1.Research on control effect of sulfoxaflor and flonicamid on Lonicera japonica.
Shao-Yan HOU ; Yu-Jie WANG ; Jian XUE ; Jia-Xin LI ; Peng-Si WANG
China Journal of Chinese Materia Medica 2018;43(2):306-308
The study was aimed to determine the efficacy of two pesticides in the control of aphids in Lonicera japonica, and study the applicability of pesticides in L. japonica. The number of insects was counted before and 2, 3, 7 and 10 days after the application of pesticide in the test area within different dosage groups. The method was 5-point sampling method. Five aphids on the L. japonica branches were selected, then the number of insects was recorded. The effect of the two pesticides on the control rate of aphid was more than 80% at 1 d after application. The results showed that the two pesticides had good efficacy. After 7 days and 10 days, the control effect was 100%. After 1 day of spraying, the effect of the two pesticides on the control of L. japonica aphids was more than 80%, which was higher than that of the control agent. The results showed that the two pesticides had good and fast effect. After 7 days and 10 days of spraying, the control effect was 100%. The control effect of two kinds pesticides for aphid sprayed in recommended dose on the L. japonica is good and showed no hytotoxicity.
Animals
;
Aphids
;
Lonicera
;
Niacinamide
;
analogs & derivatives
;
Pesticides
;
Pyridines
;
Sulfur Compounds
2.EGF Induced RET Inhibitor Resistance in CCDC6-RET Lung Cancer Cells.
Hyun CHANG ; Ji Hea SUNG ; Sung Ung MOON ; Han Soo KIM ; Jin Won KIM ; Jong Seok LEE
Yonsei Medical Journal 2017;58(1):9-18
PURPOSE: Rearrangement of the proto-oncogene rearranged during transfection (RET) has been newly identified potential driver mutation in lung adenocarcinoma. Clinically available tyrosine kinase inhibitors (TKIs) target RET kinase activity, which suggests that patients with RET fusion genes may be treatable with a kinase inhibitor. Nevertheless, the mechanisms of resistance to these agents remain largely unknown. Thus, the present study aimed to determine whether epidermal growth factor (EGF) and hepatocyte growth factor (HGF) trigger RET inhibitor resistance in LC-2/ad cells with CCDC6-RET fusion genes. MATERIALS AND METHODS: The effects of EGF and HGF on the susceptibility of a CCDC6-RET lung cancer cell line to RET inhibitors (sunitinib, E7080, vandetanib, and sorafenib) were examined. RESULTS: CCDC6-RET lung cancer cells were highly sensitive to RET inhibitors. EGF activated epidermal growth factor receptor (EGFR) and triggered resistance to sunitinib, E7080, vandetanib, and sorafenib by transducing bypass survival signaling through ERK and AKT. Reversible EGFR-TKI (gefitinib) resensitized cancer cells to RET inhibitors, even in the presence of EGF. Endothelial cells, which are known to produce EGF, decreased the sensitivity of CCDC6-RET lung cancer cells to RET inhibitors, an effect that was inhibited by EGFR small interfering RNA (siRNA), anti-EGFR antibody (cetuximab), and EGFR-TKI (Iressa). HGF had relatively little effect on the sensitivity to RET inhibitors. CONCLUSION: EGF could trigger resistance to RET inhibition in CCDC6-RET lung cancer cells, and endothelial cells may confer resistance to RET inhibitors by EGF. E7080 and other RET inhibitors may provide therapeutic benefits in the treatment of RET-positive lung cancer patients.
Adenocarcinoma/drug therapy/*genetics
;
Cell Line, Tumor
;
Cetuximab/pharmacology
;
Drug Resistance, Neoplasm/drug effects/*genetics
;
Epidermal Growth Factor/metabolism/*pharmacology
;
*Gene Rearrangement
;
Hepatocyte Growth Factor/*pharmacology
;
Humans
;
Indoles/pharmacology
;
Lung Neoplasms/drug therapy/*genetics
;
MAP Kinase Signaling System
;
*Mutation
;
Niacinamide/analogs & derivatives/pharmacology
;
Phenylurea Compounds/pharmacology
;
Piperidines/pharmacology
;
Protein Kinase Inhibitors/therapeutic use
;
Proto-Oncogene Proteins c-ret/*antagonists & inhibitors/genetics
;
Pyrroles/pharmacology
;
Quinazolines/pharmacology
;
RNA, Small Interfering/pharmacology
;
Receptor, Epidermal Growth Factor/genetics/metabolism
;
Signal Transduction/drug effects
;
fms-Like Tyrosine Kinase 3/metabolism
3.Trends and Patterns of Hepatocellular Carcinoma Treatment in Korea.
