차주의 정보에 관한 권리의 관점에서

학위논문(석사) -- 서울대학교대학원 : 법과대학 법학과, 2022. 8. 정순섭.인공지능에 기반한 대출심사 기술이 나날이 고도화되고 있다. 이러한 변화는 IT 기술의 발전으로부터 시작되어 규제샌드박스를 도입한 금융혁신법의 제정과 데이터 경제로의 전환을 촉진하는 신용정보법의 개정 등 금융당국의 적극적인 규제 완화에 의해 가속화되었다. 본 논문은 본격화된 인공지능 기반의 대출심사가 차주의 정보에 관한 권리와 일으키는 긴장관계에 따라 새롭게 발생하는 법적 문제에 대해 검토한다. 첫 번째로, 인공지능의 학습을 위한 빅데이터 수집의 방법으로 활용할 수 있는 가명정보 거래, 본인신용정보관리업자로서의 데이터 수집, 공개된 정보에 대한 자연어 처리가 적법한지, 만일 불법적인 빅데이터 수집이 이루어졌다면 차주는 어떻게 권리를 구제받을 수 있는지에 대해 검토한다. 두 번째로, 자동화평가와 관련하여 이에 활용된 알고리즘에 대한 차주의 설명요구권의 범위가 구체적으로 어떻게 되는지 또한 이에 따라 도입할 수 있는 차별적 취급 금지 규제의 구체적인 가이드라인은 무엇인지에 대해서 살펴본다. 이를 바탕으로 적절한 신용정보의 공유가 결국 차주의 정보에 관한 권리도 완결시키는바 이를 위한 적절한 균형점을 찾아야 함을 강조한다.The AI-based Lending is rapidly progressing. These changes started with development of fintech and was driven by financial authorities’ efforts such as the Special Act on Supprot for Financial Innovation and the Credit Information Use And Protection Act This paper examines the legal issues that arise when AI-based lending collides with the borrower's right to information. First, this paper review ‘Pseudonymous Data’, ‘Comparability Rule’ and ‘Published Data’ that are being used as a method of big data collection, and then review how the borrower's right to information can be remedied if it has been infringed. Second, what is the specific scope of the data subjects' right to request explanation for decision based solely on automated processing, and what is the direction of the Financial AI guidelines to prevent bias in the algorithm are examined. In conclusion, it is emphasized that an appropriate balance must be found because proper sharing of credit information ultimately completes the borrower's right to information.제 1 장 서론 1 제 1 절 연구의 배경 및 목적 1 1. 연구의 배경 1 2. 연구의 목적 2 제 2 절 연구의 방법 및 구성 3 제 2 장 인공지능 기반 대출심사 현황 6 제 1 절 인공지능 일반론 7 1. 인공지능의 개념 7 가. 인공지능의 정의 7 (1) 다양한 견해 7 (2) 법령상 정의 9 나. 인공지능의 구별 11 다. 