• IMMUNE NETWORK
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• 제20권1호
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• pp.7.1-7.11
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• 2020

Cancer immunotherapy, in the form of vaccination, adoptive cellular transfer, or immune checkpoint inhibitors, has emerged as a promising practice within the field of oncology. However, despite the developing field's potential to revolutionize cancer treatment, the presence of immunotherapeutic-resistant tumor cells in many patients present a challenge and limitation to these immunotherapies. These cells not only indicate immunotherapeutic resistance, but also show multi-modal resistance to conventional therapies, abnormal metabolism, stemness, and metastasis. How can immunotherapeutic-resistant tumor cells render multi-malignant phenotypes? We reasoned that the immune-refractory phenotype could be associated with multi-malignant phenotypes and that these phenotypes are linked together by a factor that acts as the master regulator. In this review, we discussed the role of the embryonic transcription factor NANOG as a crucial master regulator we named "common factor" in multi-malignant phenotypes and presented strategies to overcome multi-malignancy in immunotherapeutic-resistant cancer by restraining the NANOG-mediated multi-malignant signaling axis. Strategies that blunt the NANOG axis could improve the clinical management of therapy-refractory cancer.

• IMMUNE NETWORK
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• 제20권1호
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• pp.8.1-8.15
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• 2020

Immune checkpoint blockade targeting PD-1 and PD-L1 has resulted in unprecedented clinical benefit for cancer patients. Anti-PD-1/PD-L1 therapy has become the standard treatment for diverse cancer types as monotherapy or in combination with other anticancer therapies, and its indications are expanding. However, many patients do not benefit from anti-PD-1/PD-L1 therapy due to primary and/or acquired resistance, which is a major obstacle to broadening the clinical applicability of anti-PD-1/PD-L1 therapy. In addition, hyperprogressive disease, an acceleration of tumor growth following anti-PD-1/PD-L1 therapy, has been proposed as a new response pattern associated with deleterious prognosis. Anti-PD-1/PD-L1 therapy can also cause a unique pattern of adverse events termed immune-related adverse events, sometimes leading to treatment discontinuation and fatal outcomes. Investigations have been carried out to predict and monitor treatment outcomes using peripheral blood as an alternative to tissue biopsy. This review summarizes recent studies utilizing peripheral blood immune cells to predict various outcomes in cancer patients treated with anti-PD-1/PD-L1 therapy.

• Journal of Microbiology
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• 제44권6호
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• pp.641-648
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• 2006

We previously reported that Skp1, a component of the Skp1-Cullin-F-box protein (SCF) complex essential for the timely degradation of cell cycle proteins by ubiquitination, physically interacts with Bfa1, which is a key negative regulator of the mitotic exit network (MEN) in response to diverse checkpoint-activating stresses in budding yeast. In this study, we initially investigated whether the interaction of Skp1 and Bfa1 is involved in the regulation of the Bfa1 protein level during the cell cycle, especially by mediating its degradation. However, the profile of the Bfa1 protein did not change during the cell cycle in skp1-11, which is a SKP1 mutant allele in which the function of Skp1 as a part of SCF is completely impaired, thus indicating that Skp1 does not affect the degradation of Bfa1. On the other hand, we found that the skp1-12 mutant allele, previously reported to block G2-M transition, showed defects in mitotic exit and cytokinesis. The skp1-12 mutant allele also revealed a specific genetic interaction with ${\Delta}bfa1$. Bfa1 interacted with Skp1 via its 184 C-terminal residues (Bfa1-D8) that are responsible for its function in mitotic exit. In addition, the interaction between Bfa1 and the Skp1-12 mutant protein was stronger than that of Bfa1 and the wild type Skp1. We suggest a novel function of Skp1 in mitotic exit and cytokinesis, independent of its function as a part of the SCF complex. The interaction of Skp1 and Bfa1 may contribute to the function of Skp1 in the mitotic exit.

