okayama University of Science
affil-num=14
en-affil=
kn-affil=Department of Biotechnology, Graduate School of Natural Science and Technology, Okayama University
END
start-ver=1.4
cd-journal=joma
no-vol=69
cd-vols=
no-issue=3
article-no=
start-page=145
end-page=153
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2015
dt-pub=201506
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Eosinophil Cationic Protein Shows Survival Effect on H9c2 Cardiac Myoblast Cells with Enhanced Phosphorylation of ERK and Akt/GSK-3β under Oxidative Stress
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Eosinophil cationic protein (ECP) is well known as a cationic protein contained in the basic granules of activated eosinophils. Recent studies have reported that ECP exhibits novel activities on various types of cells, including rat neonatal cardiomyocytes. Here we evaluated the effects of ECP on rat cardiac myoblast H9c2 cells. Our results showed that ECP enhanced the survival of the cells, in part by promoting the ERK and Akt/GSK-3β signaling pathways. ECP attenuated the cytotoxic effects of H2O2 on H9c2 cells as well as the production of reactive oxygen species, the number of apoptotic cells and caspase 3/7 activity in the cells. In conclusion, ECP activated the ERK and Akt/GSK-3β pathways, resulting in anti-oxidative effects on H9c2 cells that attenuated apoptosis.
en-copyright=
kn-copyright=
en-aut-name=IshiiHiroko
en-aut-sei=Ishii
en-aut-mei=Hiroko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=
en-aut-name=KamikawaShigeshi
en-aut-sei=Kamikawa
en-aut-mei=Shigeshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=
en-aut-name=HirohataSatoshi
en-aut-sei=Hirohata
en-aut-mei=Satoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=
en-aut-name=MizutaniAkifumi
en-aut-sei=Mizutani
en-aut-mei=Akifumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=
en-aut-name=AbeKoji
en-aut-sei=Abe
en-aut-mei=Koji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=
en-aut-name=SenoMasaharu
en-aut-sei=Seno
en-aut-mei=Masaharu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=
en-aut-name=OohashiToshitaka
en-aut-sei=Oohashi
en-aut-mei=Toshitaka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=
en-aut-name=NinomiyaYoshifumi
en-aut-sei=Ninomiya
en-aut-mei=Yoshifumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=
affil-num=1
en-affil=
kn-affil=Departments of Molecular Biology and Biochemistry, Okayama University Graduate School of Medicine
affil-num=2
en-affil=
kn-affil=Departments of Molecular Biology and Biochemistry, Okayama University Graduate School of Medicine
affil-num=3
en-affil=
kn-affil=Departments of Molecular Biology and Biochemistry, Okayama University Graduate School of Medicine
affil-num=4
en-affil=
kn-affil=Department of Chemistry and Biotechnology, Graduate School of Natural Science and Technology, Okayama University
affil-num=5
en-affil=
kn-affil=Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences,
affil-num=6
en-affil=
kn-affil=Department of Chemistry and Biotechnology, Graduate School of Natural Science and Technology, Okayama University
affil-num=7
en-affil=
kn-affil=Departments of Molecular Biology and Biochemistry, Okayama University Graduate School of Medicine
affil-num=8
en-affil=
kn-affil=Departments of Molecular Biology and Biochemistry, Okayama University Graduate School of Medicine
en-keyword=ECP
kn-keyword=ECP
en-keyword=reactive oxygen species
kn-keyword=reactive oxygen species
en-keyword=Akt
kn-keyword=Akt
en-keyword=ERK
kn-keyword=ERK
END