Young Mi HONG ; Ki Tae YOON ; Mong CHO ; Dae Hwan KANG ; Hyung Wook KIM ; Cheol Woong CHOI ; Su Bum PARK ; Jeong HEO ; Hyun Young WOO ; Won LIM
Journal of Korean Medical Science 2016;31(3):403-409
Multiple therapeutic modalities are available for hepatocellular carcinoma (HCC) treatment. We aimed to evaluate the trends for HCC treatment in Korea. Recent trends and patterns in treatment modalities were assessed in HCC patients who first registered for the Health Insurance Review Assessment Service between 2008 and 2012. From 2009 to 2012, 57,690 patients were diagnosed with HCC. Transcatheter arterial chemoembolization (TACE) was the most common treatment modality for initial treatment. Curative treatment modalities like hepatic resection, liver transplantation, and local ablation therapy increased gradually. The 3 most common treatment modalities (hepatic resection, local ablation therapy, TACE) used after initial treatment in 2009 were studied. Following initial hepatic resection, 44.5% of patients required re-treatment. TACE was the most common modality (in 48.3% of cases), while 15.0% of patients received local ablation therapy. After local ablation therapy, 55.4% of patients were re-treated, wherein 45.0% of patients received TACE and 31.5% received local ablation therapy. Following initial TACE, 73.9% patients were re-treated, most commonly with TACE (57.7%) followed by local ablation therapy (12.8%). While there were no significant differences between the initial and re-treatment modalities, various multiple treatments followed the initial treatment. The treatment modalities were interchangeable.
Aged
;
Carcinoma, Hepatocellular/epidemiology/pathology/*therapy
;
Chemoembolization, Therapeutic
;
Combined Modality Therapy/trends
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Cross-Sectional Studies
;
Databases, Factual
;
Female
;
Humans
;
Insurance Claim Review
;
Liver Neoplasms/epidemiology/pathology/*therapy
;
Liver Transplantation
;
Male
;
Middle Aged
;
Niacinamide/administration & dosage/analogs & derivatives
;
Phenylurea Compounds/administration & dosage
;
Prevalence
;
Protein Kinase Inhibitors/administration & dosage
;
Republic of Korea/epidemiology
4.Clinical Efficacy of Sorafenib Combined with Low Dose Cytarabine for Treating Patients with FLT3+ Relapsed and Refractory Acute Myeloid Leukemia.
Xiao-Shu LIU ; Hui LONG ; Yu-Xian HUANG ; Jian-Hui XU ; Jun-Yu ZHU ; Qing-Feng DU ; Bing-Yi WU
Journal of Experimental Hematology 2016;24(2):394-398
OBJECTIVETo study the efficacy and safety of sorafenib combined with low dose cytarabine for treating patients with FLT3(+) relapsed and refractory acute myeloid leukemia (FLT3(+) RR-AML).
METHODSSeven patients with FLT3(+) RR-AML were treated with sorafenib and low dose cytarabine. The curative rate and adverse effects were observed in these patients.
RESULTSOut of 7 RR-AML patients after treatment, 5 patients achieved complete remission (CR), 2 patients achieved partial remission (PR), and the overall response rate (ORR) after one course of therapy was 100%. No severe bleeding, nausea, vomiting and other side effects were found in these patients.
CONCLUSIONSorafenib combined with low dose cytarabine can effectively induce the remission of FLT3(+) RR-AML patients, and is worth for further clinical trails to verify its safty and efficiency.