• 제어로봇시스템학회논문지
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• 제17권11호
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• pp.1074-1081
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• 2011

As robotics systems are becoming more complex there is the need to promote component based robot development, where systems can be constructed as the composition and integration of reusable building block. One of the most important challenges facing component based robot development is safeguarding against software component failures and malfunctions. The health monitoring of the robot software is most fundamental factors not only to manage system at runtime but also to analysis information of software component in design phase of the robot application. And also as a lot of monitoring events are occurred during the execution of the robot software components, a simple data treatment and efficient memory management method is required. In this paper, we propose an efficient events monitoring and data management method by modeling robot software component and monitoring factors based on robot software framework. The monitoring factors, such as component execution runtime exception, Input/Output data, execution time, checkpoint-rollback are deduced and the detail monitoring events are defined. Furthermore, we define event record and monitor record pool suitable for robot software components and propose a efficient data management method. To verify the effectiveness and usefulness of the proposed approach, a monitoring module and user interface has been implemented using OPRoS robot software framework. The proposed monitoring module can be used as monitoring tool to analysis the software components in robot design phase and plugged into self-healing system to monitor the system health status at runtime in robot systems.

• 생명과학회지
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• 제23권6호
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• pp.832-837
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• 2013

본 연구에서는 생체 내 구성요소 및 에너지원으로서 중요한 역할을 하는 글루타민 결핍에 의한 인체 전립선 PC3 암세포의 증식에 관한 기전 연구를 실시하였다. 글루타민 결핍에 의한 PC3 세포의 증식억제는 세포주기 G2/M arrest와 연관성이 있었으나, apoptosis 유발 현상은 관찰되지 않았다. 글루타민 결핍에 의한 G2/M arrest는 전사 및 번역 수준에서 Cdc2, cyclin A 및 cyclin B1의 발현 억제 및 p53 비의존적인 p21(WAF1/CIP1)의 발현 증가와 연관성이 있었다. 아울러 글루타민 결핍은 Chk1 및 Chk2의 인산화를 증가시켰으나, Cdc25C의 인산화는 감소시켰다. 본 연구의 결과는 글루타민 결핍에 의한 PC3 세포의 증식억제가 apoptosis 유발과는 상관없이 G2/M arrest를 유발시킨다는 첫 번째 증거이다.

• 한국측량학회지
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• 제26권2호
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• pp.111-116
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• 2008

본 연구는 무선조정 헬리콥터에 1000만 화소 카메라인 비측량용 카메라를 장착하였다. 그리고 상공에서 촬영되는 영상을 지상에서 제어하면서 중복도를 고려하여 촬영하였다. 획득된 영상으로부터 영상정합에 의해 불규칙 삼각망을 추출하여 수치표고모형(DEM)을 나타낼 수가 있었으며, 재래적인 측량방식인 Total Station에 의해 관측된 기준점 및 검사점과의 정확도를 비교 검토한 결과 X방향으로는 $-0.194{\sim}0.224m$, Y축으로는 $-0.088{\sim}0.180m$, Z축으로는 $-0.286{\sim}0.285m$ 정도의 오차를 얻을 수 있었다. 또한, 검사점에 대한 오차의 RMSE를 표현하면, X축 방향으로 0.021388m, Y축 방향으로 0.015285m, Z축 방향으로 0.041872m로 나타났다. 이러한 사진촬영 및 분석방법으로 기존의 Total Station 측량방법보다 더 많은 지형표고자료를 취득하는데 좋은 방법이라 판단된다.

• 한국정보과학회논문지:시스템및이론
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• 제34권12호
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• pp.610-617
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• 2007

페이지 기반 점진적 검사점은 검사점 오버헤드를 줄이기 위해 프로세스의 메모리 상태 중 변경된 페이지만 저장하는 기법이다. 그러나 점진적 검사점의 누적 크기는 검사점 횟수가 증가함에 따라 서서히 증가하게 된다. 이는 한 페이지가 검사점 작성 이후에 변경되어 검사점 작성시에 검사점에 저장되는 과정이 되풀이 되고, 이후에 삭제되지 않기 때문이다. 복구 시에 프로세스의 저장된 상태를 만들기 위해 검사점들이 모두 필요할 수 있으므로 함부로 검사점을 삭제를 할 수 없다. 본 논문에서는 페이지 기반 검사점 도구인 Pickpt를 소개하고, Pickpt가 검사점의 누적 크기 증가 문제를 해결하는 방법을 설명한다. 실험을 통해 기존 점진적 검사점에 비해 Pickpt가 점진적 검사점의 누적 크기를 현저히 줄임을 보였다.

