In Ah Kim
Seoul National University · Medicine
About the Lab
Professor In Ah Kim's research lab focuses on improving cancer therapy outcomes through molecular and translational oncology, with a strong emphasis on radiosensitization and targeted therapy in aggressive cancers such as glioblastoma, non-small cell lung cancer, and triple-negative breast cancer. The lab investigates key signaling pathways—particularly EGFR, K-RAS, PI3K, and HDACs—to overcome therapeutic resistance and enhance the efficacy of radiotherapy and chemotherapy. By integrating machine learning for imaging analysis and exploring epigenetic modulators, the lab aims to develop precision oncology strategies for personalized treatment. Their work bridges preclinical models with clinical applications, targeting molecular mechanisms that drive tumor survival and recurrence.
Research Overview
Research Output Trend
Figures are computed from collected data and may differ slightly.
Selected Papers
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
Research Areas
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