šŸ‘¤ Koji Okabayashi

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3
Articles
2
Name variants
Also published as: Haruka Okabayashi,
articles

Acquisition of

Naoki Fukunaga, Hideki Terai, Rui Nomura +17 more Ā· 2025 Ā· JTO clinical and research reports Ā· Elsevier Ā· added 2026-04-24
Histologic transformation from adenocarcinoma to SCLC is a recognized mechanism of resistance in lung cancer. However, the transformation into squamous cell carcinoma is less common, and the associate Show more
Histologic transformation from adenocarcinoma to SCLC is a recognized mechanism of resistance in lung cancer. However, the transformation into squamous cell carcinoma is less common, and the associated genomic alterations remain unclear. Here, we present a case of lung adenocarcinoma harboring an EGFR ( Show less
šŸ“„ PDF DOI: 10.1016/j.jtocrr.2025.100862
FGFR1
Haruka Okabayashi, Miki Yasuda, Chinatsu Nii +5 more Ā· 2024 Ā· Biological & pharmaceutical bulletin Ā· added 2026-04-24
Plasmalogens are a family of glycerophospholipids containing one vinyl-ether bond at the sn-1 position in the glycerol backbone, and play important roles in cellular homeostasis including neural trans Show more
Plasmalogens are a family of glycerophospholipids containing one vinyl-ether bond at the sn-1 position in the glycerol backbone, and play important roles in cellular homeostasis including neural transmission. Therefore, reductions of plasmalogens have been associated with neurodegenerative disorders, such as Alzheimer's disease (AD). To evaluate the potential protective effects of plasmalogens against the pathology of AD, protein expression levels of key factors in amyloid precursor protein (APP) metabolic processes were examined using human neuroblastoma SH-SY5Y cells. Here, phosphatidylcholine-plasmalogen-oleic acid (PC-PLS-18) was shown to reduce protein expression levels of β-site APP cleaving enzyme 1 (BACE1), clusterin, and Tau, factors involved in the amyloid β-associated pathogenesis of AD. Thus, PC-PLS-18 may have preventive effects against AD by delaying the onset risk for a certain period. Show less
no PDF DOI: 10.1248/bpb.b23-00787
BACE1
Shodai Mizuno, Ryo Seishima, Juntaro Yamasaki +8 more Ā· 2022 Ā· Journal of cancer research and clinical oncology Ā· Springer Ā· added 2026-04-24
Angiopoietin-like 4 (ANGPTL4) was recently shown to be associated with cancer progression but little is known about its contribution to cancer metabolism. The purpose of this study was to elucidate th Show more
Angiopoietin-like 4 (ANGPTL4) was recently shown to be associated with cancer progression but little is known about its contribution to cancer metabolism. The purpose of this study was to elucidate the role of ANGPTL4 in glucose metabolism in colorectal cancer (CRC). Immunohistochemical staining of CRC specimens classified 84 patients into two groups according to ANGPTL4 expression. Clinicopathological characteristics, gene mutation status obtained by next-generation sequencing, and fluorodeoxyglucose (FDG) uptake measured by positron emission tomography/computed tomography (PET/CT) were compared between the two groups. Furthermore, the impact of ANGPTL4 expression on cancer metabolism was investigated by a subcutaneous xenograft mouse model using the ANGPTL4 knockout CRC cell line, and glucose transporter (GLUT) expression was evaluated. There were significantly more cases of T3/4 tumours (94.3% vs. 57.1%, P < 0.001) and perineural invasion (42.9% vs. 22.4%, P = 0.046) in the ANGPTL4-high group than in the low group. Genetic exploration revealed a higher frequency of KRAS mutation (54.3% vs. 22.4%, P = 0.003) in the ANGPTL4-high tumours. All the FDG uptake parameters were significantly higher in ANGPTL4-high tumours. In vivo analysis showed a significant reduction in tumour size due to ANGPTL4 knockout with lower expression of GLUT1 and GLUT3, and suppression of AKT phosphorylation. ANGPTL4 regulates the expression of GLUTs by activating the PI3K-AKT pathway and thereby promoting glucose metabolism in CRC. These findings establish a new functional role of ANGPTL4 in cancer progression and lay the foundation for developing a novel therapeutic target. Show less
no PDF DOI: 10.1007/s00432-022-03960-z
ANGPTL4