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  1. Article ; Online: PD-L2 suppresses T cell signaling via coinhibitory microcluster formation and SHP2 phosphatase recruitment

    Tomohiro Takehara / Ei Wakamatsu / Hiroaki Machiyama / Wataru Nishi / Katsura Emoto / Miyuki Azuma / Kenzo Soejima / Koichi Fukunaga / Tadashi Yokosuka

    Communications Biology, Vol 4, Iss 1, Pp 1-

    2021  Volume 12

    Abstract: Takehara et al performed imaging analysis of microcluster formation between the PD-L1 and PD-L2, which are known to play a role in T cell activation in response to tumour cell signaling. Their analysis showed that the cluster formation inhibited T cell ... ...

    Abstract Takehara et al performed imaging analysis of microcluster formation between the PD-L1 and PD-L2, which are known to play a role in T cell activation in response to tumour cell signaling. Their analysis showed that the cluster formation inhibited T cell receptor signaling and could serve as a visual index for PD-L1/2-targeted cancer therapies.
    Keywords Biology (General) ; QH301-705.5
    Language English
    Publishing date 2021-05-01T00:00:00Z
    Publisher Nature Portfolio
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  2. Article: The FGF2 aptamer inhibits the growth of FGF2-FGFR pathway driven lung cancer cells

    Hamamoto, Junko / Hiroyuki Yasuda / Yosuke Nonaka / Masatoshi Fujiwara / Yoshikazu Nakamura / Kenzo Soejima / Tomoko Betsuyaku

    Biochemical and biophysical research communications. 2018 Sept. 10, v. 503, no. 3

    2018  

    Abstract: Cancers, including lung cancer, are a leading cause of death worldwide. To overcome this deadly disease, multiple modality inhibitors have been developed. These include cytotoxic agents, molecular targeted small molecules, such as tyrosine kinase ... ...

    Abstract Cancers, including lung cancer, are a leading cause of death worldwide. To overcome this deadly disease, multiple modality inhibitors have been developed. These include cytotoxic agents, molecular targeted small molecules, such as tyrosine kinase inhibitors, and neutralizing antibodies. An aptamer is a short single-stranded nucleic acid molecule that is selected in vitro from a large random sequence library based on its high and specific affinity to a target molecule. Aptamers can be applied to therapeutics of various types of diseases, including cancer, due to their strong and specific neutralizing activities. However, the efficacy of aptamer-based therapy for cancer cells is not well characterized. In this study, we aimed to show that the FGF2 aptamer is effective for the treatment of FGF2 dependent lung cancer cells. We previously developed PC9GR lung cancer cells, whose proliferation is dependent on EGFR and FGF2-FGFR pathways in a cell autonomous manner. Using PC9GR cells, we demonstrate that the addition of the FGF2 aptamer induces more significant inhibition of PC9GR cell proliferation than does the addition of EGFR inhibitor alone. Furthermore, the addition of the FGF2 aptamer more significantly inhibits the downstream signals and induces apoptosis to a higher extent than does the addition of EGFR inhibitor alone. Our results show that the FGF2 aptamer inhibits the growth of FGF2-FGFR pathway-dependent lung cancer cells. The findings provide preclinical evidence that aptamers can be useful for cancer treatment.
    Keywords DNA libraries ; apoptosis ; cell proliferation ; cytotoxicity ; death ; enzyme inhibitors ; lung neoplasms ; neoplasm cells ; neutralization ; neutralizing antibodies ; nucleic acids ; oligonucleotides ; protein-tyrosine kinases ; therapeutics
    Language English
    Dates of publication 2018-0910
    Size p. 1330-1334.
    Publishing place Elsevier Inc.
    Document type Article
    ZDB-ID 205723-2
    ISSN 0006-291X ; 0006-291X
    ISSN (online) 0006-291X
    ISSN 0006-291X
    DOI 10.1016/j.bbrc.2018.07.044
    Database NAL-Catalogue (AGRICOLA)

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  3. Article ; Online: Genotype-phenotype mapping of a patient-derived lung cancer organoid biobank identifies NKX2-1-defined Wnt dependency in lung adenocarcinoma

    Toshiki Ebisudani / Junko Hamamoto / Kazuhiro Togasaki / Akifumi Mitsuishi / Kai Sugihara / Taro Shinozaki / Takahiro Fukushima / Kenta Kawasaki / Takashi Seino / Mayumi Oda / Hikaru Hanyu / Kohta Toshimitsu / Katsura Emoto / Yuichiro Hayashi / Keisuke Asakura / Todd A. Johnson / Hideki Terai / Shinnosuke Ikemura / Ichiro Kawada /
    Makoto Ishii / Tomoyuki Hishida / Hisao Asamura / Kenzo Soejima / Hidewaki Nakagawa / Masayuki Fujii / Koichi Fukunaga / Hiroyuki Yasuda / Toshiro Sato

    Cell Reports, Vol 42, Iss 3, Pp 112212- (2023)

    2023  

    Abstract: Summary: Human lung cancer is a constellation of tumors with various histological and molecular properties. To build a preclinical platform that covers this broad disease spectrum, we obtained lung cancer specimens from multiple sources, including sputum ...