• 한국콘텐츠학회논문지
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• 제8권3호
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• pp.270-278
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• 2008

본 연구에서는 연구지역을 대상으로 LiDAR(Light Detection And Ranging) 데이터와 항공사진, 수치 지도를 이용하여 지형지물에 대한 위치정확도 분석을 실시하였다. 연구지역은 부산광역시 사하구 하단지역으로 선정하였으며, 첨단 측량기법인 항공 LiDAR 데이터와 축척 1:20,000의 항공사진을 이용하였다. 그리고 각각의 영상에 대하여 표정작업과 영상의 재배열 과정을 거쳐 최종 수치정사영상을 제작하였다. 제작된 영상을 이용하여 검사점을 선정하고, 선정된 검사점에 대한 정보를 추출하였으며, 스크린 디지타이징기법을 통한 수평위치 좌표를 추출하였다. 그리고 국토지리 정보원에서 공시한 축척 1:5,000의 수치지도를 이용하여 추출된 LiDAR 데이터 좌표와 항공사진의 좌표를 각각 비교.분석하였다. 수치지도를 기준으로 비교 분석한 결과 항공사진의 수평위치 정확도가 항공 LiDAR 측량 성과 보다 건물의 경우 x방향으로 24cm, y방향으로 26cm정도가 우수함을 알 수 있었다.

• Asian Pacific Journal of Cancer Prevention
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• 제15권1호
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• pp.475-481
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• 2014

Background: Pereskia sacharosa is a genus of cacti widely used in folk medicine for cancer-related treatment. Anti-proliferative effects have been studied in recent years against colon, breast, cervical and lung cancer cell lines, with promising results. We here extended study of anti-proliferative effects to a blood malignancy, leukemia. Materials and Methods: Two leukemic cell lines, MV4-11 (acute myeloid leukemia) and K562 (chronic myeloid leukemia), were studied. $IC_{50}$ concentrations were determined and apoptosis and cell cycle regulation were studied by flow cytometric analysis. The expression of apoptosis and cell-cycle related regulatory proteins was assessed by Western blotting. Results: P sacharosa inhibited growth of MV4-11 and K562 cells in a dose-dependent manner. The mode of cell death was via induction of intrinsic apoptotic pathways and cell cycle arrest. There was profound up-regulation of cytochrome c, caspases, p21 and p53 expression and repression of Akt and Bcl-2 expression in treated cells. Conclusions: These results suggest that P sacharosa induces leukemic cell death via apoptosis induction and changes in cell cycle checkpoint, thus deserves further study for anti-leukemic potential.

• Asian Pacific Journal of Cancer Prevention
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• 제13권4호
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• pp.1355-1360
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• 2012

Background: The cell cycle checkpoint kinase 2 (CHEK2) gene I157T variant may be associated with an increased risk of breast cancer, but it is unclear whether the evidence is sufficient to recommend testing for the mutation in clinical practice. Materials and Methods: We systematically searched PubMed, Embase, Elsevier and Springer for relevant articles published before Nov 2011. Summary odds ratio (OR) and 95% confidence interval (95% CI) incidence rates were calculated using a random-effects model with STATA (version 10.0) software. Results: A total of fifteen case-control studies, including 19,621 cases and 27,001 controls based on the search criteria, were included for analysis. A significant association was found between carrying the CHEK2 I157T variant and increased risk of unselected breast cancer (OR = 1.48, 95% CI = 1.31-1.66, P < 0.0001), familial breast cancer (OR = 1.48, 95% CI = 1.16-1.89, P < 0.0001), and early-onset breast cancer (OR = 1.47, 95% CI = 1.29-1.66, P < 0.0001). We found an even stronger significant association between the CHEK2 I157T C variant and increased risk of lobular type breast tumors (OR = 4.17, 95% CI = 2.89-6.03, P < 0.0001). Conclusion: Our research indicates that the CHEK2 I157T variant may be another important genetic mutation which increases risk of breast cancer, especially the lobular type.