The University of Tokyo · 의학
Tsuyoshi Hamada 교수의 연구실은 분자병리학적 epidemiology(MPE)를 기반으로 암의 발생 원인과 예후에 영향을 미치는 외부 및 내재적 요인, 특히 장내 미생물(예: *Fusobacterium nucleatum*)과 염증 반응, 면역 미세환경 간의 상호작용을 연구합니다. 특히 대장암에서 유전자 불안정성(MSI), T세포 침윤, 면역관문 억제제 반응성 등과의 연관성을 규명하며 정밀의료 기반 예방 및 치료 전략 개발에 기여하고 있습니다. 또한 아스피린의 면역조절 작용과 암 예후 간의 관계 등 약물-면역 상호작용에 대해서도 심층적 연구를 수행하고 있습니다.
표시된 성과는 수집된 데이터 기준으로 산출되며, 일부 차이가 있을 수 있습니다.
The presence of <i>Fusobacterium nucleatum</i> (<i>F. nucleatum</i>) in colorectal carcinoma tissue has been associated with microsatellite instability (MSI), lower-level T-cell infiltrates, and poor clinical outcomes. Considering differences in the tumor-immune microenvironment between MSI-high and non-MSI-high carcinomas, we hypothesized that the association of <i>F. nucleatum</i> with immune response might differ by tumor MSI status. Using samples from 1,041 rectal and colon cancer patients w
Purpose Blockade of the programmed cell death 1 (PDCD1, PD-1) immune checkpoint pathway can improve clinical outcomes in various malignancies. Evidence suggests that aspirin (a widely used nonsteroidal anti-inflammatory drug) not only prolongs colorectal cancer survival, but can also activate T cell-mediated antitumor immunity and synergize with immunotherapy through inhibition of prostaglandin E2 production. We hypothesized that the survival benefit associated with aspirin might be stronger in
Molecular pathological epidemiology (MPE) is an integrative transdisciplinary field that addresses heterogeneous effects of exogenous and endogenous factors (collectively termed 'exposures'), including microorganisms, on disease occurrence and consequences, utilising molecular pathological signatures of the disease. In parallel with the paradigm of precision medicine, findings from MPE research can provide aetiological insights into tailored strategies of disease prevention and treatment. Due to
The present nomogram can provide valuable information for tailored decision-making early after the diagnosis of nonresectable pancreatic cancer.
Outcomes of covered and uncovered gastroduodenal SEMS were comparable, although the lower dysfunction rate of covered SEMS observed in the analysis of randomized trials needs further investigation. Antimigration mechanisms for covered SEMS and identification of patients who can achieve longer patency from uncovered SEMS would help improve the outcomes of gastroduodenal SEMS.
Family history of pancreatic cancer was associated with increased risk of this malignancy. Family history of breast or colorectal cancer was associated with the increased risk among AJ men.
EST and EPBD can be safely performed in patients receiving antiplatelet agents. Users of anticoagulants are at high risk of bleeding, and the periprocedural management of these should be further investigated.
Inhibitors targeting the <i>PDCD1</i> (programmed cell death 1, PD-1) immune checkpoint pathway have revolutionized cancer treatment strategies. The TIME (Tumor Immunity in the MicroEnvironment) classification based on tumor <i>CD274</i> (<i>PDCD1</i> ligand 1, PD-L1) expression and tumor-infiltrating lymphocytes (TIL) has been proposed to predict response to immunotherapy. It remains to be determined clinical, pathological, and molecular features of TIME subtypes of colorectal cancer. Using 812
Severe bleeding and perforation following EUS-FNA for pancreatic masses are rare, and the procedure is safe.