Cytarabine ; therapeutic use ; Humans ; Leukemia, Myeloid, Acute ; drug therapy ; Niacinamide ; analogs & derivatives ; therapeutic use ; Phenylurea Compounds ; therapeutic use ; Recurrence ; Remission Induction ; Treatment Outcome ; fms-Like Tyrosine Kinase 3 ; metabolism
5.Painful Rashes on the Palms and Soles.
Maneesha BHULLAR ; Anisha BHULLAR ; Niranjan J ARACHCHI
Annals of the Academy of Medicine, Singapore 2016;45(10):479-480
Aged
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Antineoplastic Agents
;
adverse effects
;
Carcinoma, Hepatocellular
;
drug therapy
;
Hand-Foot Syndrome
;
diagnosis
;
etiology
;
Humans
;
Liver Neoplasms
;
drug therapy
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Male
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Neoplasms, Multiple Primary
;
drug therapy
;
Niacinamide
;
adverse effects
;
analogs & derivatives
;
Phenylurea Compounds
;
adverse effects
6.Sorafenib as salvage therapy in refractory relapsed acute myeloid leukemia with positive FLT3 mutation.
Yu ZHANG ; Li XUAN ; Zhiping FAN ; Fen HUANG ; Qianli JIANG ; Na XU ; Ya GAO ; Jing SUN ; Qifa LIU
Chinese Journal of Hematology 2016;37(4):292-296
OBJECTIVETo analyze the effect of sorafenib as salvage therapy used before and/or after allogeneic hematopoietic stem cell transplantation (allo-HSCT) in refractory relapsed FLT3-positive acute myeloid leukemia (AML).
METHODSA total of 16 patients with refractory relapsed FLT3-positive AML, including 10 refractory relapsed pre-transplantation and 6 relapsed after allo-HSCT, were enrolled in this retrospective study. Sorafenib treatment protocols included sorafenib in combination with chemotherapy inducing remission, and sorafenib monotherapy as mauntenance treatment after complete remission (CR).
RESULTSThirteen of the 16 patients achieved CR after one or two courses of induction therapy, including 7 refractory relapsed pre-transplantation and 6 relapsed after allo-HSCT. With a median follow up of 472 (range, 59-1569) days post-transplantation, 12 patients survived and 4 died. Causes of death included leukemia relapse (n=3) and acute graft-versus-host disease (n=1). The 2-year overall and disease-free survival post-transplantation of the 16 patients were (75.0±10.8) % and (50.5±13.7) % respectively. The main side effect of sorafenib was the skin rash. The incidence of rash was lower in the patients used sorafenib pre-transplantation than those post-transplantation (30.0% vs 75.0%, P=0.043).
CONCLUSIONSorafenib used as salvage therapy befor and/or after transplantation for refractory relapsed FLT3-positive AML could reduce the relapse rate and improve the survival.
Antineoplastic Agents ; therapeutic use ; Disease-Free Survival ; Graft vs Host Disease ; Hematopoietic Stem Cell Transplantation ; Humans ; Induction Chemotherapy ; Leukemia, Myeloid, Acute ; genetics ; therapy ; Mutation ; Niacinamide ; analogs & derivatives ; therapeutic use ; Phenylurea Compounds ; therapeutic use ; Recurrence ; Remission Induction ; Retrospective Studies ; Salvage Therapy ; Treatment Outcome ; fms-Like Tyrosine Kinase 3 ; genetics
7.Survival outcomes of hepatic resection compared with transarterial chemoembolization or sorafenib for hepatocellular carcinoma with portal vein tumor thrombosis.
