Kyushu University · Medicine
Professor Kentaro Tanaka's research lab focuses on molecular mechanisms underlying immune regulation and cancer development, particularly in T cell differentiation and hepatocellular carcinoma. The lab investigates key signaling molecules such as SOCS1 in autoimmune diseases and explores hormonal and genetic factors contributing to cancer progression, including EGFR mutations in non-small cell lung cancer. Their work bridges immunology, oncology, and molecular medicine to identify therapeutic targets and resistance mechanisms in cancer. The lab employs both murine disease models and clinical cohort studies to translate molecular insights into potential clinical applications.
Figures are computed from collected data and may differ slightly.
Suppressor of cytokine signaling 1 (SOCS1) is an important negative regulator for cytokines; however, the role of SOCS1 in Th17 differentiation has not been clarified. We generated T cell-specific SOCS1-deficient mice and found that these mice were extremely resistant to a Th17-dependent autoimmune disease model, experimental autoimmune encephalomyelitis. SOCS1-deficient naive CD4(+) T cells were predominantly differentiated into Th1 and poorly into Th17 in vitro. These phenotypes were canceled
The reason for the large male predominance in the occurrence of hepatocellular carcinoma (HCC) remains unknown, and sex hormones may contribute to this phenomenon. We examined possible associations of serum levels of testosterone, free testosterone, estradiol, sex hormone binding globulin, and testosterone:estradiol ratio (T:E2 ratio) with HCC development in a follow-up study of 46 Japanese male patients with liver cirrhosis predominantly of hepatitis C virus origin (76%). Serum samples were col
The T790M secondary mutation of the epidermal growth factor receptor (EGFR) gene accounts for 50% to 60% of cases of resistance to the first-generation EGFR tyrosine kinase inhibitors (TKIs) gefitinib and erlotinib. The prevalence of T790M in <i>EGFR</i> mutation-positive patients who acquire resistance to the irreversible, second-generation EGFR-TKI afatinib has remained unclear, however. We here determined the frequency of T790M acquisition at diagnosis of progressive disease in patients with
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