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( Yu Ri Kim ),( Soo-jeong Kim ),( June-won Cheong ),( Yundeok Kim ),( Ji Eun Jang ),( Hyunsoo Cho ),( Haerim Chung ),( Yoo Hong Min ),( Woo Ick Yang ),( Arthur Cho ),( Jin Seok Kim ) 대한내과학회 2021 The Korean Journal of Internal Medicine Vol.36 No.0
Background/Aims: Although the use of surveillance 18F-fluorodeoxyglucose (FDG) positron emission tomography/computed tomography (PET/CT) is discouraged in patients with diffuse large B-cell lymphoma, its usefulness in different subtypes has not been thoroughly investigated. Methods: We retrospectively evaluated 157 patients who showed positive results on surveillance FDG-PET/CT every 6 months following complete response for up to 5 years. All of the patients also underwent biopsies. Results: Seventy-eight (49.6%) of 157 patients had true positive results; the remaining 79 (50.3%), including eight (5.1%) with secondary malignancies, were confirmed to yield false positive results. Among the 78 patients with true positive results, the disease in seven (8.9%) had transformed to a different subtype. The positive predictive value (PPV) of FDG-PET/CT for aggressive B-cell non-Hodgkin’s lymphoma (NHL) was lower than that for indolent B-cell or aggressive T-cell NHL (p = 0.003 and p = 0.018, respectively), especially in patients with a low/low-intermediate international prognostic index (IPI) upon a positive PET/CT finding. On the other hand, indolent B-cell and aggressive T-cell NHL patients showed PPVs of > 60%, including those with low/low-intermediate secondary IPIs. Conclusions: The role of FDG-PET/CT surveillance is limited, and differs according to the lymphoma subtype. FDG-PET/CT may be useful in detecting early relapse in patients with aggressive T-cell NHL, including those with low/low-intermediate risk secondary IPI; as already known, FDG-PET/CT has no role in aggressive B-cell NHL. Repeat biopsy should be performed to discriminate relapse or transformation from false positive findings in patients with positive surveillance FDG-PET/CT results.
( Yu Ri Cho ),( Eun Ju Cho ),( Jung Hwan Yoon ),( Jung Hee Kwon ),( Jeong Hoon Lee ),( Su Jong Yu ),( Hyo Suk Lee ),( Chung Yong Kim ) 대한간학회 2012 춘·추계 학술대회 (KASL) Vol.2012 No.1
Background: The crosstalk between tumor cells and their microenvironment plays a crucial role in the development, progression and metastasis of HCC. Hypoxia, a common feature of advanced hepatocellular carcinoma (HCC), has been known to modulate the development and evolution of the tumor microenvironment. However, the mechanism and functional impact of the tumor-stroma co-evolution in hypoxic HCC remains poorly understood. In this study, we investigated the effects of hypoxia on the tumor-stroma crosstalk in HCC. Methods: Human HCC cells (Huh-BAT and HepG2) were co-cultured with activated human hepatic stellate cells (HSCs; LX-2) either in a normoxic or hypoxic condition. Cell growth, migration capacity and apoptosis were assessed using the MTS assay, wound healing assay and DAPI staining. The expression of various growth factors was detected by quantitative RT-PCR and ELISA. Results: Among several growth factors derived from cocultured cells, PDGF-BB was most abundantly upregulated in hypoxic condition. Hypoxic microenvironment-derived PDGFBB induced tumor cell proliferation, migration and attenuated DC or TRAIL cytotoxicity. Consistent with these findings, co-culturing HCC cells with HSCs in hypoxia significantly enhanced proliferation and migration of both cells as compared to normoxic condition. Co-culturing also decreased DC- or TRAIL-induced HCC cell apoptosis. The effects of hypoxic tumor-stroma crosstalk on proliferation and migration were meaningfully inhibited by the PI3K inhibitor compared to cells in a normoxic condition. Conclusions: These results indicate that hypoxia induced upregulation of PDGF-BB accelerates the evolution of the tumorstroma crosstalk at least in part through PI3/AKT pathway.
( Yu Ri Cho ),( Dong Hyeon Lee ),( Jeong Hoon Lee ),( Su Jong Yu ),( Jung Hwan Yoon ),( Hyo Suk Lee ),( Yoon Jun Kim ) 대한내과학회 2011 대한내과학회 추계학술발표논문집 Vol.2011 No.1
Background: Antiviral resistance is a major challenge for the treatments that are currently available for hepatitis B virus. However, the efficacy of adefovir (ADV) and entecavir (ETV) combination therapy in patients who developed antiviral resistance was not fully evaluated. In this study, we aimed to evaluate the efficacy of ADV and ETV combination therapy as compared to the efficacy of LAM and ADV in patients with antiviral resistant chronic hepatitis B (CHB). Methods: Antiviral resistance was defined as follows: persistently detectable HBV DNA after 36 weeks after LAM or ADV therapy ; virological breakthrough with previous LAM or ADV therapy ; or documented LAM or ADV-resistant mutations. We assessed 90 patients with antiviral resistant CHB. Of these, 27 patients were treated with a combination of ADV+ETV and 63 patients were treated with a combination of LAM+ADV. The virological and biochemical parameters were compared between the two groups at 3, 6, 9 and 12 months, respectively. Results: Treatment with a combination of ADV+ETV resulted significant difference in virological response compared to that in the LAM+ADV group through 12 months (p=0.001). At 12 months, the HBV DNA declined more in the ADV+ETV group than that in the LAM+ADV group (-4.52±1.956 vs. -2.65±1.723 log10IU/ml; p=0.001). The rate of a virological non-response, which is defined as <1 log10IU/ml reduction in HBV DNA concentration at 3 months was significantly greater in the LAM+ADV group than that in the ADV+ETV group (26.78% vs. 7.40%, p=0.022). Also, the rate of a virological complete response at 12 months was greater in the ADV+ETV group than that in the LAM+ADV group (73.68% vs. 31.48%, p=0.005). In the multivariate analysis, parameters related to a virological response at Month 12 were the baseline HBV DNA level [OR, 0.403 ; p=0.004] and virological non-response at Month 3 [OR, 0.102 ; p=0.028]. Conclusion: In patients with antiviral resistant CHB, the response to ADV+ETV was significantly superior compared to that of the LAM+ADV group for suppressing HBV DNA through 12 months. The result indicates that ADV+ETV should be used in the patients antiviral resistant CHB, especially in the area where tenofovir is not available.