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Jason Joon Bock Lee,Jinhyun Choi,Sung Gwe Ahn,Joon Jeong,Ik Jae Lee,Kwangwoo Park,Kangpyo Kim,Jun Won Kim 대한방사선종양학회 2017 Radiation Oncology Journal Vol.35 No.2
Purpose: To report the results of a correlation analysis of skin dose assessed by in vivo dosimetry and the incidence of acute toxicity. This is a phase 2 trial evaluating the feasibility of intraoperative radiotherapy (IORT) as a boost for breast cancer patients. Materials and Methods: Eligible patients were treated with IORT of 20 Gy followed by whole breast irradiation (WBI) of 46 Gy. A total of 55 patients with a minimum follow-up of 1 month after WBI were evaluated. Optically stimulated luminescence dosimeter (OSLD) detected radiation dose delivered to the skin during IORT. Acute toxicity was recorded according to the Common Terminology Criteria for Adverse Events v4.0. Clinical parameters were correlated with seroma formation and maximum skin dose. Results: Median follow-up after IORT was 25.9 weeks (range, 12.7 to 50.3 weeks). Prior to WBI, only one patient developed acute toxicity. Following WBI, 30 patients experienced grade 1 skin toxicity and three patients had grade 2 skin toxicity. Skin dose during IORT exceeded 5 Gy in two patients: with grade 2 complications around the surgical scar in one patient who received 8.42 Gy. Breast volume on preoperative images (p = 0.001), ratio of applicator diameter and breast volume (p = 0.002), and distance between skin and tumor (p = 0.003) showed significant correlations with maximum skin dose. Conclusions: IORT as a boost was well-tolerated among Korean women without severe acute complication. In vivo dosimetry with OSLD can help ensure safe delivery of IORT as a boost.
Negative Regulation of Hypoxic Responses via Induced Reptin Methylation
Lee, Jason S.,Kim, Yunho,Kim, Ik Soo,Kim, Bogyou,Choi, Hee June,Lee, Ji Min,Shin, Hi-Jai R.,Kim, Jung Hwa,Kim, Ji-Young,Seo, Sang-Beom,Lee, Ho,Binda, Olivier,Gozani, Or,Semenza, Gregg L.,Kim, Minhyung Elsevier 2010 Molecular cell Vol.39 No.1
<P><B>Summary</B></P><P>Lysine methylation within histones is crucial for transcriptional regulation and thus links chromatin states to biological outcomes. Although recent studies have extended lysine methylation to nonhistone proteins, underlying molecular mechanisms such as the upstream signaling cascade that induces lysine methylation and downstream target genes modulated by this modification have not been elucidated. Here, we show that Reptin, a chromatin-remodeling factor, is methylated at lysine 67 in hypoxic conditions by the methyltransferase G9a. Methylated Reptin binds to the promoters of a subset of hypoxia-responsive genes and negatively regulates transcription of these genes to modulate cellular responses to hypoxia.</P> <P><B>Highlights</B></P><P>► Reptin is a target of G9a methyltransferase ► Reptin K67 methylation is induced by hypoxia ► Genome-wide identification of hypoxia target genes negatively regulated by Reptin ► Hypoxia-driven Reptin methylation negatively regulates tumorigenic behavior in vivo</P>
Lee, Jason Joon Bock,Choi, Jinhyun,Ahn, Sung Gwe,Jeong, Joon,Lee, Ik Jae,Park, Kwangwoo,Kim, Kangpyo,Kim, Jun Won The Korean Society for Radiation Oncology 2017 Radiation Oncology Journal Vol.35 No.2
Purpose: To report the results of a correlation analysis of skin dose assessed by in vivo dosimetry and the incidence of acute toxicity. This is a phase 2 trial evaluating the feasibility of intraoperative radiotherapy (IORT) as a boost for breast cancer patients. Materials and Methods: Eligible patients were treated with IORT of 20 Gy followed by whole breast irradiation (WBI) of 46 Gy. A total of 55 patients with a minimum follow-up of 1 month after WBI were evaluated. Optically stimulated luminescence dosimeter (OSLD) detected radiation dose delivered to the skin during IORT. Acute toxicity was recorded according to the Common Terminology Criteria for Adverse Events v4.0. Clinical parameters were correlated with seroma formation and maximum skin dose. Results: Median follow-up after IORT was 25.9 weeks (range, 12.7 to 50.3 weeks). Prior to WBI, only one patient developed acute toxicity. Following WBI, 30 patients experienced grade 1 skin toxicity and three patients had grade 2 skin toxicity. Skin dose during IORT exceeded 5 Gy in two patients: with grade 2 complications around the surgical scar in one patient who received 8.42 Gy. Breast volume on preoperative images (p = 0.001), ratio of applicator diameter and breast volume (p = 0.002), and distance between skin and tumor (p = 0.003) showed significant correlations with maximum skin dose. Conclusions: IORT as a boost was well-tolerated among Korean women without severe acute complication. In vivo dosimetry with OSLD can help ensure safe delivery of IORT as a boost.
