Pub Date : 2019-07-20DOI: 10.3760/CMA.J.ISSN.1673-419X.2019.04.005
Haiyan Li, L. Lilan, Xuejun Liu, Fang Lu, Jiang Lihong
Objective To investigate the establishment and verification of immortal lymphoblastic cell lines from platelets CD36 deficient individuals. Methods From January 2012 to January 2018, eight individuals with platelet CD36 deficiency were selected as the study subjects. Among them, six cases were blood donors from Nanning Blood Center, one case was patient with platelet transfusion refractoriness (PTR) hospitalized in Guangxi 923 Hospital, and 1 case was mother of a child with fetal/neonatal alloimmune thrombocytopenia (FNAIT) hospitalized in Maternal and Child Health Hospital of Guangxi Zhuang Autonomous Region. All the subjects′ ages ranged from 15 to 66 years. The subjects were identified as platelet CD36 deficiency by flow cytometry, monoclonal antibody immobilization of platelet (MAIPA) and CD36 genotyping. Among them, one case was a CD36 mutant heterozygote of 538T>C, three cases were mutant heterozygote of 380C>T, one case was mutant homozygous of 329-330del, and 3 cases were mutant heterozygote of 329-330del. Volume of 5 mL heparin anticoagulant blood was collected from participants and their lymphocytes were isolated. Epstein-Barr virus (EBV) and cyclosporine were used to treat peripheral blood lymphocytes of participants with platelet CD36 deficiency to obtain immortal lymphoblast cell lines, which were frozen after stable passages. Resuscitation activity and mycoplasma detection of these cell lines were performed, and the CD36 gene was sequenced for verification. The procedure of this study is accordance with the requirement of the revised World Medical Association Declaration of Helsinki in 2013. Informed consent was obtained from each participant. Results ① After EBV and cyclosporine treatment, the peripheral blood lymphocytes of the participants were cultured for 7 d, and blastoformation of the cells with prickly edges were observed, and some of the cells were agglutinated in clusters. After continuous replacement of the complete culture medium for about 1 month, a large number of cells proliferated and grew vigorously, and more clonal spheres could be seen to form by naked eyes, and immortalized lymphoblastic cell line was successfully obtained. ② CD36 deficient immortalized lymphoblastic cell lines were subcultured for 20 generations, then frozen in liquid nitrogen. All of them were successfully resuscitated, and the cell lines were observed growing well under inverted phase contrast microscope. ③ Mycoplasma test results of the CD36 deficient immortalized lymphoblastic cell lines showed negative. ④ DNA of CD36 deficient immortalized lymphoblastic cell lines were amplified and sequenced by PCR, and comparison results showed that the DNA of immortalized lymphoblastic cell lines were identical to those of individuals with CD36 deficiency, and no gene mutation occurred. The genotypes of CD36 deficient immortalized lymphoblastic cell lines established in this study included 1 case of CD36 gene 538T>C mutant heterozygote, thre
{"title":"Establishment and verification of immortalized lymphoblastic cell lines derived from platelets CD36 deficient individuals","authors":"Haiyan Li, L. Lilan, Xuejun Liu, Fang Lu, Jiang Lihong","doi":"10.3760/CMA.J.ISSN.1673-419X.2019.04.005","DOIUrl":"https://doi.org/10.3760/CMA.J.ISSN.1673-419X.2019.04.005","url":null,"abstract":"Objective \u0000To investigate the establishment and verification of immortal lymphoblastic cell lines from platelets CD36 deficient individuals. \u0000 \u0000 \u0000Methods \u0000From January 2012 to January 2018, eight individuals with platelet CD36 deficiency were selected as the study subjects. Among them, six cases were blood donors from Nanning Blood Center, one case was patient with platelet transfusion refractoriness (PTR) hospitalized in Guangxi 923 Hospital, and 1 case was mother of a child with fetal/neonatal alloimmune thrombocytopenia (FNAIT) hospitalized in Maternal and Child Health Hospital of Guangxi Zhuang Autonomous Region. All the subjects′ ages ranged from 15 to 66 years. The subjects were identified