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Monoclonal antibodies and Fc-fusion proteins used clinically are Fc-based therapeutics that grow fastest in the pharmaceutical industry. Since they both contain an Fc fragment, engineering of Fc fragments could be a platform for improving Fc-based drug efficacy. Fc engineering includes various aspects: stabilization of Fc; regulation of effector functions including antibody-dependent cell-mediated cytotoxicity, complement-dependent cytotoxicity; extension of serum half-life by modification of neonatal Fc receptor (FcRn) binding; monomerization or heterodimerization of Fc for design of new Fc formats. Currently, many new methods are being used in Fc engineering. Compared to traditional methods such as site mutagenesis on certain positions by amino acid replacement, new methods such as display-based technology can confer high throughput screening and obtain optimized variants relatively quickly, accelerating the drug development process. With the new methods, many new Fc variants were identified. On this Research Topic we are going to review the progress in current Fc engineering including the new engineering methods and the Fc variants or constructs they have produced, and the potential of these new Fcs in clinical use.

effector function --- Fc receptor --- heterodimeric Fc --- Fc-fusion protein --- monomeric Fc --- Monoclonal antibody --- Fc engineering

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The book gives an overview on the progress that has been made in the treatment of acute lymphoblastic leukemia (ALL), of acute and chronic myeloid leukemia (AML, CML) and of juvenile myelomonocytic leukemia (JMML). Leukemia is the most common malignant disease in children, and 80% of patients are diagnosed with ALL and 15–20% with AML, whereas CML and JMML are rather rare. Although ALL was considered an incurable disease until the early 1960s, with the availability of cytotoxic drugs and the start of clinical multicenter studies, ALL has become an almost curable disease with a survival rate exceeding 90 % in high-income countries. These impressive results have mainly been achieved by a deeper understanding of the genomic landscape of the disease and the introduction of risk stratifications based on genetic features and response to chemotherapy as determined by the presence or absence of minimal residual disease (MRD). Immunotherapies including bispecific T-cell Engagers (BiTEs), Chimeric Antigen Receptor (CAR) T cells, monoclonal antibodies and improvements in the outcome of allogeneic stem cell transplantation (HSCT) have shown impressive results in chemorefractory or relapsed patients, and it is anticipated that the cure rate can be further increased. For countries with less resources, therapies have to be adapted to increase survival as well. This book also updates on the progress made in the treatment of AML. As in ALL, risk classification based on genetic factors and response to chemotherapy is most important for therapy guidance. The book also provides updates and guidance for the treatment of CML and JMML.

Research & information: general --- Chemistry --- acute lymphoblastic leukemia --- pediatric --- advances --- diagnosis --- treatment --- immunotherapy --- bispecific T-cell engager (BiTE) --- BCP-ALL --- leukemia --- TRAIL --- antibody --- Fc-engineering --- xenograft --- CD19 --- juvenile myelomonocytic leukemia --- RAS signaling --- hematopoietic stem cell transplantation --- 5-azacitidine --- myelodysplastic/myeloproliferative disorders --- targeted therapy --- ADC --- antibody–drug conjugate --- pediatric leukemia --- ALL --- AML --- allogeneic stem cell transplantation --- acute myeloid leukemia --- minimal residual disease --- conditioning regimen --- alternative donors --- B-ALL --- DUX4 --- IKZF1 --- PAX5 --- Ph-like --- ZNF384 --- NUTM1 --- T-ALL --- NOTCH1 --- BCL11B --- transcriptome --- genome --- chronic myeloid leukemia --- CML --- tyrosine kinase inhibitor --- immunizations --- COVID-19 --- childhood acute lymphoblastic leukemia --- low-risk ALL --- risk-stratified treatment --- treatment related toxicity --- L-asparaginase --- acute pancreatitis --- polymorphism --- SNV --- ABCC4 --- CFTR --- other extramedullary relapse --- lymphoblastic leukemia --- children --- prognosis --- evolution of CAR T cells --- FDA-approved CAR products --- TcR versus CAR --- limitations and complications of CAR T cell therapy --- future directions of CAR T cell therapy --- n/a --- antibody-drug conjugate