인공지능의 권리능력 12 2. 인공지능의 특징 16 가. 데이터 수집 16 (1) 데이터와 정보 그리고 빅데이터 16 (2) 인공지능과 데이터 17 나. 데이터 가공 및 이용 19 (1) 가공과 이용 그리고 자동화 평가 19 (2) 인공지능의 자동화 평가 20 제 2 절 대출심사의 변화 23 1. 인공지능의 빅데이터 수집 23 가. 공개된 정보의 활용 24 나. 데이터 거래 25 다. 본인신용정보관리업 진출 27 2. 인공지능의 데이터 가공 및 이용 30 가. 금융혁신지원 특별법 30 (1) 배경 및 제정 경과 30 (2) 주요내용 33 나. 활용현황 35 (1) 신용평가 35 (2) 담보평가 36 1) 부동산 평가 36 2) 동산 평가 38 제 3 장 인공지능과 차주의 정보에 관한 권리 40 제 1 절 인공지능의 데이터 수집과 차주의 권리 41 1. 개관 41 2. 데이터 일반론 42 가. 데이터의 법적성격 42 (1) 데이터의 권리주체 42 1) 데이터 생산자 42 2) 정보주체 43 (2) 데이터 유형에 다른 현행법상 지위 45 1) 개인정보(신용정보 포함)인 데이터 46 2) 개인정보가 아닌 데이터 46 - 지적재산권법의 보호를 받는 데이터 46 - 일반 민법의 보호를 받는 데이터 49 나. 데이터 소유권론의 검토 50 (1) 데이터의 물건성 50 1) 민법 제98조 물건의 정의 50 2) 데이터의 물건성에 대한 통설 50 3) 민법 제98조의 개정논의 51 (2) 데이터 소유권론의 실익 52 1) 찬성론 53 2) 반대론 54 3) 소결 56 3. 빅데이터 기술과 개인정보자기결정권 57 가. 개인정보자기결정권의 새로운 균형 57 (1) 신용정보 수집 및 처리에 대한 예외 58 1) 신용정보법의 개정 내용 58 2) 대법원 2016.8.17. 선고 2014다235080 판결 59 3) 대출심사를 위해 공개된 정보를 수집하는 경우 61 (2) 신용정보 제공 및 이용에 대한 예외 63 1) 신용정보법의 개정 내용 63 2) 가명정보 제공 및 이용 65 3) 당초 수집목적과 상충되지 않는 제공 및 이용 67 나. 인공지능과 불법행위 책임 71 (1) 고의 또는 과실의 입증 72 1) 입증책임의 전환 72 2) 무과실책임으로의 전환 가능성 73 (2) 손해의 입증 74 (3) 불법행위 책임의 주체 75 제 2 절 인공지능의 데이터 가공 및 이용과 차주의 권리 77 1. 개관 77 2. 자동화평가의 개념 78 가. 자동화평가의 알고리즘 78 (1) 알고리즘 함수와 결정경계 78 (2) 알고리즘의 성능 79 나. 자동화평가의 법적 성질 80 3. 자동화평가에 대한 설명요구권 81 가. 설명가능한 알고리즘 문제 81 (1) 논의의 배경: GDPR 81 (2) 불투명성의 원인 83 나. 차주의 설명요구권 85 (1) 필요성 85 (2) 개념 87 1) 관련 법령 87 2) 법적 성질 88 다. 은행의 권리 89 (1) 은행의 신용위험관리 침해 89 (2) 은행의 영업비밀 침해 90 1) 영업비밀의 정의 및 요건 90 2) 인공지능 기술의 경우 91 라. 설명의 범위 문제 92 (1) 딜레마 상황 92 (2) 설명요구권 행사 범위의 구체화 92 4. 자동화평가에 의한 차별적 취급 금지 95 가. 자동화평가에 의한 차별의 개념 95 (1) 법령상 차별적 취급금지 원칙 95 (2) 자동화평가에 의한 차별 95 나. 자동화평가에 의한 차별의 규제 97 (1) 입력값 규제 98 1) 불변적 특징 98 2) 가변적 특징 100 (2) 출력값 규제 102 다. 자동화평가에 대한 자율적 윤리원칙 구축 103 (1) 필요성 103 (2) 미국의 사례 104 (3) 금융분야 AI 가이드라인의 발전을 통한 윤리원칙의 구축 106 제 4 장 결론 109 참고문헌 111 Abstract 125석

