Nagoya University · 의학
아오키 교수의 연구실은 신경종양, 특히 저-grade 뇌신경종양의 유전적 기반과 진행 메커니즘을 규명하는 데 초점을 맞추고 있습니다. IDH 돌연변이와 1p/19q 코드레션과 같은 분자적 특성에 기반한 종양 분류와 생존 예측 모델링을 통해 개인화된 치료 전략을 개발하고 있으며, 특히 액체 생검(liquid biopsy) 기반의 비침습적 조기 진단 기술 개발에도 주력하고 있습니다. 또한, 종양의 진행 과정을 수학적 모델링으로 분석함으로써 치료 유도 유전적 변화를 이해하고자 합니다.
표시된 성과는 수집된 데이터 기준으로 산출되며, 일부 차이가 있을 수 있습니다.
BACKGROUND: Diffuse lower-grade gliomas (LGGs) are genetically classified into 3 distinct subtypes based on isocitrate dehydrogenase (IDH) mutation status and codeletion of chromosome 1p and 19q (1p/19q). However, the subtype-specific effects of additional genetic lesions on survival are largely unknown. METHODS: Using Cox proportional hazards regression modeling, we investigated the subtype-specific effects of genetic alterations and clinicopathological factors on survival in each LGG subtype,
There are no accurate mass screening methods for early detection of central nervous system (CNS) tumors. Recently, liquid biopsy has received a lot of attention for less-invasive cancer screening. Unlike other cancers, CNS tumors require efforts to find biomarkers due to the blood-brain barrier, which restricts molecular exchange between the parenchyma and blood. Additionally, because a satisfactory way to collect urinary biomarkers is lacking, urine-based liquid biopsy has not been fully invest
A condition is derived for reciprocal altruism to evolve by kin or group selection. It is assumed that many additively acting genes of small effect and the environment determine the probability that an individual is a reciprocal altruist, as opposed to being unconditionally selfish. The particular form of reciprocal altruism considered is TIT FOR TAT, a strategy that involves being altruistic on the first encounter with another individual and doing whatever the other did on the previous encounte
Isocitrate dehydrogenase-mutant low-grade gliomas (IDHmut-LGG) grow slowly but frequently undergo malignant transformation, which eventually leads to premature death. Chemotherapy and radiotherapy treatments prolong survival, but can also induce genetic (or epigenetic) alterations involved in transformation. Here, we developed a mathematical model of tumor progression based on serial tumor volume data and treatment history of 276 IDHmut-LGGs classified by chromosome 1p/19q codeletion (IDH<sup>mu
