• IMMUNE NETWORK
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• v.21 no.3
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• pp.23.1-23.16
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• 2021

Chemokines are key factors that influence the migration and maintenance of relevant immune cells into an infected tissue or a tumor microenvironment. Therefore, it is believed that the controlled administration of chemokines in the tumor microenvironment may be an effective immunotherapy against cancer. Previous studies have shown that CCL3, also known as macrophage inflammatory protein 1-alpha, facilitates the recruitment of dendritic cells (DCs) for the presentation of tumor Ags and promotes T cell activation. Here, we investigated the role of CCL3 in regulating the tumor microenvironment using a syngeneic mouse tumor model. We observed that MC38 tumors overexpressing CCL3 (CCL3-OE) showed rapid regression compared with the wild type MC38 tumors. Additionally, these CCL3-OE tumors showed an increase in the proliferative and functional tumor-infiltrating T cells. Furthermore, PD-1 immune checkpoint blockade accelerated tumor regression in the CCL3-OE tumor microenvironment. Next, we generated a modified CCL3 protein for pre-clinical use by fusing recombinant CCL3 (rCCL3) with a non-cytolytic hybrid Fc (HyFc). Administering a controlled dose of rCCL3-HyFc via subcutaneous injections near tumors was effective in tumor regression and improved survival along with activated myeloid cells and augmented T cell responses. Furthermore, combination therapy of rCCL3-HyFc with PD-1 blockade exhibited prominent effect to tumor regression. Collectively, our findings demonstrate that appropriate concentrations of CCL3 in the tumor microenvironment would be an effective adjuvant to promote anti-tumor immune responses, and suggest that administering a long-lasting form of CCL3 in combination with PD-1 blockers can have clinical applications in cancer immunotherapy.

• Molecules and Cells
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• v.37 no.10
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• pp.713-718
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• 2014

Alteration in chromosome numbers and structures instigate and foster massive genetic instability. As Boveri has seen a hundred years ago (Boveri, 1914; 2008), aneuploidy is hall-mark of many cancers. However, whether aneuploidy is the cause or the result of cancer is still at debate. The molecular mechanism behind aneuploidy includes the chromosome mis-segregation in mitosis by the compromise of spindle assembly checkpoint (SAC). SAC is an elaborate network of proteins, which monitor that all chromosomes are bipolarly attached with the spindles. Therefore, the weakening of the SAC is the major reason for chromosome number instability, while complete compromise of SAC results in detrimental death, exemplified in natural abortion in embryonic stage. Here, I will review on the recent progress on the understanding of chromosome missegregation and cancer, based on the comparison of different mouse models of BubR1, the core component of SAC.

• 제어로봇시스템학회:학술대회논문집
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• 2004.08a
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• pp.1012-1016
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• 2004

In this paper, we propose a simple but optimized NC code generating technique for disk cams by means of tool path error control in a five-axis CNC machining center. Using the geometric theorem of the triangle made between manufacturing points and error checkpoint, the tool path error has been studied for disk cams profile generation and an improvement in the profile has been obtained. Then, based on the present manufacturing approach a computer program is developed on $C^{++}$ language to perform and to verify the shape design, the manufacturing simulation, and the optimized generation of the NC code.

• Tuberculosis and Respiratory Diseases
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• v.83 no.1
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• pp.14-19
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• 2020

Lung cancer remains the most common cause of cancer-related deaths worldwide. Although there are many possible treatments, including targeted therapies such as epidermal growth factor receptor tyrosine kinase inhibitors and anaplastic lymphoma kinase inhibitors, new therapeutic strategies are needed to improve clinical outcomes. Immunotherapy through the use of immune checkpoint inhibitors has provided one of the most important breakthroughs in the management of solid tumors, including lung cancers, and has shown promising results in numerous clinical trials. This review will present the current status of immunotherapy for lung cancer and future perspectives on these treatments.

• Journal of Korea Society of Industrial Information Systems
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• v.22 no.2
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• pp.15-25
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• 2017

A System can be more Dependable from some types of Threats if the Dependability Level Against the Threat on the System is Increased. However, The Dependability-performance Tradeoff should be Considered because the Increased Dependability may Degrade the Performance of the System. Therefore, it is Efficient to Temporally Increase the Dependability Level to High only when an Threat is Predicted on the System in a Short time while Maintaining the Level in Low or mid in Normal Situations. In this Paper, we Present a Threat Prevention Strategy for a Networked Node by Dynamically Changing the Dependability Level According to the Threat Situation on its Logically/physically Neighboring Nodes. As case Studies, we Employ our Strategy to an Internet Server Against TCP SYN Flood Attacks and to a Checkpoint and Rollback System Against Transient Faults. Our Performance Analysis Shows that our Strategy can Effectively Relieve the Damage of the Failure without Serious Performance Degradation.