Spatiotemporal genomic architecture informs precision oncology in glioblastoma
Lee, Jin-Ku,Wang, Jiguang,Sa, Jason K,Ladewig, Erik,Lee, Hae-Ock,Lee, In-Hee,Kang, Hyun Ju,Rosenbloom, Daniel S,Camara, Pablo G,Liu, Zhaoqi,van Nieuwenhuizen, Patrick,Jung, Sang Won,Choi, Seung Won,Ki Nature Pub. Co 2017 Nature genetics Vol.49 No.4
<P>Precision medicine in cancer proposes that genomic characterization of tumors can inform personalized targeted therapies1-5. However, this proposition is complicated by spatial and temporal heterogeneity6-14. Here we study genomic and expression profiles across 127 multisector or longitudinal specimens from 52 individuals with glioblastoma (GBM). Using bulk and single-cell data, we find that samples from the same tumor mass share genomic and expression signatures, whereas geographically separated, multifocal tumors and/or long-term recurrent tumors are seeded from different clones. Chemical screening of patient-derived glioma cells (PDCs) shows that therapeutic response is associated with genetic similarity, and multifocal tumors that are enriched with PIK3CA mutations have a heterogeneous drug-response pattern. We show that targeting truncal events is more efficacious than targeting private events in reducing the tumor burden. In summary, this work demonstrates that evolutionary inference from integrated genomic analysis in multisector biopsies can inform targeted therapeutic interventions for patients with GBM.</P>
Pharmacogenomic landscape of patient-derived tumor cells informs precision oncology therapy
Lee, Jin-Ku,Liu, Zhaoqi,Sa, Jason K.,Shin, Sang,Wang, Jiguang,Bordyuh, Mykola,Cho, Hee Jin,Elliott, Oliver,Chu, Timothy,Choi, Seung Won,Rosenbloom, Daniel I. S.,Lee, In-Hee,Shin, Yong Jae,Kang, Hyun J Nature Pub. Co 2018 Nature genetics Vol.50 No.10
Choi, Yong Seok,Park, Jin Kyun,Kang, Eun Ha,Lee, Young-Kyun,Kim, Tae Kyun,Chung, Jin-Haeng,Zimmerer, Jason M,Carson III, William E,Song, Yeong Wook,Lee, Yun Jong BioMed Central 2013 ARTHRITIS RESEARCH AND THERAPY Vol.15 No.6
<P><B>Introduction</B></P><P>Although IL-1β is believed to be crucial in the pathogenesis of osteoarthritis (OA), the IL-1β blockade brings no therapeutic benefit in human OA and results in OA aggravation in several animal models. We explored the role of a cytokine signaling 1 (SOCS1) suppressor as a regulatory modulator of IL-1β signaling in chondrocytes.</P><P><B>Methods</B></P><P>Cartilage samples were obtained from patients with knee OA and those without OA who underwent surgery for femur-neck fracture. SOCS1 expression in cartilage was assessed with immunohistochemistry. IL-1β-induced SOCS1 expression in chondrocytes was analyzed with quantitative polymerase chain reaction and immunoblot. The effect of SOCS1 on IL-1β signaling pathways and the synthesis of matrix metalloproteinases (MMPs) and aggrecanase-1 was investigated in SOCS1-overexpressing or -knockdown chondrocytes.</P><P><B>Results</B></P><P>SOCS1 expression was significantly increased in OA cartilage, especially in areas of severe damage (<I>P</I> < 0.01). IL-1β stimulated SOCS1 mRNA expression in a dose-dependent pattern (<I>P</I> < 0.01). The IL-1β-induced production of MMP-1, MMP-3, MMP-13, and ADAMTS-4 (aggrecanase-1, a disintegrin and metalloproteinase with thrombospondin motifs 4) was affected by SOCS1 overexpression or knockdown in both SW1353 cells and primary human articular chondrocytes (all <I>P</I> values < 0.05). The inhibitory effects of SOCS1 were mediated by blocking p38, c-Jun N-terminal kinase (JNK), and nuclear factor κB (NF-κB) activation, and by downregulating transforming growth factor-β-activated kinase 1 (TAK1) expression.</P><P><B>Conclusions</B></P><P>Our results show that SOCS1 is induced by IL1-β in OA chondrocytes and suppresses the IL-1β-induced synthesis of matrix-degrading enzymes by inhibiting IL-1β signaling at multiple levels. It suggests that the IL-1β-inducible SOCS1 acts as a negative regulator of the IL-1β response in OA cartilage.</P>
