Kyushu University · Medicine
Professor Naoki Ikenaga's research lab focuses on the molecular mechanisms underlying tumor microenvironment remodeling and fibrotic stroma formation in gastrointestinal cancers, particularly pancreatic ductal adenocarcinoma (PDAC) and liver fibrosis. The lab investigates key regulators such as LOXL2 and kindlin-2 in extracellular matrix remodeling and cancer progression, as well as the role of intratumoral bacteria like *Fusobacterium nucleatum* in shaping the immune microenvironment and influencing clinical outcomes. A central theme is identifying novel therapeutic targets through the integration of cancer biology, fibrosis, and tumor microbiome research. The lab also evaluates surgical outcomes, particularly in laparoscopic-assisted distal gastrectomy, with a focus on quality of life and long-term patient outcomes.
Figures are computed from collected data and may differ slightly.
LOXL2 mediates collagen crosslinking and fibrotic matrix stabilisation during liver fibrosis, and independently promotes fibrogenic HPC differentiation. By blocking these two convergent profibrotic pathways, therapeutic LOXL2 inhibition attenuates both parenchymal and biliary fibrosis and promotes fibrosis reversal.
Several studies have revealed the diagnostic value of fluorodeoxyglucose-positron emission tomography for breast carcinomas. However, breast carcinomas display considerable variation in 18F-labeled 2-fluoro-2-deoxy-D-glucose uptake, and few papers have reported the clinical utility of the standardized uptake values (SUV). The purpose of this study is to investigate the relationship between SUV assessed by positron emission tomography (PET) and the clinicopathological characteristics of breast ca
Intratumor bacteria modify the tumor immune microenvironment and influence outcomes of various tumors. Periodontal pathogen Fusobacterium nucleatum has been detected in pancreatic cancer tissues and is associated with poor prognosis. However, it remains unclear how F. nucleatum affects pancreatic cancer. Here, we compared clinical features with F. nucleatum colonization in pancreatic cancer tissues. F. nucleatum was detected in 15.5% (13/84) of pancreatic cancer patients. The tumor size was sign
Pancreatic cancer cells are capable of collagen internalization, which is enhanced by EMT. This ECM clearance system may be a novel mechanism for cellular invasion and a potential therapeutic target in pancreatic cancer.
Kindlin-2 expression in stromal components is significantly associated with poor prognosis of patients with PDAC, suggesting that kindlin-2 is a prognostic marker for patients with PDAC.
LADG has an equivocal effect on long-term quality of life. Satisfaction with the surgical procedure was greater in patients who underwent the LADG method; however, complications that impaired the quality of life were also seen. The usefulness of LADG should be assessed in view of the immediate and relatively short-term outcomes and their effect on long-term quality of life.
Suppression of an epithelial marker and over expression of a mesenchymal marker suggest that epithelial-mesenchymal transition is induced in CD105(+) pancreatic cancer cells. CD105(+) pancreatic cancer cell migration is strongly enhanced by PSCs, suggesting that these cells play a role in the pancreatic cancer microenvironment.
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