• Proceedings of the Korea Information Processing Society Conference
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• 2003.11a
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• pp.397-400
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• 2003

TMR(Triple Modular redundancy)은 공간여분(W/H 및 S/W)을 정적으로 활용하는 가장 간단한 구조를 지닌 대표적인 고장포용 기법중의 하나이다. TMR 구조 고장시 TMR 시스템 고장복구를 위해 잘못된 결과를 가지고 있는 프로그램의 일부분을 재실행 또는 프로그래밍 전체를 재시작하는 기법을 적용하는 것은 일반적으로 상당한 시간을 필요로 한다. 이러한 단점을 극복하기 위해 본 논문에서는 TMR 고장을 효과적으로 복구하기 위해 또 다른 형태의 시간여분 기법인 rollback과 rol1-forward 기법에 checkpoint들을 적용하여 처리하는 시간 및 공간여분을 혼용하는 기법을 제안하였다.

• ETRI Journal
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• v.42 no.3
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• pp.388-398
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• 2020

We herein propose a heuristic redundancy selection algorithm that combines resubmission, replication, and checkpointing redundancies to reduce the resiliency overhead in fault-tolerant workflow scheduling. The appropriate combination of these redundancies for workflow tasks is obtained in two consecutive phases. First, to compute the replication vector (number of task replicas), we apportion the set of provisioned resources among concurrently executing tasks according to their needs. Subsequently, we obtain the optimal checkpointing interval for each task as a function of the number of replicas and characteristics of tasks and computational environment. We formulate the problem of obtaining the optimal checkpointing interval for replicated tasks in situations where checkpoint files can be exchanged among computational resources. The results of our simulation experiments, on both randomly generated workflow graphs and real-world applications, demonstrated that both the proposed replication vector computation algorithm and the proposed checkpointing scheme reduced the resiliency overhead.

• BMB Reports
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• v.53 no.10
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• pp.512-520
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• 2020

T-cell-based cancer immunotherapies, such as immune checkpoint blockers (ICBs) and chimeric antigen receptor (CAR)-T-cells, have significant anti-tumor effects against certain types of cancer, providing a new paradigm for cancer treatment. However, the activity of tumor infiltrating T-cells (TILs) can be effectively neutralized in the tumor microenvironment (TME) of most solid tumors, rich in various immunosuppressive factors and cells. Therefore, to improve the clinical outcomes of established T-cell-based immunotherapy, adjuvants that can comprehensively relieve multiple immunosuppressive mechanisms of TME are needed. In this regard, recent studies have revealed that metformin has several beneficial effects on anti-tumor immunity. In this mini-review, we understand the immunosuppressive properties of TME and how metformin comprehensively enhances anti-tumor immunity. Finally, we will discuss this old friend's potential as an adjuvant for cancer immunotherapy.

• Proceedings of the Korean Society of Developmental Biology Conference
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• 2006.07a
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• pp.5-5
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• 2006

• BMB Reports
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• v.43 no.12
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• pp.795-800
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• 2010

Huntingtin-interacting protein 1-related (HIP1r) is known to function in clathrin-mediated endocytosis and regulation of the actin cytoskeleton, which occurs continuously in non-dividing cells. This study reports a new function for HIP1r in mitosis. Green fluorescent protein-fused HIP1r localizes to the mitotic spindles. Depletion of HIP1r by RNA interference induces misalignment of chromosomes and prolonged mitosis, which is associated with decreased proliferation of HIP1r-deficeint cells. Chromosome misalignment leads to missegregation and ultimately production of multinucleated cells. Depletion of HIP1r causes persistent activation of the spindle checkpoint in misaligned chromosomes. These findings suggest that HIP1r plays an important role in regulating the attachment of spindle microtubules to chromosomes during mitosis, an event that is required for accurate congression and segregation of chromosomes. This finding may provide new insights that improve the understanding of various human diseases involving HIP1r as well as its fusion genes.