as platelet CD36 deficiency by flow cytometry, monoclonal antibody immobilization of platelet (MAIPA) and CD36 genotyping. Among them, one case was a CD36 mutant heterozygote of 538T>C, three cases were mutant heterozygote of 380C>T, one case was mutant homozygous of 329-330del, and 3 cases were mutant heterozygote of 329-330del. Volume of 5 mL heparin anticoagulant blood was collected from participants and their lymphocytes were isolated. Epstein-Barr virus (EBV) and cyclosporine were used to treat peripheral blood lymphocytes of participants with platelet CD36 deficiency to obtain immortal lymphoblast cell lines, which were frozen after stable passages. Resuscitation activity and mycoplasma detection of these cell lines were performed, and the CD36 gene was sequenced for verification. The procedure of this study is accordance with the requirement of the revised World Medical Association Declaration of Helsinki in 2013. Informed consent was obtained from each participant. \u0000 \u0000 \u0000Results \u0000① After EBV and cyclosporine treatment, the peripheral blood lymphocytes of the participants were cultured for 7 d, and blastoformation of the cells with prickly edges were observed, and some of the cells were agglutinated in clusters. After continuous replacement of the complete culture medium for about 1 month, a large number of cells proliferated and grew vigorously, and more clonal spheres could be seen to form by naked eyes, and immortalized lymphoblastic cell line was successfully obtained. ② CD36 deficient immortalized lymphoblastic cell lines were subcultured for 20 generations, then frozen in liquid nitrogen. All of them were successfully resuscitated, and the cell lines were observed growing well under inverted phase contrast microscope. ③ Mycoplasma test results of the CD36 deficient immortalized lymphoblastic cell lines showed negative. ④ DNA of CD36 deficient immortalized lymphoblastic cell lines were amplified and sequenced by PCR, and comparison results showed that the DNA of immortalized lymphoblastic cell lines were identical to those of individuals with CD36 deficiency, and no gene mutation occurred. The genotypes of CD36 deficient immortalized lymphoblastic cell lines established in this study included 1 case of CD36 gene 538T>C mutant heterozygote, thre","PeriodicalId":13774,"journal":{"name":"International Journal of Blood Transfusion and Hematology","volume":"42 1","pages":"305-312"},"PeriodicalIF":0.0,"publicationDate":"2019-07-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"46870196","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2019-07-20DOI: 10.3760/CMA.J.ISSN.1673-419X.2019.04.010
Xiting Jia, Z. Cai
Chronic myeloid leukemia (CML) is a malignant myeloproliferative neoplasm that occurs in pluripotent hematopoietic stem cells. Pathogenesis of CML is slow, and leukocytosis and splenomegaly are main clinical features of patients with CML. The introduction of tyrosine kinase inhibitor (TKI) imatinib mesylate (IM) has changed the natural progression of CML and significantly improved survival of CML patients. However, with the prolonged application of IM, IM resistance has become a major challenge in the treatment of CML. Many studies are currently working to elucidate the mechanisms of CML resistance and to research and develop new TKI. There is a urgent need to replace new drug targets and new therapeutic strategies for BCR/ABL1 fusion gene in response to IM-resistant CML patients. This article focuses on the development of CML-related TKI and non-TKI latest drugs for IM-resistant CML patients, and describes immunological approaches activating specific T cell responses against CML cells. Key words: Leukemia, myelogenous, chronic, BCR-ABL positive; Receptor protein-tyrosine kinases; Drug resistance, neoplasm; Immunotherapy; Therapeutic uses