Renal intravascular large B cell lymphoma: the first case report in Korea and a review of the literature

Herein, we describe the first case of renal intravascular large B cell lymphoma in Korea occurring in a 66-year-old female. She presented with mild fever and dyspnea. On physical and laboratory evaluations, hemophagocytic lymphohistiocytosis was suspected, but the bone marrow biopsy results were unremarkable. During the work-up, massive proteinuria developed, which led to a renal biopsy. The renal architecture was relatively well-preserved, but the glomeruli were hypercellular with the infiltration of atypical, large lymphoid cells with increased nucleus-cytoplasm ratio and clumped chromatin. Similar cells were also present in the peritubular capillaries. The tumor cells exhibited membranous staining for CD20 and CD79a. After the diagnosis of intravascular large B cell lymphoma, the patient received rituximab-based chemotherapy under close follow-up.ope

Arsenic trioxide synergistically promotes the antileukaemic activity of venetoclax by downregulating Mcl-1 in acute myeloid leukaemia cells

Background: The evasion of apoptosis through dysregulated Bcl-2 family members is a hallmark of leukaemia stem cells (LSCs) in acute myeloid leukaemia (AML). Therefore, targeting Bcl-2 with venetoclax has been suggested as an attractive strategy for inducing apoptosis in AML LSCs. However, the selective inhibition of Bcl-2 in AML often leads to upregulation of Mcl-1, another dominant anti-apoptotic Bcl-2 family protein conferring venetoclax resistance. Methods: We assessed the combined effect of venetoclax and arsenic trioxide (ATO) on leukaemic cell viability, apoptosis, combination index, and cell cycle in the human LSC-like KG1 and KG1a cells. The synergistic effect of venetoclax and ATO on apoptosis was also examined in primary CD34+ and CD34+CD38- LSCs from the bone marrow (BM) of AML patients, and compared with those from healthy donors. Results: Venetoclax efficiently impaired cell viability and dose-dependently promoted apoptosis when combined with ATO; their synergism was aptly represented by the combination index. The combination of venetoclax and ATO impaired cell cycle progression by restricting cells within the sub-G1 phase and facilitating caspase-dependent apoptotic cell death associated with the loss of mitochondrial membrane potential, while sparing healthy BM haematopoietic stem cells. Mechanistically, ATO mitigated venetoclax-induced upregulation of Mcl-1 by the inhibition of AKT and ERK, along with activation of GSK-3β. This led to the Mcl-1 destabilisation, triggering Noxa and Bim to facilitate apoptosis and the consequent activation of the apoptosis executioner protein Bak. Moreover, the combination promoted phosphorylation of ATM, Chk2, p38, and H2AX, indicating an active DNA damage response. Conclusions: Our findings demonstrate the synergistic, preferential antileukaemic effects of venetoclax and ATO on LSCs, providing a rationale for preclinical and clinical trials by combining these agents already being used in clinical practice to treat acute leukaemia.ope

PERK/NRF2 and Autophagy Form a Resistance Mechanism Against G9a Inhibition in Leukemia Stem Cells

Background: The histone methyltransferase G9a has recently been identified as a potential target for epigenetic therapy of acute myeloid leukemia (AML). However, the effect of G9a inhibition on leukemia stem cells (LSCs), which are responsible for AML drug resistance and recurrence, is unclear. In this study, we investigated the underlying mechanisms of the LSC resistance to G9a inhibition. Methods: We evaluated the effects of G9a inhibition on the unfolded protein response and autophagy in AML and LSC-like cell lines and in primary CD34+CD38- leukemic blasts from patients with AML and investigated the underlying mechanisms. The effects of treatment on cells were evaluated by flow cytometry, western blotting, confocal microscopy, reactive oxygen species (ROS) production assay. Results: The G9a inhibitor BIX-01294 effectively induced apoptosis in AML cell lines; however, the effect was limited in KG1 LSC-like cells. BIX-01294 treatment or siRNA-mediated G9a knockdown led to the activation of the PERK/NRF2 pathway and HO-1 upregulation in KG1 cells. Phosphorylation of p38 and intracellular generation of reactive oxygen species (ROS) were suppressed. Pharmacological or siRNA-mediated inhibition of the PERK/NRF2 pathway synergistically enhanced BIX-01294-induced apoptosis, with suppressed HO-1 expression, increased p38 phosphorylation, and elevated ROS generation, indicating that activated PERK/NRF2 signaling suppressed ROS-induced apoptosis in KG1 cells. By contrast, cotreatment of normal hematopoietic stem cells with BIX-01294 and a PERK inhibitor had no significant proapoptotic effect. Additionally, G9a inhibition induced autophagy flux in KG1 cells, while autophagy inhibitors significantly increased the BIX-01294-induced apoptosis. This prosurvival autophagy was not abrogated by PERK/NRF2 inhibition. Conclusions: PERK/NRF2 signaling plays a key role in protecting LSCs against ROS-induced apoptosis, thus conferring resistance to G9a inhibitors. Treatment with PERK/NRF2 or autophagy inhibitors could overcome resistance to G9a inhibition and eliminate LSCs, suggesting the potential clinical utility of these unique targeted therapies against AML.ope

DRP1 Inhibition Enhances Venetoclax-Induced Mitochondrial Apoptosis in TP53-Mutated Acute Myeloid Leukemia Cells through BAX/BAK Activation

