김인아 교수
In Ah Kim
서울대학교 방사선종양학과 · 의학
연구실 소개
김인아 교수의 연구실은 뇌신경종양, 특히 간질성 뇌종양(GBM)의 치료 내성과 재발 문제를 해결하기 위해 기계학습 기반 진단 도구 개발과 함께, 표적치료 전략의 기반을 마련하고자 합니다. 특히 EGFR, MGMT, PARP 및 HDAC 등 핵심 신호전달 경로를 타겟으로 방사선과 화학요법의 효과를 향상시키는 다학제 치료 전략을 연구하고 있으며, 신호전달 경로의 분자 기전을 규명함으로써 개인화된 암 치료의 가능성을 모색하고 있습니다. 최근에는 방사선 감수성 유발을 위한 타겟 기반 약물 개발과 함께, 영상 기반 인공지능 진단 모델 개발을 융합한 종양 진단 및 예후 평가 시스템 구축에도 주력하고 있습니다.
연구 현황
연구 성과 추이
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주요 논문
15We aimed to investigate the feasibility of machine learning (ML) algorithm to distinguish pseudoprogression (PsPD) from progression (PD) in patients with glioblastoma (GBM). We recruited the patients diagnosed as primary GBM who received gross total resection (GTR) and concurrent chemoradiotherapy in two institutions from April 2010 to April 2017 and presented suspicious contrast-enhanced lesion on brain magnetic resonance imaging (MRI) during follow-up. Patients from two institutions were alloc
BACKGROUND: Despite aggressive treatment with radiation therapy and concurrent adjuvant temozolomide (TMZ), glioblastoma multiform (GBM) still has a dismal prognosis. We aimed to identify strategies to improve the therapeutic outcome of combined radiotherapy and TMZ in GBM by targeting pro-survival signaling from the epidermal growth factor receptor (EGFR). METHODS: Glioma cell lines U251, T98G were used. Colony formation, DNA damage repair, mode of cell death, invasion, migration and vasculogen
Several studies have shown solid evidence for the potential value of targeting epidermal growth factor receptor (EGFR) signaling to enhance the antitumor activity of radiation. However, therapeutic resistance has emerged as an important clinical issue. Here, we investigated whether strategies for targeting EGFR-associated downstream signaling would radiosensitize a panel of non-small cell lung cancer cell lines. Inhibition of K-RAS using RNA interference attenuated downstream signaling and incre
Combined pre- and postchemoradiotherapy CEA levels could be useful as a prognostic factor for disease-free survival in patients with rectal cancer who undergo treatment with neoadjuvant chemoradiotherapy and curative resection. Postchemoradiotherapy CEA may be helpful in a selection of patients who want more conservative surgery after chemoradiotherapy.
Histone deacetylase inhibitors (HDI) are emerging as potentially useful components of the anticancer armamentarium and as useful tools to dissect mechanistic pathways. HDIs that globally inhibit histone deacetylases (HDAC) have radiosensitizing effects, but the relative contribution of specific HDAC classes remains unclear. Newly characterized HDIs are now available that preferentially inhibit specific HDAC classes, including SK7041 (inhibits class I HDACs) and splitomicin (inhibits class III HD
BACKGROUND: Triple-negative breast cancer (TNBC) shows aggressive clinical behavior, but the treatment options are limited due to lack of a specific target. TNBC shares many clinical and pathological similarities with BRCA-deficient breast cancer, for which poly(ADP-ribose) polymerase (PARP) inhibitor is effective, but PARP inhibitor alone failed to show clinical effects in patients with sporadic TNBC. Radiation induces DNA double-strand breaks, and the phosphoinositide 3-kinase (PI3K) signaling
INTRODUCTION: Evaluating the expression of signaling molecule proteins from the mitogen-activated protein kinase (MAPK) pathway and the phosphatidylinositol-3-kinase (PI3K) pathway in invasive breast cancers may identify prognostic marker(s) associated with early relapse. METHODS: Immunohistochemical analyses of phosphatase and tensin homologue deleted on chromosome 10 (PTEN), PI3K-p110alpha, phospho-AKT, phospho-p70S6 kinase, phospho-S6 ribosomal protein, phospho-RAF, phospho-p44/42 MAPK, and h
Several studies have indicated the potential value of targeting HER-2 signaling to enhance the anti-tumor activity of ionizing radiation. However, therapeutic resistance resulting from several factors, including activation of the downstream pathway, represents a major obstacle to treatment. Here, we investigated whether inhibitors targeting downstream of HER-2 signaling would radiosensitize SKBR3 breast cancer cells that exhibit overamplification of HER2. Selective inhibition of MEK-ERK signalin
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