{"title":"Research progress in treatment of chronic myeloid leukemia patients with imatinib resistance","authors":"Xiting Jia, Z. Cai","doi":"10.3760/CMA.J.ISSN.1673-419X.2019.04.010","DOIUrl":"https://doi.org/10.3760/CMA.J.ISSN.1673-419X.2019.04.010","url":null,"abstract":"Chronic myeloid leukemia (CML) is a malignant myeloproliferative neoplasm that occurs in pluripotent hematopoietic stem cells. Pathogenesis of CML is slow, and leukocytosis and splenomegaly are main clinical features of patients with CML. The introduction of tyrosine kinase inhibitor (TKI) imatinib mesylate (IM) has changed the natural progression of CML and significantly improved survival of CML patients. However, with the prolonged application of IM, IM resistance has become a major challenge in the treatment of CML. Many studies are currently working to elucidate the mechanisms of CML resistance and to research and develop new TKI. There is a urgent need to replace new drug targets and new therapeutic strategies for BCR/ABL1 fusion gene in response to IM-resistant CML patients. This article focuses on the development of CML-related TKI and non-TKI latest drugs for IM-resistant CML patients, and describes immunological approaches activating specific T cell responses against CML cells. \u0000 \u0000 \u0000Key words: \u0000Leukemia, myelogenous, chronic, BCR-ABL positive; Receptor protein-tyrosine kinases; Drug resistance, neoplasm; Immunotherapy; Therapeutic uses","PeriodicalId":13774,"journal":{"name":"International Journal of Blood Transfusion and Hematology","volume":"42 1","pages":"338-343"},"PeriodicalIF":0.0,"publicationDate":"2019-07-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43396996","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2019-07-20DOI: 10.3760/CMA.J.ISSN.1673-419X.2019.04.009
Wen-FuThomas Lai
T-lymphoblastic lymphoma(T-LBL) is a rare and highly aggressive lymphoma, with poor prognosis. It occurs mostly in children and male adolescents, and its main symptoms are mediastinal mass, lymphadenectasis, bone marrow invasion and central nervous system(CNS) invasion, etc.. The diagnosis of T-LBL is mainly based on lymph node biopsy, bone marrow cell morphology, immunology, cytogenetics and gene detection. After definitive diagnosis of T-LBL, the patients should be treated with extensive combined chemotherapy and sequential hematopoietic stem cell transplantation (HSCT) or maintenance treatment. There are many factors influencing the prognosis of T-LBL patients, such as age, bone marrow invasion, CNS invasion, disease stage and gene mutations. This article intends to introduce the development of diagnosis, therapy and prognostic factors of T-LBL to provide reference for the diagnosis and therapy of T-LBL. Key words: Precursor T-cell lymphoblastic leukemia-lymphoma; Genetics; Immunology; Diagnosis; Therapy
{"title":"Current research status of diagnosis, treatment and prognostic factors of T-lymphoblastic lymphoma","authors":"Wen-FuThomas Lai","doi":"10.3760/CMA.J.ISSN.1673-419X.2019.04.009","DOIUrl":"https://doi.org/10.3760/CMA.J.ISSN.1673-419X.2019.04.009","url":null,"abstract":"T-lymphoblastic lymphoma(T-LBL) is a rare and highly aggressive lymphoma, with poor prognosis. It occurs mostly in children and male adolescents, and its main symptoms are mediastinal mass, lymphadenectasis, bone marrow invasion and central nervous system(CNS) invasion, etc.. The diagnosis of T-LBL is mainly based on lymph node biopsy, bone marrow cell morphology, immunology, cytogenetics and gene detection. After definitive diagnosis of T-LBL, the patients should be treated with extensive combined chemotherapy and sequential hematopoietic stem cell transplantation (HSCT) or maintenance treatment. There are many factors influencing the prognosis of T-LBL patients, such as age, bone marrow invasion, CNS invasion, disease stage and gene mutations. This article intends to introduce the development of diagnosis, therapy and prognostic factors of T-LBL to provide reference for the diagnosis and therapy of T-LBL. \u0000 \u0000 \u0000Key words: \u0000Precursor T-cell lymphoblastic leukemia-lymphoma; Genetics; Immunology; Diagnosis; Therapy","PeriodicalId":13774,"journal":{"name":"International Journal of Blood Transfusion and Hematology","volume":"42 1","pages":"332-337"},"PeriodicalIF":0.0,"publicationDate":"2019-07-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"47926776","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2019-07-20DOI: 10.3760/CMA.J.ISSN.1673-419X.2019.04.012
