7 results match your criteria: "Hiroshima University. Electronic address: nhattori@hiroshima-u.ac.jp.[Affiliation]"

Role of PAI-1 in the progression and treatment resistance of non-small cell lung cancer.

Biomed J

September 2025

Department of Molecular and Internal Medicine, Graduate School of Biomedical and Health Sciences, Hiroshima University. Electronic address:

Background: Lung cancer is the leading cause of cancer-related mortality worldwide. Although immune checkpoint inhibitors (ICIs), chemotherapy, and molecular targeted therapies have improved survival rates, therapeutic resistance remains a major barrier to curative outcomes. Recently, plasminogen activator inhibitor-1 (PAI-1) has been implicated in lung cancer progression and treatment resistance.

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Suplatast tosilate reduces radiation-induced lung injury in mice through suppression of oxidative stress.

Free Radic Biol Med

May 2019

Department of Molecular and Internal Medicine, Graduate School of Biomedical & Health Sciences, Hiroshima University, 1-2-3 Kasumi, Minami-ku, Hiroshima, 734-8551, Japan. Electronic address:

Purpose: Although radiotherapy is important in the treatment of malignant thoracic tumors, it has harmful effects on healthy tissues. We previously showed that suplatast tosilate, an anti-allergic agent, scavenged reactive oxygen species (ROS), including hydroxyl radicals. Because ROS-mediated oxidative stress is involved in radiation-induced lung injury, we hypothesized that suplatast tosilate could reduce radiation-induced lung injury via suppression of oxidative stress.

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Article Synopsis
  • Polymorphic epithelial mucin (MUC1) is overexpressed in many adenocarcinomas, including breast cancer, and is linked to resistance against chemotherapy and immune evasion.
  • This study investigates how MUC1 expression levels and distribution impact the effectiveness of trastuzumab-mediated antibody-dependent cell-mediated cytotoxicity (ADCC) in breast cancer cells.
  • Findings reveal that breast cancer cells with high and uniform MUC1 expression resist trastuzumab treatment, but this resistance can be reversed with MUC1 knockdown or anti-KL-6/MUC1 antibodies, suggesting both the amount and arrangement of MUC1 affect treatment sensitivity.
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Intratracheal Administration of siRNA Dry Powder Targeting Vascular Endothelial Growth Factor Inhibits Lung Tumor Growth in Mice.

Mol Ther Nucleic Acids

September 2018

Department of Molecular and Internal Medicine, Graduate School of Biomedical & Health Sciences, Hiroshima University, 1-2-3 Kasumi, Minami-ku, Hiroshima 734-8551, Japan. Electronic address:

Inhalation therapy using small-interfering RNA (siRNA) is a potentially effective therapeutic strategy for lung cancer because of its high gene-silencing effects and sequence specificity. Previous studies reported that intratracheal administration of siRNA using pressurized metered dose inhalers or nebulizers could suppress tumor growth in murine lung metastatic models. Although dry powder inhalers are promising devices due to their low cost, good portability, and preservability, the anti-tumor effects of siRNA dry powder have not been elucidated.

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Suplatast tosilate protects the lung against hyperoxic lung injury by scavenging hydroxyl radicals.

Free Radic Biol Med

May 2017

Department of Molecular and Internal Medicine, Graduate School of Biomedical & Health Sciences, Hiroshima University, 1-2-3 Kasumi, Minami-ku, Hiroshima, Hiroshima 734-8551, Japan. Electronic address:

Prolonged exposure to hyperoxia produces extraordinary amounts of reactive oxygen species (ROS) in the lung and causes hyperoxic lung injury. Although supraphysiological oxygen is routinely administered for the management of respiratory failure, there is no effective strategy to prevent hyperoxic lung injury. In our previous study, we showed that suplatast tosilate, an asthma drug that inhibits T helper 2 (Th2) cytokines, ameliorated bleomycin-induced lung injury and fibrosis through Th2-independent mechanisms.

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FAM13A polymorphism as a prognostic factor in patients with idiopathic pulmonary fibrosis.

Respir Med

February 2017

Department of Molecular and Internal Medicine, Graduate School of Biomedical Science, Hiroshima University, Hiroshima, Japan; Hiroshima Cosmopolitan University, Hiroshima, Japan. Electronic address:

Background: Family with sequence similarity 13, member A (FAM13A) variants have been associated with susceptibility to chronic lung diseases. A recent genome-wide association study has shown an association between a polymorphism in FAM13A rs2609255 and idiopathic interstitial pneumonias in a Caucasian population. However, the relationship between rs2609255 polymorphism and prognosis in idiopathic interstitial pneumonias has not been investigated.

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Background: Acute exacerbation (AE) is a major cause of death in idiopathic pulmonary fibrosis (IPF). However, little is known about sensitive biomarkers for predicting AE. The aim of our study was to investigate the significance of KL-6 and CC-Chemokine Ligand 18 (CCL18) as predictors for AE of IPF.

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