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Upfront consolidation treatment with 131I-mIBG followed by myeloablative chemotherapy and hematopoietic stem cell transplantation in high-risk neuroblastoma

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Pediatric Investigation 2020年第3期4卷 168-177页

作者： Jianhua Feng Frankie WT Cheng Alex WK Leung Vincent Lee Eva WM Yeung Hoi Ching Lam Jeanny Cheung Grace KS Lam terry tw chow Carol LS Yan Chi Kong Li Department of Paediatrics The Chinese University of Hong KongHong KongChina Department of Paediatrics The First Affiliated Hospital of Wenzhou Medical UniversityWenzhouChina Department of Paediatrics and Adolescent Medicine Hong Kong Children’s HospitalHong KongChina Department of Clinical Oncology Prince of Wales HospitalThe Chinese University of Hong KongHong KongChina

Importance:131I-metaiodobenzylguanidine(131I-mIBG)has a significant targeted antitumor effect for neuroblastoma.However,currently there is a paucity of data for the use of 131I-mIBG as a"front-line"therapeutic agent in those patients with newly diagnosed high-risk neuroblastoma as part of the conditioning regimen for myeloablative chemotherapy(MAC).Objective:To evaluate the feasibility of upfront consolidation treatment with 131I-mIBG plus MAC and hematopoietic stem cell transplantation(HSCT)in high-risk neuroblastoma patients.Methods:A retrospective,single-center study was conducted from 2003-2019 on newly diagnosed high-risk neuroblastoma patients without progressive disease(PD)after the completion of induction therapy.They received 131I-mIBG infusion and MAC followed by HSCT.Results:A total of 24 high-risk neuroblastoma patients were enrolled with a median age of 3.0 years at diagnosis.After receiving this sequential consolidation treatment,3 of 13 patients who were in partial response(PR)before 131I-mIBG treatment achieved either complete response(CR)(n=1)or very good partial response(VGPR)(n=2)after HSCT.With a median follow-up duration of 13.0 months after 131I-mIBG therapy,the 5-year event-free survival and overall survival rates estimated were 29%and 38%for the entire cohort,and 53%and 67%for the patients who were in CR/VGPR at the time of 131I-mIBG treatment.Interpretation:Upfront consolidation treatment with 131I-mIBG plus MAC and HSCT is feasible and tolerable in high-risk neuroblastoma patients,however the survival benefit of this 131I-mIBG regimen is only observed in the patients who were in CR/VGPR at the time of 131I-mIBG treatment.

关键词： Neuroblastoma 131I-mIBG Transplantation

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Cellular & Molecular Immunology 2021年第4期18卷 1005-1015页

作者： Xuezhen Zeng Jingying Zhou Zhewen Xiong Hanyong Sun Weiqin Yang Myth T.S.Mok Jing Wang Jingqing Li Man Liu Wenshu Tang Yu Feng Hector Kwong-Sang W ang Shun-Wa Tsang King-Lau chow Philip Chun Yeung John Wong Paul Bo-San Lai Anthony Wing-Hung Chan Ka Fai To Stephen Lam Chan Qiang Xia Jing Xue Xiao Chen Jun Yu Sui Peng Joseph Jao-Yiu Sung Ming Kuang Alfred Sze-Lok Cheng School of Biomedical Sciences The Chinese University of Hong KongHong Kong SARChina lnstitute of Precision Medicine The First Affiliated HospitalSun Yat-sen UniversityGuangzhouChina Department of Liver Surgery The First Affiliated HospitalSun Yat-sen UniversityGuangzhouChina Department of Pharmacy The First Affiliated HospitalSun Yat-sen UniversityGuangzhouChina Department of Anatomical and Cellular Pathology The Chinese University of Hong KongHong Kong SARChina Department of Liver Surgery Ren Ji HospitalSchool of MedicineShanghai Jiao Tong UniversityShanghaiChina Department of Gastroenterology The First Affiliated HospitalSun Yat-sen UniversityGuangzhouChina Division of Life Science Hong Kong University of Science and TechnologyHong Kong SARChina Department of Surgery The Chinese University of Hong KongHong Kong SARChina State Key Laboratory of Translational Oncology The Chinese University of Hong KongHong Kong SARChina Department of Clinical Oncology The Chinese University of Hong KongHong Kong SARChina State Key Laboratory of Oncogenes and Related Genes Stem Cell Research CenterRen Ji HospitalSchool of MedicineShanghai Cancer InstituteShanghai Jiao Tong UniversityShanghaiChina Department of Medicine and Therapeutics The Chinese University of Hong KongHong Kong SARChina State Key Laboratory of Digestive Disease The Chinese University of Hong KongHong Kong SARChina Clinical Trial Unit The First Affiliated HospitalSun Yat-sen UniversityGuangzhouChina Cancer Center The First Affiliated HospitalSun Yat-sen UniversityGuangzhouChina

The liver is an immunologically tolerant organ and a common metastatic site of multiple cancer types.Although a role for cancer cell invasion programs has been well characterized,whether and how liver-intrinsic factors drive metastatic spread is incompletely understood.Here,we show that aberrantly activated hepatocyte-intrinsic cell cycle-related kinase(CCRK)signaling in chronic liver diseases is critical for cancer metastasis by reprogramming an immunosuppressive microenvironment.Using an inducible liverspecific transgenic model,we found that CCRK overexpression dramatically increased both B16F10 melanoma and MC38 colorectal cancer(CRC)metastasis to the liver,which was highly infiltrated by polymorphonuclear-myeloid-derived suppressor cells(PMNMDSCs)and lacking natural killer T(NKT)cells.Depletion of PMN-MDSCs in CCRK transgenic mice restored NKT cell levels and their interferon gamma production and reduced liver metastasis to 2.7% and 0.7%(metastatic tumor weights)in the melanoma and CRC models,respectively.Mechanistically,CCRK activated nuclear factor-kappa B(NF-κB)signaling to increase the PMN-MDSC trafficking chemokine C-X-C motif ligand 1(CXCL1),which was positively correlated with liver-infiltrating PMN-MDSC levels in CCRK transgenic mice.Accordingly,CRC liver metastasis patients exhibited hyperaaivation of hepatic CCRK/NF-κB/CXCL1 signaling,which was associated with accumulation of PMN-MDSCs and paucity of NKT cells compared to healthy liver transplantation donors.In summary,this study demonstrates that immunosuppressive reprogramming by hepatic CCRK signaling undermines antimetastatic immunosurveillance.Our findings offer new mechanistic insights and therapeutic targets for liver metastasis intervention.

关键词： Cell cycle related kinase liver metastasis liver immune microenvironment myeloid-derived suppressor cell natural killer T cell

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