{"title":"慢性髓性白血病","authors":"Letícia Antunes Muniz Ferreira","doi":"10.5772/intechopen.90604","DOIUrl":null,"url":null,"abstract":"Chronic myelogenous leukemia (CML) is a chronic clonal myeloproliferative disease characterized by left leukocytosis, splenomegaly, and the presence of the Philadelphia (Ph) chromosome, which results from the reciprocal and balanced translocation between the long arms of chromosomes 9q34 and 22q11, generating the hybrid protein BCR-ABL, with increased tyrosine kinase activity. The BCR-ABL protein is present in all patients with CML, and its hyperactivity triggers the release of effectors of cell proliferation and inhibitors of apoptosis, and its activity is responsible for the initial oncogenesis of CML. This chapter will review CML from its discovery, molecular and epigenetic mechanisms of disease progression to current treatments.","PeriodicalId":74639,"journal":{"name":"Rare diseases (Austin, Tex.)","volume":"1 1","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2020-02-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.5772/intechopen.90604","citationCount":"1","resultStr":"{\"title\":\"Chronic Myeloid Leukemia\",\"authors\":\"Letícia Antunes Muniz Ferreira\",\"doi\":\"10.5772/intechopen.90604\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"Chronic myelogenous leukemia (CML) is a chronic clonal myeloproliferative disease characterized by left leukocytosis, splenomegaly, and the presence of the Philadelphia (Ph) chromosome, which results from the reciprocal and balanced translocation between the long arms of chromosomes 9q34 and 22q11, generating the hybrid protein BCR-ABL, with increased tyrosine kinase activity. The BCR-ABL protein is present in all patients with CML, and its hyperactivity triggers the release of effectors of cell proliferation and inhibitors of apoptosis, and its activity is responsible for the initial oncogenesis of CML. This chapter will review CML from its discovery, molecular and epigenetic mechanisms of disease progression to current treatments.\",\"PeriodicalId\":74639,\"journal\":{\"name\":\"Rare diseases (Austin, Tex.)\",\"volume\":\"1 1\",\"pages\":\"\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2020-02-06\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://sci-hub-pdf.com/10.5772/intechopen.90604\",\"citationCount\":\"1\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Rare diseases (Austin, Tex.)\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.5772/intechopen.90604\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Rare diseases (Austin, Tex.)","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.5772/intechopen.90604","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
Chronic myelogenous leukemia (CML) is a chronic clonal myeloproliferative disease characterized by left leukocytosis, splenomegaly, and the presence of the Philadelphia (Ph) chromosome, which results from the reciprocal and balanced translocation between the long arms of chromosomes 9q34 and 22q11, generating the hybrid protein BCR-ABL, with increased tyrosine kinase activity. The BCR-ABL protein is present in all patients with CML, and its hyperactivity triggers the release of effectors of cell proliferation and inhibitors of apoptosis, and its activity is responsible for the initial oncogenesis of CML. This chapter will review CML from its discovery, molecular and epigenetic mechanisms of disease progression to current treatments.
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