Jung Min LEE ; Byoung Kuk JANG ; Yoo Jin LEE ; Wang Yong CHOI ; Sei Myong CHOI ; Woo Jin CHUNG ; Jae Seok HWANG ; Koo Jeong KANG ; Young Hwan KIM ; Anil Kumar CHAUHAN ; Soo Young PARK ; Won Young TAK ; Young Oh KWEON ; Byung Seok KIM ; Chang Hyeong LEE
Clinical and Molecular Hepatology 2016;22(1):160-167
BACKGROUND/AIMS: Treating hepatocellular carcinoma (HCC) with portal vein tumor thrombosis (PVTT) remains controversial. We compared the outcomes of hepatic resection (HR), transarterial chemoembolization (TACE), and sorafenib therapy as treatments for HCC with PVTT. METHODS: Patients diagnosed as HCC with PVTT between January 2000 and December 2011 who received treatment with sorafenib, HR, or TACE were included. Patients with main PVTT, superior mesenteric vein tumor thrombosis, or Child-Turcotte-Pugh (CTP) class C were excluded. The records of 172 patients were analyzed retrospectively. HR, TACE, and sorafenib treatment were performed is 40, 80, and 52 patients respectively. PVTT was classified as either involving the segmental branch (type I) or extending to involve the right or left portal vein (type II). RESULTS: The median survival time was significantly longer in the HR group (19.9 months) than in the TACE and sorafenib groups (6.6 and 6.2 months, respectively; both p<0.001), and did not differ significantly between the latter two groups (p=0.698). Among patients with CTP class A, type I PVTT or unilobar-involved HCC, the median survival time was longer in the HR group than in the TACE and sorafenib groups (p=0.006). In univariate analyses, the initial treatment method, tumor size, PVTT type, involved lobe, CTP class, and presence of cirrhosis or ascites were correlated with overall survival. The significant prognostic factors for overall survival in Cox proportional-hazards regression analysis were initial treatment method (HR vs. TACE: hazard ratio=1.750, p=0.036; HR vs. sorafenib: hazard ratio=2.262, p=0.006), involved lobe (hazard ratio=1.705, p=0.008), PVTT type (hazard ratio=1.617, p=0.013), and CTP class (hazard ratio=1.712, p=0.012). CONCLUSIONS: Compared with TACE or sorafenib, HR may prolong the survival of patients with HCC in cases of CTP class A, type I PVTT or unilobar-involved HCC.
Adult
;
Aged
;
Antineoplastic Agents/*therapeutic use
;
Carcinoma, Hepatocellular/complications/drug therapy/*therapy
;
Chemoembolization, Therapeutic
;
Combined Modality Therapy
;
Female
;
Follow-Up Studies
;
Humans
;
Liver Neoplasms/complications/drug therapy/*therapy
;
Male
;
Middle Aged
;
Niacinamide/*analogs & derivatives/therapeutic use
;
Phenylurea Compounds/*therapeutic use
;
Portal Vein
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Proportional Hazards Models
;
Retrospective Studies
;
Severity of Illness Index
;
Survival Rate
;
Treatment Outcome
;
Venous Thrombosis/*complications
8.Sorafenib-induced Thyroiditis in FMS-like Tyrosine Kinase 3-internal Tandem Duplication-mutated Acute Myeloid Leukemia.
Jie SUN ; Juan HU ; Yan HUANG ; Shuang-Wei YING ; Xiao-Yan HAN ; Yan-Long ZHENG ; He HUANG
Chinese Medical Journal 2016;129(20):2512-2513
Adult
;
Female
;
Humans
;
Leukemia, Myeloid, Acute
;
enzymology
;
genetics
;
Mutation
;
genetics
;
Niacinamide
;
adverse effects
;
analogs & derivatives
;
Phenylurea Compounds
;
adverse effects
;
Tandem Repeat Sequences
;
genetics
;
Thyroiditis
;
chemically induced
;
enzymology
;
genetics
;
fms-Like Tyrosine Kinase 3
;
genetics
9.Low-dose steroid-induced tumor lysis syndrome in a hepatocellular carcinoma patient.