Yu Tian
Anthracyclines (ANT) are cytotoxic drugs that are highly effective against a variety of malignancies and are widely used in the treatment of childhood malignancies.But the dose-cumulative cardiotoxicity associated with anthracyclines can affect the quality of life in children, and even cause heart failure. In recent years, with the recognition of the cardiotoxicity of ANT, cardiac monitoring has become necessary to patients treated with ANT and to take early interventions to prevent or treat heart failure.This article reviews the recent advances in the pathogenesis, diagnosis and treatment of ANT related cardiotoxicity. Key words: Anthracyclines; Drug toxicity; Cardiotoxins; Heart failure; Dexrazoxane
{"title":"Research progress in pathogenesis, diagnosis and treatment of anthracyclines related cardiotoxicity","authors":"Yu Tian","doi":"10.3760/CMA.J.ISSN.1673-419X.2019.04.012","DOIUrl":"https://doi.org/10.3760/CMA.J.ISSN.1673-419X.2019.04.012","url":null,"abstract":"Anthracyclines (ANT) are cytotoxic drugs that are highly effective against a variety of malignancies and are widely used in the treatment of childhood malignancies.But the dose-cumulative cardiotoxicity associated with anthracyclines can affect the quality of life in children, and even cause heart failure. In recent years, with the recognition of the cardiotoxicity of ANT, cardiac monitoring has become necessary to patients treated with ANT and to take early interventions to prevent or treat heart failure.This article reviews the recent advances in the pathogenesis, diagnosis and treatment of ANT related cardiotoxicity. \u0000 \u0000 \u0000Key words: \u0000Anthracyclines; Drug toxicity; Cardiotoxins; Heart failure; Dexrazoxane","PeriodicalId":13774,"journal":{"name":"International Journal of Blood Transfusion and Hematology","volume":"42 1","pages":"351-357"},"PeriodicalIF":0.0,"publicationDate":"2019-07-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42593383","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2019-07-20DOI: 10.3760/CMA.J.ISSN.1673-419X.2019.04.001
Junying Wu
The clinical presentation and prognosis for patients with primary myelofibrosis (PMF) are of highly heterogeneous. Several risk stratification models are raised in order to stratify patients accurately and guide appropriate treatment decisions. Recently, the cytogenetic and molecular pathogenesis of patients with PMF have been elucidated considerably. Therefore, prognostic scoring systems are updating to improve prognostic effectiveness and guidance value for therapy decisions. This article summarizes the advances of prognostic factors, the advantages and disadvantages of different prognostic scoring systems and the practical usefulness of the prognostic scoring systems in terms of clinical decision making. Key words: Primary myelofibrosis; Myeloproliferative disorders; Myelofibrosis; Prognostic factors; Prognostic scoring systems; Genetics
{"title":"Current research status of prognostic scoring systems in primary myelofibrosis","authors":"Junying Wu","doi":"10.3760/CMA.J.ISSN.1673-419X.2019.04.001","DOIUrl":"https://doi.org/10.3760/CMA.J.ISSN.1673-419X.2019.04.001","url":null,"abstract":"The clinical presentation and prognosis for patients with primary myelofibrosis (PMF) are of highly heterogeneous. Several risk stratification models are raised in order to stratify patients accurately and guide appropriate treatment decisions. Recently, the cytogenetic and molecular pathogenesis of patients with PMF have been elucidated considerably. Therefore, prognostic scoring systems are updating to improve prognostic effectiveness and guidance value for therapy decisions. This article summarizes the advances of prognostic factors, the advantages and disadvantages of different prognostic scoring systems and the practical usefulness of the prognostic scoring systems in terms of clinical decision making. \u0000 \u0000 \u0000Key words: \u0000Primary myelofibrosis; Myeloproliferative disorders; Myelofibrosis; Prognostic factors; Prognostic scoring systems; Genetics","PeriodicalId":13774,"journal":{"name":"International Journal of Blood Transfusion and Hematology","volume":"42 1","pages":"277-282"},"PeriodicalIF":0.0,"publicationDate":"2019-07-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"47265909","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2019-07-20DOI: 10.3760/CMA.J.ISSN.1673-419X.2019.04.014
