Anticancer activities of Licochalcone D (LCD) in human colorectal cancer (CRC) cells HCT116 and oxaliplatin-resistant HCT116 (HCT116-OxR) were determined. Cell viability assay and soft agar assay were used to analyze antiproliferative activity of LCD.Flow cytometry was performed to determine effects of LCD on apoptosis, cell cycle distribution, reactive oxygen species (ROS), mitochondrial membrane potential (MMP) dysfunction, and multi-caspase activity in CRC cells. Western blot analysis was used to monitor levels of proteins involved in cell cycle and apoptosis signaling pathways. LCD suppressed the growth and anchorageindependent colony formation of both HCT116 and HCT116-OxR cells. Cell cycle analysis by flow cytometry indicated that LCD induced cell cycle arrest and increased cells in sub-G1 phase. In parallel with the antiproliferative effect of LCD, LCD up-regulated levels of p21 and p27 while downregulating cyclin B1 and cdc2. In addition, phosphorylation levels of JNK and p38 mitogen-activated protein kinase (MAPK) were increased by LCD. Inhibition of these kinases somehow prevented the antiproliferative effect of LCD. Moreover, LCD increased ROS and deregulated mitochondrial membrane potential, leading to the activation of multiple caspases. An ROS scavenger N-acetyl-cysteine (NAC) or pan-caspase inhibitor Z-VAD-FMK prevented the antiproliferative effect of LCD, supporting that ROS generation and caspase activation mediated LCD-induced apoptosis in CRC cells. In conclusion, LCD exerted antitumor activity in CRC cells by inducing ROS generation and phosphorylation of JNK and p38 MAPK. These results support that LCD could be further developed as a chemotherapeutic agent for treating CRC.

Purpose: This multicenter, open-label, phase II trial evaluated the efficacy and safety of bortezomib combined with dexamethasone for the treatment of relapsed/refractory cutaneous T-cell lymphoma (CTCL) in previously treated patients across 14 institutions in South Korea. Materials and Methods: Between September 2017 and July 2020, 29 patients with histologically confirmed CTCL received treatment, consisting of eight 4-week cycles of induction therapy followed by maintenance therapy, contingent upon response, for up to one year. The primary endpoint was the proportion of patients achieving an objective global response. Results: Thirteen of the 29 patients (44.8%) achieved an objective global response, including two complete responses. The median progression-free survival (PFS) was 5.8 months, with responders showing a median PFS of 14.0 months. Treatment-emergent adverse events were generally mild, with a low incidence of peripheral neuropathy and hematologic toxicities. Despite the trend toward shorter PFS in patients with higher mutation burdens, genomic profiling before and after treatment showed no significant emergence of new mutations indicative of disease progression. Conclusion This study supports the use of bortezomib and dexamethasone as a viable and safe treatment option for previously treated CTCL, demonstrating substantial efficacy and manageability in adverse effects. Further research with a larger cohort is suggested to validate these findings and explore the prognostic value of mutation profiles.

Anticancer activities of Licochalcone D (LCD) in human colorectal cancer (CRC) cells HCT116 and oxaliplatin-resistant HCT116 (HCT116-OxR) were determined. Cell viability assay and soft agar assay were used to analyze antiproliferative activity of LCD.Flow cytometry was performed to determine effects of LCD on apoptosis, cell cycle distribution, reactive oxygen species (ROS), mitochondrial membrane potential (MMP) dysfunction, and multi-caspase activity in CRC cells. Western blot analysis was used to monitor levels of proteins involved in cell cycle and apoptosis signaling pathways. LCD suppressed the growth and anchorageindependent colony formation of both HCT116 and HCT116-OxR cells. Cell cycle analysis by flow cytometry indicated that LCD induced cell cycle arrest and increased cells in sub-G1 phase. In parallel with the antiproliferative effect of LCD, LCD up-regulated levels of p21 and p27 while downregulating cyclin B1 and cdc2. In addition, phosphorylation levels of JNK and p38 mitogen-activated protein kinase (MAPK) were increased by LCD. Inhibition of these kinases somehow prevented the antiproliferative effect of LCD. Moreover, LCD increased ROS and deregulated mitochondrial membrane potential, leading to the activation of multiple caspases. An ROS scavenger N-acetyl-cysteine (NAC) or pan-caspase inhibitor Z-VAD-FMK prevented the antiproliferative effect of LCD, supporting that ROS generation and caspase activation mediated LCD-induced apoptosis in CRC cells. In conclusion, LCD exerted antitumor activity in CRC cells by inducing ROS generation and phosphorylation of JNK and p38 MAPK. These results support that LCD could be further developed as a chemotherapeutic agent for treating CRC.