    Abstract Summary: Human lung cancer is a constellation of tumors with various histological and molecular properties. To build a preclinical platform that covers this broad disease spectrum, we obtained lung cancer specimens from multiple sources, including sputum and circulating tumor cells, and generated a living biobank consisting of 43 lines of patient-derived lung cancer organoids. The organoids recapitulated the histological and molecular hallmarks of the original tumors. Phenotypic screening of niche factor dependency revealed that EGFR mutations in lung adenocarcinoma are associated with the independence from Wnt ligands. Gene engineering of alveolar organoids reveals that constitutive activation of EGFR-RAS signaling provides Wnt independence. Loss of the alveolar identity gene NKX2-1 confers Wnt dependency, regardless of EGFR signal mutation. Sensitivity to Wnt-targeting therapy can be stratified by the expression status of NKX2-1. Our results highlight the potential of phenotype-driven organoid screening and engineering for the fabrication of therapeutic strategies to combat cancer.
    Keywords CP: Stem cell research ; CP: Cancer ; Biology (General) ; QH301-705.5
    Subject code 610
    Language English
    Publishing date 2023-03-01T00:00:00Z
    Publisher Elsevier
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  4. Article ; Online: Mimicking the niche of lung epithelial stem cells and characterization of several effectors of their in vitro behavior

    Ahmed E. Hegab / Daisuke Arai / Jingtao Gao / Aoi Kuroda / Hiroyuki Yasuda / Makoto Ishii / Katsuhiko Naoki / Kenzo Soejima / Tomoko Betsuyaku

    Stem Cell Research, Vol 15, Iss 1, Pp 109-

    2015  Volume 121

    Abstract: The niche surrounding stem cells regulate their fate during homeostasis and after injury or infection. The 3D organoid assay has been widely used to study stem cells behavior based on its capacity to evaluate self-renewal, differentiation and the effect ... ...

    Abstract The niche surrounding stem cells regulate their fate during homeostasis and after injury or infection. The 3D organoid assay has been widely used to study stem cells behavior based on its capacity to evaluate self-renewal, differentiation and the effect of various medium supplements, drugs and co-culture with supportive cells. We established an assay to study both lung and trachea stem cells in vitro. We characterized their proliferation and differentiation spectrum at baseline then evaluated the effect of co-culturing with fibroblasts and endothelial cells and/or treating with several biologically relevant substances as possible contributors to their niche. We found that lung epithelial (but not tracheal basal) stem cells require co-culture with stromal cells to undergo clonal proliferation and differentiation. Fibroblasts were more efficient than endothelial cells in offering this support and the pattern of support varied based on the tissue origin of the stromal cells. Treating distal lung epithelial or basal stem cells with FGF2, FGF9, FGF10, LIF as well as ALK5 and ROCK inhibitors increased their colony formation efficiency and resulted in variable effects on colonies number, size and differentiation spectrum. This model and findings pave the way for better understanding of lung stem cell niche components and factors that can manipulate lung stem cell behavior.
    Keywords Biology (General) ; QH301-705.5
    Subject code 571
    Language English
    Publishing date 2015-07-01T00:00:00Z
    Publisher Elsevier
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  5. Article ; Online: DNA methylation profiles at precancerous stages associated with recurrence of lung adenocarcinoma.

    Takashi Sato / Eri Arai / Takashi Kohno / Koji Tsuta / Shun-ichi Watanabe / Kenzo Soejima / Tomoko Betsuyaku / Yae Kanai

    PLoS ONE, Vol 8, Iss 3, p e

    2013  Volume 59444

    Abstract: The aim of this study was to clarify the significance of DNA methylation alterations at precancerous stages of lung adenocarcinoma. Using single-CpG resolution Infinium array, genome-wide DNA methylation analysis was performed in 36 samples of normal ... ...