Xiangliang Ren
In the case of intravascular hemolysis in patients with hemolytic diseases such as paroxysmal nocturnal hemoglobinuria (PNH) and sickle cell disease (SCD), patients′ body can produce a large amount of free hemoglobin (FHb) and release intracellular arginase. FHb can rapidly scavenge nitric oxide (NO) and arginase can degrade L-arginine, which is substrate for NO synthesis. All together with the increased amount of reactive oxygen species (ROS) after hemolysis, NO appears to be depleted in the circulation, which results damages to endothelial and dysfunction of microcirculation, as well as eventually lead to acute and chronic impair to multiple organs. In recent years, with the in-depth study of the mechanisms beneath NO depletion in intravascular hemolytic disorders, the common pathological mechanisms of such diseases have been elucidated, and NO replacement therapy seems to be an all new approach. In view of this, this article reviews the research progress in the field of NO depletion and its replacement therapy in intravascular hemolytic diseases. Key words: Hemolytic disease; Nitric oxide; Depletion; Replacement therapy; Intravascular hemolysis
{"title":"Research progress on nitric oxide depletion and its replacement therapy in intravascular hemolytic diseases","authors":"Xiangliang Ren","doi":"10.3760/CMA.J.ISSN.1673-419X.2019.04.014","DOIUrl":"https://doi.org/10.3760/CMA.J.ISSN.1673-419X.2019.04.014","url":null,"abstract":"In the case of intravascular hemolysis in patients with hemolytic diseases such as paroxysmal nocturnal hemoglobinuria (PNH) and sickle cell disease (SCD), patients′ body can produce a large amount of free hemoglobin (FHb) and release intracellular arginase. FHb can rapidly scavenge nitric oxide (NO) and arginase can degrade L-arginine, which is substrate for NO synthesis. All together with the increased amount of reactive oxygen species (ROS) after hemolysis, NO appears to be depleted in the circulation, which results damages to endothelial and dysfunction of microcirculation, as well as eventually lead to acute and chronic impair to multiple organs. In recent years, with the in-depth study of the mechanisms beneath NO depletion in intravascular hemolytic disorders, the common pathological mechanisms of such diseases have been elucidated, and NO replacement therapy seems to be an all new approach. In view of this, this article reviews the research progress in the field of NO depletion and its replacement therapy in intravascular hemolytic diseases. \u0000 \u0000 \u0000Key words: \u0000Hemolytic disease; Nitric oxide; Depletion; Replacement therapy; Intravascular hemolysis","PeriodicalId":13774,"journal":{"name":"International Journal of Blood Transfusion and Hematology","volume":"42 1","pages":"362-365"},"PeriodicalIF":0.0,"publicationDate":"2019-07-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"44732498","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2019-05-20DOI: 10.3760/CMA.J.ISSN.1673-419X.2019.03.015
Xiyan Wang
Endothelial protein C receptor (EPCR) is one of the components of protein C anticoagulation system, which has important significance in anticoagulation regulation and cell protection. It has been found that EPCR is one of the surface markers of hematopoietic stem cells (HSC) and can be used for sorting and purification of HSC. EPCR can participate in the regulation of HSC and its microenvironment through protease-activated receptor (PAR)1 signaling and other pathways, and it can mediate the retention and hematopoietic function reconstitution of HSC in bone marrow. This article intends to review the application of EPCR in HSC sorting and purification, as well as the research progress of EPCR on the regulation of HSC and its related mechanisms. Key words: Endothelial cells; Hematopoietic stem cells; Protease activated receptor 1; Endothelial protein C receptor; Protein C; Activated protein C