CD55 polymorphisms and risk of aspirin-exacerbated respiratory disease
LEE, JIN SOL,BAE, JOON SEOL,KIM, JEONG-HYUN,KIM, JASON YONGHA,PARK, TAE JOON,PASAJE, CHARISSE FLERIDA,PARK, BYUNG-LAE,CHEONG, HYUN SUB,UH, SOO-TAEK,JANG, AN-SOO,CHOI, INSEON S.,PARK, CHOON-SIK,SHIN, H Spandidos Publications 2012 MOLECULAR MEDICINE REPORTS Vol.6 No.5
<P>Aspirin-exacerbated respiratory disease (AERD) is a respiratory disease characterized by acute bronchial responses upon the administration of non-steroidal anti?inflammatory drugs (NSAIDs) and the immune response by mast cells is regarded as one of the noteworthy causes of AERD pathogenesis. The complement cascade is regarded as a key mechanism for clearing pathogens from the host. CD55 is one of the proteins involved in self-recognition, a central component of the complement system and autoimmunity. To investigate the associations between CD55 single nucleotide polymorphisms (SNPs) and the risk of AERD, we carried out logistic analyses with three genetic models and further regression analysis was performed with the fall rate of forced expiratory volume in 1?sec (FEV1) by aspirin provocation. However, our results demonstrate that no CD55 polymorphisms are associated with the risk of AERD and the fall rate of FEV1 (P>0.05). Therefore, our results suggest that CD55 polymorphisms are not genetic markers of aspirin?induced bronchospasm, including FEV1, in the population studied. Although the genetic role of CD55 has been found to be integral to human immunity, our results indicate that genetic variations of CD55 do not influence the risk of AERD and the fall rate of FEV1 in the population studied.</P>
Sungpill Choi,Kyuho Jason Lee,Youngwoo Kim,Hoi-Jun Yoo 대한전자공학회 2020 Journal of semiconductor technology and science Vol.20 No.3
The 3D hand gesture interface (HGI) for virtual reality and mixed reality on smart mobile devices is strongly dependent upon the robust depth-estimation with low latency and power consumption. However, the conventional depth-estimation hardware such as active depth sensors and stereo matching accelerators cannot realize the always-on and natural 3D HGI on mobile platform due to their large power consumption from active depth sensors and computations as well as the massive external memory bandwidth, respectively. To resolve the limit, we propose a depth-estimation processor that realizes the always-on and natural 3D HGI with algorithm and hardware co-optimization. The processor features: 1) shifter-based adaptive support weight aggregation that replaces complex floating-point operations with integer operations to reduce power and bandwidth by 92.2% and 69.1%; 2) line streaming 7-stage pipeline architecture with aggregation pipeline reordering optimization to realize 94% utilization and 43.9% memory reduction; and 3) shifting register-based pipeline buffer optimization to reduce 29.8% area. The proposed depth-estimation processor realizes a real-time 3D HGI with 9.52 ms of latency under QVGA stereo inputs. It achieves external memory bandwidth reduction to 18.93 MB/s with 15.56 mW power and 2.8 mm2 area, which are 4.1x and 6.9x more efficient than state-of-the-arts [9, 10], respectively.