Purpose: This multicenter, open-label, phase II trial evaluated the efficacy and safety of bortezomib combined with dexamethasone for the treatment of relapsed/refractory cutaneous T-cell lymphoma (CTCL) in previously treated patients across 14 institutions in South Korea. Materials and Methods: Between September 2017 and July 2020, 29 patients with histologically confirmed CTCL received treatment, consisting of eight 4-week cycles of induction therapy followed by maintenance therapy, contingent upon response, for up to one year. The primary endpoint was the proportion of patients achieving an objective global response. Results: Thirteen of the 29 patients (44.8%) achieved an objective global response, including two complete responses. The median progression-free survival (PFS) was 5.8 months, with responders showing a median PFS of 14.0 months. Treatment-emergent adverse events were generally mild, with a low incidence of peripheral neuropathy and hematologic toxicities. Despite the trend toward shorter PFS in patients with higher mutation burdens, genomic profiling before and after treatment showed no significant emergence of new mutations indicative of disease progression. Conclusion This study supports the use of bortezomib and dexamethasone as a viable and safe treatment option for previously treated CTCL, demonstrating substantial efficacy and manageability in adverse effects. Further research with a larger cohort is suggested to validate these findings and explore the prognostic value of mutation profiles.

Anticancer activities of Licochalcone D (LCD) in human colorectal cancer (CRC) cells HCT116 and oxaliplatin-resistant HCT116 (HCT116-OxR) were determined. Cell viability assay and soft agar assay were used to analyze antiproliferative activity of LCD.Flow cytometry was performed to determine effects of LCD on apoptosis, cell cycle distribution, reactive oxygen species (ROS), mitochondrial membrane potential (MMP) dysfunction, and multi-caspase activity in CRC cells. Western blot analysis was used to monitor levels of proteins involved in cell cycle and apoptosis signaling pathways. LCD suppressed the growth and anchorageindependent colony formation of both HCT116 and HCT116-OxR cells. Cell cycle analysis by flow cytometry indicated that LCD induced cell cycle arrest and increased cells in sub-G1 phase. In parallel with the antiproliferative effect of LCD, LCD up-regulated levels of p21 and p27 while downregulating cyclin B1 and cdc2. In addition, phosphorylation levels of JNK and p38 mitogen-activated protein kinase (MAPK) were increased by LCD. Inhibition of these kinases somehow prevented the antiproliferative effect of LCD. Moreover, LCD increased ROS and deregulated mitochondrial membrane potential, leading to the activation of multiple caspases. An ROS scavenger N-acetyl-cysteine (NAC) or pan-caspase inhibitor Z-VAD-FMK prevented the antiproliferative effect of LCD, supporting that ROS generation and caspase activation mediated LCD-induced apoptosis in CRC cells. In conclusion, LCD exerted antitumor activity in CRC cells by inducing ROS generation and phosphorylation of JNK and p38 MAPK. These results support that LCD could be further developed as a chemotherapeutic agent for treating CRC.

Purpose: This multicenter, open-label, phase II trial evaluated the efficacy and safety of bortezomib combined with dexamethasone for the treatment of relapsed/refractory cutaneous T-cell lymphoma (CTCL) in previously treated patients across 14 institutions in South Korea. Materials and Methods: Between September 2017 and July 2020, 29 patients with histologically confirmed CTCL received treatment, consisting of eight 4-week cycles of induction therapy followed by maintenance therapy, contingent upon response, for up to one year. The primary endpoint was the proportion of patients achieving an objective global response. Results: Thirteen of the 29 patients (44.8%) achieved an objective global response, including two complete responses. The median progression-free survival (PFS) was 5.8 months, with responders showing a median PFS of 14.0 months. Treatment-emergent adverse events were generally mild, with a low incidence of peripheral neuropathy and hematologic toxicities. Despite the trend toward shorter PFS in patients with higher mutation burdens, genomic profiling before and after treatment showed no significant emergence of new mutations indicative of disease progression. Conclusion This study supports the use of bortezomib and dexamethasone as a viable and safe treatment option for previously treated CTCL, demonstrating substantial efficacy and manageability in adverse effects. Further research with a larger cohort is suggested to validate these findings and explore the prognostic value of mutation profiles.

The Controlling Nutritional Status (CONUT) score and the prognostic nutritional index (PNI) have emerged as important nutritional indices because they provide an objective assessment based on data. We aimed to investigate how these nutritional indices relate to outcomes in patients with sepsis. Methods: Data were collected retrospectively at five hospitals for patients aged ≥18 years receiving treatment for sepsis between January 1, 2017, and December 31, 2021. Serum albumin and total cholesterol concentrations, and peripheral lymphocytes were used to calculate the CONUT score and PNI. To identify predictors correlated with 30-day mortality, analyses were conducted using univariate and multivariate Cox proportional hazards models. Results: The 30-day mortality rate among 9,763 patients was 15.8% (n=1,546). The median CONUT score was 5 (interquartile range [IQR], 3–7) and the median PNI score was 39.6 (IQR, 33.846.4). Higher 30-day mortality rates were associated with individuals with moderate (CONUT score: 5–8; PNI: 35–38) or severe (CONUT: 9–12; PNI: <35) malnutrition compared with those with no malnutrition (CONUT: 0–1; PNI: >38). With CONUT scores, the hazard ratio (HR) associated with moderate malnutrition was 1.52 (95% confidence interval [CI], 1.24–1.87; P<0.001); for severe, HR=2.42 (95% CI, 1.95–3.02; P<0.001). With PNI scores, the HR for moderate malnutrition was 1.29 (95% CI, 1.09–1.53; P=0.003); for severe, HR=1.88 (95% CI, 1.67–2.12; P<0.001). Conclusions: The nutritional indices CONUT score and PNI showed significant associations with mortality of sepsis patients within 30 days.