{"title":"Role of endothelial cell protein C receptor in hematopoietic stem cells","authors":"Xiyan Wang","doi":"10.3760/CMA.J.ISSN.1673-419X.2019.03.015","DOIUrl":"https://doi.org/10.3760/CMA.J.ISSN.1673-419X.2019.03.015","url":null,"abstract":"Endothelial protein C receptor (EPCR) is one of the components of protein C anticoagulation system, which has important significance in anticoagulation regulation and cell protection. It has been found that EPCR is one of the surface markers of hematopoietic stem cells (HSC) and can be used for sorting and purification of HSC. EPCR can participate in the regulation of HSC and its microenvironment through protease-activated receptor (PAR)1 signaling and other pathways, and it can mediate the retention and hematopoietic function reconstitution of HSC in bone marrow. This article intends to review the application of EPCR in HSC sorting and purification, as well as the research progress of EPCR on the regulation of HSC and its related mechanisms. \u0000 \u0000 \u0000Key words: \u0000Endothelial cells; Hematopoietic stem cells; Protease activated receptor 1; Endothelial protein C receptor; Protein C; Activated protein C","PeriodicalId":13774,"journal":{"name":"International Journal of Blood Transfusion and Hematology","volume":"42 1","pages":"259-263"},"PeriodicalIF":0.0,"publicationDate":"2019-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"45261232","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2019-05-20DOI: 10.3760/CMA.J.ISSN.1673-419X.2019.03.009
Guangqiang Meng
The number of acute myeloid leukemia (AML) patients aged over 80 years are increasing year by year. They have poor treatment effects and shorter survival period because of elderly age, more underlying diseases, poor tolerance to chemotherapy. At present, there are many treatments reported, including supportive therapy, standard-dose chemotherapy, reduced-dose chemotherapy, demethylation therapy, hematopoietic stem cell transplantation(HSCT) and adoptive cellular immunotherapy, and various treatments have achieved some good effects in AML patients aged over 80 years. However, the survival of this group of patients is still poor. And there are lack of unified and effective therapeutic strategies for elderly patients with AML. This article reviewed the present status and research progresses on treatment of AML aged over 80 years. Key words: Leukemia, myeloid, acute; Aged; Life support care; Prognosis; Drug therapy
{"title":"Present status and research progresses in treatment of acute myeloid leukemia patients aged over 80 years","authors":"Guangqiang Meng","doi":"10.3760/CMA.J.ISSN.1673-419X.2019.03.009","DOIUrl":"https://doi.org/10.3760/CMA.J.ISSN.1673-419X.2019.03.009","url":null,"abstract":"The number of acute myeloid leukemia (AML) patients aged over 80 years are increasing year by year. They have poor treatment effects and shorter survival period because of elderly age, more underlying diseases, poor tolerance to chemotherapy. At present, there are many treatments reported, including supportive therapy, standard-dose chemotherapy, reduced-dose chemotherapy, demethylation therapy, hematopoietic stem cell transplantation(HSCT) and adoptive cellular immunotherapy, and various treatments have achieved some good effects in AML patients aged over 80 years. However, the survival of this group of patients is still poor. And there are lack of unified and effective therapeutic strategies for elderly patients with AML. This article reviewed the present status and research progresses on treatment of AML aged over 80 years. \u0000 \u0000 \u0000Key words: \u0000Leukemia, myeloid, acute; Aged; Life support care; Prognosis; Drug therapy","PeriodicalId":13774,"journal":{"name":"International Journal of Blood Transfusion and Hematology","volume":"42 1","pages":"229-232"},"PeriodicalIF":0.0,"publicationDate":"2019-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"44694709","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2019-05-20DOI: 10.3760/CMA.J.ISSN.1673-419X.2019.03.011
Minmin Liang, Xiaobo Ni, Yan Wang