Although TP53 mutations in acute myeloid leukemia (AML) are associated with poor response to venetoclax, the underlying resistance mechanism remains unclear. Herein, we investigated the functional role of dynamin-related protein 1 (DRP1) in venetoclax sensitivity in AML cells with respect to TP53 mutation status. Effects of DRP1 inhibition on venetoclax-induced cell death were compared in TP53-mutated (THP-1 and Kasumi-1) and TP53 wild-type leukemia cell lines (MOLM-13 and MV4-11), as well as in primary AML cells obtained from patients. Venetoclax induced apoptosis in TP53 wild-type AML cells but had limited effects in TP53-mutated AML cells. DRP1 expression was downregulated in MOLM-13 cells after venetoclax treatment but was unaffected in THP-1 cells. Cotreatment of THP-1 cells with venetoclax and a TP53 activator NSC59984 downregulated DRP1 expression and increased apoptosis. Combination treatment with the DRP1 inhibitor Mdivi-1 and venetoclax significantly increased mitochondria-mediated apoptosis in TP53-mutated AML cells. The combination of Mdivi-1 and venetoclax resulted in noticeable downregulation of MCL-1 and BCL-xL, accompanied by the upregulation of NOXA, PUMA, BAK, and BAX. These findings suggest that DRP1 is functionally associated with venetoclax sensitivity in TP53-mutated AML cells. Targeting DRP1 may represent an effective therapeutic strategy for overcoming venetoclax resistance in TP53-mutated AML.ope

ULK1 Inhibition as a Targeted Therapeutic Strategy for FLT3-ITD-mutated Acute Myeloid Leukemia

Background: In acute myeloid leukemia (AML), internal tandem duplication mutations in the FLT3 tyrosine kinase receptor (FLT3-ITD) are associated with a dismal outcome. Although uncoordinated 51-like kinase 1 (ULK1), which plays a central role in the autophagy pathway, has emerged as a novel therapeutic target for various cancers, its role in FLT3-ITD AML remains elusive. In this study, we evaluated the effects of ULK1 inhibition on leukemia cell death in FLT3-ITD AML. Method: We evaluated ULK1 expression and the levels of apoptosis and autophagy following ULK1 inhibition in FLT3-ITD AML cell lines and investigated the mechanism underlying apoptosis induced by ULK1 inhibition. Statistical analysis was performed using GraphPad Prism 4.0 (GraphPad Software Inc). Results: FLT3-ITD AML cells showed significantly higher ULK1 expression than FLT3-wild-type (WT) AML cells. Two ULK1 inhibitors, MRT 68921 and SBI-0206965, induced apoptosis in FLT3-ITD AML cells, with relatively minimal effects on FLT3-WT AML cells and normal CD34-positive cells. Apoptosis induction by ULK1 inhibition was associated with caspase pathway activation. Interestingly, ULK1 inhibition paradoxically also induced autophagy, showing synergistic interaction with autophagy inhibitors. Hence, autophagy may act as a prosurvival mechanism in FLT3-ITD AML cells. FLT3-ITD protein degradation and inhibition of the ERK, AKT, and STAT5 pathways were also observed in FLT3-ITD AML cells following treatment with ULK1 inhibitors. Conclusion: ULK1 is a viable drug target and ULK1 inhibition may represent a promising therapeutic strategy against FLT3-ITD AML.ope

Clinical characteristics and treatment outcomes of isolated myeloid sarcoma without bone marrow involvement: a single-institution experience

BACKGROUND: Isolated myeloid sarcoma (MS) is a rare extramedullary tumor mass composed of malignant myeloid precursor cells without any evidence of leukemia in the peripheral blood and bone marrow. We describe the clinical characteristics and outcomes of patients diagnosed with isolated MS at our institution. METHODS: We retrospectively reviewed 9 of 497 acute myeloid leukemia (AML) patients (1.8%) with isolated MS. Isolated MS patients were divided into 2 groups according to the first-line treatment strategy: systemic treatment only (S) or local treatment with or without systemic treatment (LS). RESULTS: The most common site of MS occurrence was the head and neck area (N=4, 44.4%), followed by the anterior mediastinum (N=2, 22.2%) and the gastrointestinal tract (N=2, 22.2%). The tumors of 4 patients (44.4%) eventually evolved to AML, in a median time of 13.4 months (range, 2.4-20.1 mo). The number of patients achieving complete remission after first-line treatment was higher in the LS group (N=5, 83.3%) than in the S group (N=1, 33.3%) (P =0.226). All patients in the LS group survived, but those in the S group died (P=0.012). CONCLUSION: Accurate and rapid diagnosis using various modalities and the early initiation of intensive combined treatment may be the optimal strategies to reduce the risk of isolated MS subsequently evolving to AML. To fully understand the characteristics of isolated MS, a larger number of patients from a multinational study is necessary.ope

Immunosuppressive role of CD11b + CD33 + HLA-DR - myeloid-derived suppressor cells-like blast subpopulation in acute myeloid leukemia