    Abstract The aim of this study was to clarify the significance of DNA methylation alterations at precancerous stages of lung adenocarcinoma. Using single-CpG resolution Infinium array, genome-wide DNA methylation analysis was performed in 36 samples of normal lung tissue obtained from patients without any primary lung tumor, 145 samples of non-cancerous lung tissue (N) obtained from patients with lung adenocarcinomas, and 145 samples of tumorous tissue (T). Stepwise progression of DNA methylation alterations from normal lung tissue to non-cancerous lung tissue obtained from patients with lung adenocarcinomas, and then tumorous tissue samples, was observed at 3,270 CpG sites, suggesting that non-cancerous lung tissue obtained from patients with lung adenocarcinomas was at precancerous stages with DNA methylation alterations. At CpG sites of 2,083 genes, DNA methylation status in samples of non-cancerous lung tissue obtained from patients with lung adenocarcinomas was significantly correlated with recurrence after establishment of lung adenocarcinomas. Among such recurrence-related genes, 28 genes are normally unmethylated (average β-values based on Infinium assay in normal lung tissue samples was less than 0.2) and their DNA hypermethylation at precancerous stages was strengthened during progression to lung adenocarcinomas (Δβ(T-N)>0.1). Among these 28 genes, we focused on 6 for which implications in transcription regulation, apoptosis or cell adhesion had been reported. DNA hypermethylation of the ADCY5, EVX1, GFRA1, PDE9A, and TBX20 genes resulted in reduced mRNA expression in tumorous tissue samples. 5-Aza-2'-deoxycytidine treatment of lung cancer cell lines restored the mRNA expression levels of these 5 genes. Reduced mRNA expression in tumorous tissue samples was significantly correlated with tumor aggressiveness. These data suggest that DNA methylation alterations at precancerous stages determine tumor aggressiveness and outcome through silencing of specific genes.
    Keywords Medicine ; R ; Science ; Q
    Language English
    Publishing date 2013-01-01T00:00:00Z
    Publisher Public Library of Science (PLoS)
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  6. Article ; Online: Safety of postoperative administration of human urinary trypsin inhibitor in lung cancer patients with idiopathic pulmonary fibrosis.

    Yoshikane Yamauchi / Yotaro Izumi / Masanori Inoue / Hiroaki Sugiura / Taichiro Goto / Masaki Anraku / Takashi Ohtsuka / Mitsutomo Kohno / Kenzo Soejima / Hiroaki Nomori

    PLoS ONE, Vol 6, Iss 12, p e

    2011  Volume 29053

    Abstract: Patients with idiopathic pulmonary fibrosis (IPF) undergoing pulmonary resection for lung cancer carry risks of acute exacerbations of IPF (AE) postoperatively. Currently, agents which may attenuate AE are actively sought. Urinary trypsin inhibitor, ... ...

    Abstract Patients with idiopathic pulmonary fibrosis (IPF) undergoing pulmonary resection for lung cancer carry risks of acute exacerbations of IPF (AE) postoperatively. Currently, agents which may attenuate AE are actively sought. Urinary trypsin inhibitor, ulinastatin, is a synthetic glycoprotein which may potentially inhibit various inflammatory factors associated with the development and progression of IPF. The present study was done to evaluate the effects of administration of high dose ulinastatin in lung cancer patients with IPF immediately following lung resection.Patients with IPFs radiologically diagnosed on high resolution CT, and histologically diagnosed resectable lung cancers, were eligible for the study. The effects of escalating doses of ulinastatin 3×10(5), 6×10(5), and 9×10(5) units/body/day, administered postoperatively for 3 days were evaluated. The endpoints were safety and feasibility.Nine patients were evaluated, in cohorts of 3 patients per dosage. Postoperative follow up ranged from 3 to 12 months (median 9 months). The postoperative courses were uneventful in all patients. No subjective adverse events such as abdominal symptoms or skin rashes, or objective adverse events as per serum laboratory tests, such as liver or kidney dysfunctions potentially attributable to ulinastatin administration were observed. AE was seen in one patient at 3 months after surgery, but since this occurred shortly after administration of chemotherapy, it was considered to be attributable to the chemotherapy rather than surgery.Ulinastatin administration after lung resection in lung cancer patients with IPF was considered to be safe and feasible. Further study is planned at the highest dose of this study to evaluate efficacy.UMIN.ac.jp/ctr/UMIN000002410.
    Keywords Medicine ; R ; Science ; Q
    Subject code 610 ; 616
    Language English
    Publishing date 2011-01-01T00:00:00Z
    Publisher Public Library of Science (PLoS)
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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