The Controlling Nutritional Status (CONUT) score and the prognostic nutritional index (PNI) have emerged as important nutritional indices because they provide an objective assessment based on data. We aimed to investigate how these nutritional indices relate to outcomes in patients with sepsis. Methods: Data were collected retrospectively at five hospitals for patients aged ≥18 years receiving treatment for sepsis between January 1, 2017, and December 31, 2021. Serum albumin and total cholesterol concentrations, and peripheral lymphocytes were used to calculate the CONUT score and PNI. To identify predictors correlated with 30-day mortality, analyses were conducted using univariate and multivariate Cox proportional hazards models. Results: The 30-day mortality rate among 9,763 patients was 15.8% (n=1,546). The median CONUT score was 5 (interquartile range [IQR], 3–7) and the median PNI score was 39.6 (IQR, 33.846.4). Higher 30-day mortality rates were associated with individuals with moderate (CONUT score: 5–8; PNI: 35–38) or severe (CONUT: 9–12; PNI: <35) malnutrition compared with those with no malnutrition (CONUT: 0–1; PNI: >38). With CONUT scores, the hazard ratio (HR) associated with moderate malnutrition was 1.52 (95% confidence interval [CI], 1.24–1.87; P<0.001); for severe, HR=2.42 (95% CI, 1.95–3.02; P<0.001). With PNI scores, the HR for moderate malnutrition was 1.29 (95% CI, 1.09–1.53; P=0.003); for severe, HR=1.88 (95% CI, 1.67–2.12; P<0.001). Conclusions: The nutritional indices CONUT score and PNI showed significant associations with mortality of sepsis patients within 30 days.

The Controlling Nutritional Status (CONUT) score and the prognostic nutritional index (PNI) have emerged as important nutritional indices because they provide an objective assessment based on data. We aimed to investigate how these nutritional indices relate to outcomes in patients with sepsis. Methods: Data were collected retrospectively at five hospitals for patients aged ≥18 years receiving treatment for sepsis between January 1, 2017, and December 31, 2021. Serum albumin and total cholesterol concentrations, and peripheral lymphocytes were used to calculate the CONUT score and PNI. To identify predictors correlated with 30-day mortality, analyses were conducted using univariate and multivariate Cox proportional hazards models. Results: The 30-day mortality rate among 9,763 patients was 15.8% (n=1,546). The median CONUT score was 5 (interquartile range [IQR], 3–7) and the median PNI score was 39.6 (IQR, 33.846.4). Higher 30-day mortality rates were associated with individuals with moderate (CONUT score: 5–8; PNI: 35–38) or severe (CONUT: 9–12; PNI: <35) malnutrition compared with those with no malnutrition (CONUT: 0–1; PNI: >38). With CONUT scores, the hazard ratio (HR) associated with moderate malnutrition was 1.52 (95% confidence interval [CI], 1.24–1.87; P<0.001); for severe, HR=2.42 (95% CI, 1.95–3.02; P<0.001). With PNI scores, the HR for moderate malnutrition was 1.29 (95% CI, 1.09–1.53; P=0.003); for severe, HR=1.88 (95% CI, 1.67–2.12; P<0.001). Conclusions: The nutritional indices CONUT score and PNI showed significant associations with mortality of sepsis patients within 30 days.

The Controlling Nutritional Status (CONUT) score and the prognostic nutritional index (PNI) have emerged as important nutritional indices because they provide an objective assessment based on data. We aimed to investigate how these nutritional indices relate to outcomes in patients with sepsis. Methods: Data were collected retrospectively at five hospitals for patients aged ≥18 years receiving treatment for sepsis between January 1, 2017, and December 31, 2021. Serum albumin and total cholesterol concentrations, and peripheral lymphocytes were used to calculate the CONUT score and PNI. To identify predictors correlated with 30-day mortality, analyses were conducted using univariate and multivariate Cox proportional hazards models. Results: The 30-day mortality rate among 9,763 patients was 15.8% (n=1,546). The median CONUT score was 5 (interquartile range [IQR], 3–7) and the median PNI score was 39.6 (IQR, 33.846.4). Higher 30-day mortality rates were associated with individuals with moderate (CONUT score: 5–8; PNI: 35–38) or severe (CONUT: 9–12; PNI: <35) malnutrition compared with those with no malnutrition (CONUT: 0–1; PNI: >38). With CONUT scores, the hazard ratio (HR) associated with moderate malnutrition was 1.52 (95% confidence interval [CI], 1.24–1.87; P<0.001); for severe, HR=2.42 (95% CI, 1.95–3.02; P<0.001). With PNI scores, the HR for moderate malnutrition was 1.29 (95% CI, 1.09–1.53; P=0.003); for severe, HR=1.88 (95% CI, 1.67–2.12; P<0.001). Conclusions: The nutritional indices CONUT score and PNI showed significant associations with mortality of sepsis patients within 30 days.