Objective: Myeloid-derived suppressor cells (MDSCs) facilitate tumor growth and development by suppressing T cell function; however, their role in acute myeloid leukemia (AML) remains unclear. Here, we investigated the immunosuppressive role and prognostic value of blasts with an MDSC-like phenotype. Methods: CD11b+ CD33+ HLA-DR- MDSC-like blasts from bone marrow mononuclear cells of patients with AML were analyzed. To investigate their T cell-suppressing function, MDSC-like blasts were isolated using flow cytometry and co-cultured with CD8+ cytotoxic T cells and NB4 leukemic cells. Treatment outcomes were then compared between the MDSC-like blasts low (≤9.76%) and high (>9.76%) groups to identify clinical significance. Results: MDSC-like blasts showed higher expression of arginase-1 and inducible nitric oxide synthase. Isolated MDSC-like blasts significantly suppressed CD8+ T cell proliferation induced by phytohemagglutinin A. NB4 cell proliferation was significantly suppressed upon co-culture with CD8+ cytotoxic T cells and partially restored upon co-culture with MDSC-like blasts. Patients with high MDSC-like blasts at diagnosis showed substantially shorter overall survival and leukemia-free survival relative to low MDSC-like blasts patients, with subgroup analysis showing statistically significant differences in patients not receiving allogeneic hematopoietic stem cell transplantation. Conclusion: We demonstrated that MDSC-like blasts drive AML-specific immune-escape mechanisms by suppressing T cell proliferation and restoring T cell-suppressed NB4 cell proliferation, with clinically higher fractions of MDSC-like blasts at diagnosis resulting in poor prognosis.ope

Predictive Factors of Event-Free Survival at 24 Months in Patients with Peripheral T-Cell Lymphoma: A Retrospective Study

Purpose: Event-free survival at 24 months (EFS24) is known to be a surrogate marker for overall survival (OS) for patients with peripheral T-cell lymphoma (PTCL). We examined the role of EFS24 in PTCL compared to diffuse large B-cell lymphoma (DLBCL), and then assessed the clinical predictive factors of achieving EFS24. Materials and methods: Patients with newly diagnosed PTCL treated with anthracycline-based chemotherapy were included. Subsequent OS was defined as the time elapsed from 24 months after diagnosis until death from any cause in those who achieved EFS24. Results: Overall, 153 patients were evaluated, and 51 patients (33.3%) achieved EFS24. Patients who achieved EFS24 showed superior OS compared to patients who did not (p < 0.001). EFS24 could stratify the subsequent OS although it did not reach to that of the general population. After matching the PTCL group to the DLBCL group based on the international prognostic index, the subsequent OS in patients who achieved EFS24 was similar between the two groups (p=0.094). Advanced stage was a significant factor to predict the failing EFS24 by multivariable analysis (p < 0.001). Conclusion: Patients with PTCL who achieve EFS24 could have a favorable subsequent OS. Since advanced disease stage is a predictor of EFS24 failure, future efforts should focus on developing novel therapeutic strategies for PTCL patients presenting with advanced disease.ope

Cytogenetic testing by fluorescence in situ hybridization is improved by plasma cell sorting in multiple myeloma

Accurate detection of cytogenetic abnormalities has become more important for improving risk-adapted treatment strategies in multiple myeloma (MM). However, precise cytogenetic testing by fluorescence in situ hybridization (FISH) is challenged by the dilution effect of bone marrow specimens and poor growth of plasma cells ex vivo. It has been suggested that FISH should be performed in combination with plasma cell enrichment strategies. We examined cytogenetic abnormalities in newly diagnosed MM and compared the efficacy of three different enrichment modalities for FISH: direct FISH (n = 137), fluorescence immunophenotyping and interphase cytogenetics as a tool for the investigation of neoplasms (FICTION) technique (n = 224), and a plasma cell sorting FISH with fluorescence-activated cell sorter (FACS) (n = 132). FISH disclosed cytogenetic abnormalities in 38.0% of samples by direct FISH, 56.3% by FICTION, and 95.5% by FACS-FISH, and the percentage of cells with abnormal signals detected by FISH was significantly higher by FACS-FISH than direct FISH or FICTION. Our results suggest that the efficacy of FISH is dependent on the plasma cell enrichment modalities and reveal that plasma cell sorting FISH with FACS enables better detection of cytogenetic abnormalities in diagnostic MM samples.ope