Currently, steroid refractory acute graft versus host disease (SR-aGVHD) is one of severe complications in patients with hematological diseases who accept allogeneic hematopoietic stem cell transplantation (allo-HSCT). Glucocorticoids are first-line treatments for acute graft versus host disease (aGVHD), whereas 25%-30% of patients with aGVHD are ineffective to these drugs, which usually have a poor prognosis. The 2-year overall survival (OS) rate is about 10% or even lower of these patients. Mesenchymal stem cell (MSC), pluripotent progenitor cell with extensive immunomodulatory capacity, is thought to induce immunosuppression and delay the inflammatory state triggered by SR-aGVHD. Recent studies have confirmed that intravenous infusion of MSC is feasible and effective in the treatment of SR-aGVHD, and has gradually become a hot topic. In order to widely apply MSC in the treatment of SR-aGVHD, this article intends to summarize the biological characteristics, the mechanism of treatment in patients with SR-aGVHD and the progress of clinical application of MSC. Key words: Graft vs host disease; Mesenchymal stem cells; Immunoregulatory; Cell adhesion molecules; Steroid refractory acute graft versus host disease; Indoleamine 2, 3-dioxygenase
{"title":"Research progress of mesenchymal stem cell in treatment of steroid refractory acute graft versus host disease","authors":"Minmin Liang, Xiaobo Ni, Yan Wang","doi":"10.3760/CMA.J.ISSN.1673-419X.2019.03.011","DOIUrl":"https://doi.org/10.3760/CMA.J.ISSN.1673-419X.2019.03.011","url":null,"abstract":"Currently, steroid refractory acute graft versus host disease (SR-aGVHD) is one of severe complications in patients with hematological diseases who accept allogeneic hematopoietic stem cell transplantation (allo-HSCT). Glucocorticoids are first-line treatments for acute graft versus host disease (aGVHD), whereas 25%-30% of patients with aGVHD are ineffective to these drugs, which usually have a poor prognosis. The 2-year overall survival (OS) rate is about 10% or even lower of these patients. Mesenchymal stem cell (MSC), pluripotent progenitor cell with extensive immunomodulatory capacity, is thought to induce immunosuppression and delay the inflammatory state triggered by SR-aGVHD. Recent studies have confirmed that intravenous infusion of MSC is feasible and effective in the treatment of SR-aGVHD, and has gradually become a hot topic. In order to widely apply MSC in the treatment of SR-aGVHD, this article intends to summarize the biological characteristics, the mechanism of treatment in patients with SR-aGVHD and the progress of clinical application of MSC. \u0000 \u0000 \u0000Key words: \u0000Graft vs host disease; Mesenchymal stem cells; Immunoregulatory; Cell adhesion molecules; Steroid refractory acute graft versus host disease; Indoleamine 2, 3-dioxygenase","PeriodicalId":13774,"journal":{"name":"International Journal of Blood Transfusion and Hematology","volume":"42 1","pages":"238-243"},"PeriodicalIF":0.0,"publicationDate":"2019-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"46344195","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2019-05-20DOI: 10.3760/CMA.J.ISSN.1673-419X.2019.03.008
Yunguang Hong, R. Wen, Zhigang Yang
Myeloproliferative neoplasms (MPN) are a group of abnormal clonal diseases of hematopoietic stem cell, which characterized by sustained clonal proliferation of relatively mature differentiated one or more myeloid cells. MPN mainly include chronic myeloid leukemia (CML) and Ph-/MPN. In recent years, studies have reported that abnormal number and function of regulatory T cell (Treg) play an important role in the occurrence and development of MPN. Therefore, this article reviews recent research advances in the biological characteristics of Treg, relationship between number of Treg in CML patients and CML clinical phase, Sokal score, efficacy and transcription level of BCR-ABL fusion gene, as well as the role of Treg in the pathogenesis and progression of Ph- MPN. Key words: T-lymphocytes; T-lymphocytes, regulatory; Myeloproliferative disorders; Leukemia, myelogenous, chronic, BCR-ABL positive; Treatment outcome; Neoplasm staging
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