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• Reference Manager
• EndNote
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The book gives an overview on the progress that has been made in the treatment of acute lymphoblastic leukemia (ALL), of acute and chronic myeloid leukemia (AML, CML) and of juvenile myelomonocytic leukemia (JMML). Leukemia is the most common malignant disease in children, and 80% of patients are diagnosed with ALL and 15–20% with AML, whereas CML and JMML are rather rare. Although ALL was considered an incurable disease until the early 1960s, with the availability of cytotoxic drugs and the start of clinical multicenter studies, ALL has become an almost curable disease with a survival rate exceeding 90 % in high-income countries. These impressive results have mainly been achieved by a deeper understanding of the genomic landscape of the disease and the introduction of risk stratifications based on genetic features and response to chemotherapy as determined by the presence or absence of minimal residual disease (MRD). Immunotherapies including bispecific T-cell Engagers (BiTEs), Chimeric Antigen Receptor (CAR) T cells, monoclonal antibodies and improvements in the outcome of allogeneic stem cell transplantation (HSCT) have shown impressive results in chemorefractory or relapsed patients, and it is anticipated that the cure rate can be further increased. For countries with less resources, therapies have to be adapted to increase survival as well. This book also updates on the progress made in the treatment of AML. As in ALL, risk classification based on genetic factors and response to chemotherapy is most important for therapy guidance. The book also provides updates and guidance for the treatment of CML and JMML.

Research & information: general --- Chemistry --- acute lymphoblastic leukemia --- pediatric --- advances --- diagnosis --- treatment --- immunotherapy --- bispecific T-cell engager (BiTE) --- BCP-ALL --- leukemia --- TRAIL --- antibody --- Fc-engineering --- xenograft --- CD19 --- juvenile myelomonocytic leukemia --- RAS signaling --- hematopoietic stem cell transplantation --- 5-azacitidine --- myelodysplastic/myeloproliferative disorders --- targeted therapy --- ADC --- antibody-drug conjugate --- pediatric leukemia --- ALL --- AML --- allogeneic stem cell transplantation --- acute myeloid leukemia --- minimal residual disease --- conditioning regimen --- alternative donors --- B-ALL --- DUX4 --- IKZF1 --- PAX5 --- Ph-like --- ZNF384 --- NUTM1 --- T-ALL --- NOTCH1 --- BCL11B --- transcriptome --- genome --- chronic myeloid leukemia --- CML --- tyrosine kinase inhibitor --- immunizations --- COVID-19 --- childhood acute lymphoblastic leukemia --- low-risk ALL --- risk-stratified treatment --- treatment related toxicity --- L-asparaginase --- acute pancreatitis --- polymorphism --- SNV --- ABCC4 --- CFTR --- other extramedullary relapse --- lymphoblastic leukemia --- children --- prognosis --- evolution of CAR T cells --- FDA-approved CAR products --- TcR versus CAR --- limitations and complications of CAR T cell therapy --- future directions of CAR T cell therapy --- acute lymphoblastic leukemia --- pediatric --- advances --- diagnosis --- treatment --- immunotherapy --- bispecific T-cell engager (BiTE) --- BCP-ALL --- leukemia --- TRAIL --- antibody --- Fc-engineering --- xenograft --- CD19 --- juvenile myelomonocytic leukemia --- RAS signaling --- hematopoietic stem cell transplantation --- 5-azacitidine --- myelodysplastic/myeloproliferative disorders --- targeted therapy --- ADC --- antibody-drug conjugate --- pediatric leukemia --- ALL --- AML --- allogeneic stem cell transplantation --- acute myeloid leukemia --- minimal residual disease --- conditioning regimen --- alternative donors --- B-ALL --- DUX4 --- IKZF1 --- PAX5 --- Ph-like --- ZNF384 --- NUTM1 --- T-ALL --- NOTCH1 --- BCL11B --- transcriptome --- genome --- chronic myeloid leukemia --- CML --- tyrosine kinase inhibitor --- immunizations --- COVID-19 --- childhood acute lymphoblastic leukemia --- low-risk ALL --- risk-stratified treatment --- treatment related toxicity --- L-asparaginase --- acute pancreatitis --- polymorphism --- SNV --- ABCC4 --- CFTR --- other extramedullary relapse --- lymphoblastic leukemia --- children --- prognosis --- evolution of CAR T cells --- FDA-approved CAR products --- TcR versus CAR --- limitations and complications of CAR T cell therapy --- future directions of CAR T cell therapy