大阪大学 · Medicine
Tetsuo Takehara 교수의 연구실은 간세포암(hepatocellular carcinoma, HCC)의 발병 기전과 치료 저항성 메커니즘을 중심으로 다각도의 분석을 수행하고 있습니다. 특히, 자가분해 작용인 아폽토시스와 자가포식(autophagy)의 역할, Bcl-xL을 통한 세포 생존 기전, 그리고 간경변 및 지방간과 연관된 미세환경 변화를 다루며, 다중오믹스 기반의 종양 분류와 바이오마커 탐색에도 주력하고 있습니다. 이는 치료 반응 예측 및 개인화 치료 전략 개발에 기여하고자 하는 핵심 목표를 지닙니다.
표시된 성과는 수집된 데이터 기준으로 산출되며, 일부 차이가 있을 수 있습니다.
Multikinase inhibitor sorafenib inhibits proliferation and angiogenesis of tumors by suppressing the Raf/MEK/ERK signaling pathway and VEGF receptor tyrosine kinase. It significantly prolongs median survival of patients with advanced hepatocellular carcinoma (HCC) but the response is disease-stabilizing and cytostatic rather than one of tumor regression. To examine the mechanisms underlying the relative resistance in HCC, we investigated the role of autophagy, an evolutionarily conserved self-di
Transformed hepatocytes survive various apoptotic insults during their growth in vivo. However, molecular mechanisms that inhibit apoptosis and support their survival are not well understood. In this study, we investigated the expression and role of Bcl-xL, an antiapoptotic member of the Bcl-2 family, in human hepatocellular carcinoma (HCC). The Bcl-xL protein was expressed in HepG2, Hep3B, and Huh7 human hepatoma cell lines at high levels, but none of these cells expressed Bcl-2. Down-modulatio
Multiomics stratified nonviral HCCs according to prognosis or TIME. We identified the link between intratumoral steatosis and immune-exhausted immunotherapy-susceptible TIME.
TSP-2 may be a useful biomarker for NASH and advanced fibrosis diagnosis in patients with NAFLD.
H pylori CagA induces aberrant epigenetic silencing of let-7 expression, leading to Ras upregulation.
Connective tissue growth factor (CTGF) is a matricellular protein related to hepatic fibrosis. This study aims to clarify the roles of CTGF in hepatocellular carcinoma (HCC), which usually develops from fibrotic liver. CTGF was overexpressed in 93 human HCC compared with nontumorous tissues, primarily in tumor cells. Increased CTGF expression was associated with clinicopathologic malignancy of HCC. CTGF was upregulated in hepatoma cells in hepatocyte-specific Kras-mutated mice (Alb-Cre Kras<sup>