Jin Ok KIM ; Dae Won JUN ; Hye Jin TAE ; Kang Nyeong LEE ; Hang Lak LEE ; Oh Young LEE ; Ho Soon CHOI ; Byung Chul YOON ; Joon Soo HAHM
Clinical and Molecular Hepatology 2015;21(1):85-88
Tumor lysis syndrome is rare in hepatocellular carcinoma (HCC), but it has been reported more frequently recently in response to treatments such as transcatheter arterial chemoembolization (TACE), radiofrequency thermal ablation (RFTA), and sorafenib. Tumor lysis syndrome induced by low-dose steroid appears to be very unusual in HCC. We report a patient with hepatitis-C-related liver cirrhosis and HCC in whom tumor lysis syndrome occurred due to low-dose steroid (10 mg of prednisolone). The patient was a 90-year-old male who presented at the emergency room of our hospital with general weakness and poor oral intake. He had started to take prednisolone to treat adrenal insufficiency 2 days previously. Laboratory results revealed hyperuricemia, hyperphosphatemia, and increased creatinine. These abnormalities fulfilled the criteria in the Cairo-Bishop definition of tumor lysis syndrome. Although the patient received adequate hydration, severe metabolic acidosis and acute kidney injury progressed unabated. He finally developed multiple organ failure, and died 3 days after admission. This was a case of tumor lysis syndrome caused by administration of low-dose steroid in a patient with HCC.
Acute Kidney Injury/pathology
;
Aged, 80 and over
;
Antineoplastic Agents/therapeutic use
;
Carcinoma, Hepatocellular/*pathology/therapy
;
Chemoembolization, Therapeutic
;
Creatinine/blood
;
Humans
;
Liver Neoplasms/*pathology/*therapy
;
Male
;
Niacinamide/analogs & derivatives/therapeutic use
;
Phenylurea Compounds/therapeutic use
;
Steroids/adverse effects/therapeutic use
;
Tomography, X-Ray Computed
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Tumor Lysis Syndrome/*diagnosis/drug therapy
10.Combined treatment with silibinin and either sorafenib or gefitinib enhances their growth-inhibiting effects in hepatocellular carcinoma cells.
Ha Ra GU ; Su Cheol PARK ; Su Jin CHOI ; Jae Cheol LEE ; You Cheoul KIM ; Chul Ju HAN ; Jin KIM ; Ki Young YANG ; Yeon Joo KIM ; Geum Youb NOH ; So Hyeon NO ; Jae Hoon JEONG
Clinical and Molecular Hepatology 2015;21(1):49-59
BACKGROUND/AIMS: Silibinin, the main component of silymarin, is used as a hepatoprotectant and exhibits anticancer effects against various cancer cells. This study evaluated the effects of a combination of silibinin with either gefitinib or sorafenib on hepatocellular carcinoma (HCC) cells. METHODS: Several different human HCC cell lines were used to test the growth-inhibiting effects and cell toxicity of silibinin both alone and in combination with either gefitinib or sorafenib. The cell viability and growth inhibition were assessed using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay, trypan blue staining, and a colony-forming assay. Furthermore, changes in epidermal growth factor receptor (EGFR)-related signals were evaluated by Western blot analysis. RESULTS: Gefitinib, sorafenib, and silibinin individually exhibited dose-dependent antiproliferative effects on HCC cells. Combined treatment with silibinin enhanced the gefitinib-induced growth-inhibiting effects in some HCC cell lines. The combination effect of gefitinib and silibinin was synergistic in the SNU761 cell line, but was only additive in the Huh-BAT cell line. The combination effect may be attributable to inhibition of EGFR-dependent Akt signaling. Enhanced growth-inhibiting effects were also observed in HCC cells treated with a combination of sorafenib and silibinin. CONCLUSIONS: Combined treatment with silibinin enhanced the growth-inhibiting effects of both gefitinib and sorafenib. Therefore, the combination of silibinin with either sorafenib or gefitinib could be a useful treatment approach for HCC in the future.
Antineoplastic Agents/*pharmacology
;
Carcinoma, Hepatocellular/metabolism/pathology
;
Cell Line, Tumor
;
Cell Proliferation/*drug effects
;
Cell Survival/drug effects
;
Down-Regulation/drug effects
;
Drug Screening Assays, Antitumor
;
Drug Synergism
;
Humans
;
Liver Neoplasms/metabolism/pathology
;
Niacinamide/*analogs & derivatives/pharmacology
;
Phenylurea Compounds/*pharmacology
;
Proto-Oncogene Proteins c-akt/metabolism
;
Quinazolines/*pharmacology
;
Receptor, Epidermal Growth Factor/metabolism
;
Signal Transduction/drug effects
;
Silymarin/*pharmacology

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