Chronic myeloid leukemia

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  • Harrison's Internal Medicine Chapter 104. Acute and Chronic Myeloid Leukemia Acute and Chronic Myeloid Leukemia: Introduction The myeloid leukemias are a heterogeneous group of diseases characterized by infiltration of the blood, bone marrow, and other tissues by neoplastic cells of the hematopoietic system. In 2006 the estimated number of new myeloid leukemia cases in the United States was 16,430. These leukemias comprise a spectrum of malignancies that, untreated, range from rapidly fatal to slowly growing.

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  • Tham khảo tài liệu 'chapter 104. acute and chronic myeloid leukemia (part 10)', y tế - sức khoẻ, y học thường thức phục vụ nhu cầu học tập, nghiên cứu và làm việc hiệu quả

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  • Tham khảo tài liệu 'chapter 104. acute and chronic myeloid leukemia (part 14)', y tế - sức khoẻ, y học thường thức phục vụ nhu cầu học tập, nghiên cứu và làm việc hiệu quả

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  • Chronic myeloid leukemia (CML) is characterized by the accumulation of Philadelphia chromosome-positive (Ph+) myeloid cells. Ph+ cells occur via a reciprocal translocation between the long arms of chromosomes 9 and 22 resulting in constitutively active Bcr-abl fusion protein.

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  • Development of a new inhibitor of BCR-ABL tyrosine kinase is necessary for the treatment of chronic myeloid leukemia (CML) because of increasing resistance and tolerance to Imatinid efforts. Herein, we reported Plumbagin can significantly inhibit the growth of CML.

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  • Chronic Myelogenous Leukemia: Treatment The therapy of CML is changing rapidly because we have a proven curative treatment (allogeneic transplantation) that has significant toxicity and a new targeted treatment (imatinib) with excellent outcome based on 5-year follow-up data. Therefore, physician experience and patient preference must be factored into the treatment selection process. Discussion of both treatment options with a patient is indicated. The decision should focus on the outcomes, risks, and toxicities of the various approaches.

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  • Table 104-1 Acute Myeloid Leukemia (AML) Classification Systems World Health Organization Classificationa I. AML with recurrent genetic abnormalities AML with t(8;21)(q22;q22);RUNX1/RUNX1T1b AML with abnormal bone marrow eosinophils [inv(16)(p13q22) or t(16;16)(p13;q22);CBFB/MYH11]b Acute promyelocytic leukemia [AML with t(15;17)(q22;q12) (PML/RARα) and variants]b AML with 11q23 (MLL) abnormalities II. AML with multilineage dysplasia Following a myelodysplastic syndrome or myelodysplastic syndrome/myeloproliferative disorder Without antecedent myelodysplastic syndrome III.

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  • Acute Myeloid Leukemia: Treatment Treatment of the newly diagnosed patient with AML is usually divided into two phases, induction and postremission management (Fig. 104-2). The initial goal is to quickly induce CR. Once CR is obtained, further therapy must be used to prolong survival and achieve cure. The initial induction treatment and subsequent postremission therapy are often chosen based on the patient's age.

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  • Chronic Myelogenous Leukemia Incidence The incidence of chronic myelogenous leukemia (CML) is 1.5 per 100,000 people per year, and the age-adjusted incidence is higher in men than in women (2.0 versus 1.2). The incidence of CML increases slowly with age until the middle forties, when it starts to rise rapidly. CML incidence for males decreased slightly (4.4%) between 1997 and 2003 as compared to 1977–1997. Definition The diagnosis of CML is established by identifying a clonal expansion of a hematopoietic stem cell possessing a reciprocal translocation between chromosomes 9 and 22.

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  • We investigated the effect of (-)-epigallocatechin-3-gallate (EGCG) in overcoming imatinib mesylate -resistance in chronic myeloid leukaemia cells. Cell proliferation was determined by trypan blue dye exclusion test. Western blot analysis was performed to test the expression of key proteins.

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  • Immunophenotype and Relevance to the WHO Classification The immunophenotype of human leukemia cells can be studied by multiparameter flow cytometry after the cells are labeled with monoclonal antibodies to cell-surface antigens. This can be important for separating AML from acute lymphoblastic leukemia (ALL) and identifying some types of AML. For example, AML that is minimally differentiated (immature morphology and no lineage-specific cytochemical reactions) is diagnosed by flow-cytometric demonstration of the myeloid-specific antigens cluster designation (CD) 13 or 33.

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  • Clinical Presentation Symptoms The clinical onset of the chronic phase is generally insidious. Accordingly, some patients are diagnosed while still asymptomatic, during health-screening tests; other patients present with fatigue, malaise, and weight loss or have symptoms resulting from splenic enlargement, such as early satiety and left upper quadrant pain or mass. Less common are features related to granulocyte or platelet dysfunction, such as infections, thrombosis, or bleeding.

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  • Clinical Presentation Symptoms Patients with AML most often present with nonspecific symptoms that begin gradually or abruptly and are the consequence of anemia, leukocytosis, leukopenia or leukocyte dysfunction, or thrombocytopenia. Nearly half have had symptoms for ≤3 months before the leukemia was diagnosed. Half mention fatigue as the first symptom, but most complain of fatigue or weakness at the time of diagnosis. Anorexia and weight loss are common. Fever with or without an identifiable infection is the initial symptom in ~10% of patients.

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  • Morphology of AML cells. A. Uniform population of primitive myeloblasts with immature chromatin, nucleoli in some cells, and primary cytoplasmic granules. B. Leukemic myeloblast containing an Auer rod. C. Promyelocytic leukemia cells with prominent cytoplasmic primary granules.

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  • Treatment of Promyelocytic Leukemia Tretinoin is an oral drug that induces the differentiation of leukemic cells bearing the t(15;17). APL is responsive to cytarabine and daunorubicin, but about 10% of patients treated with these drugs die from DIC induced by the release of granule components by dying tumor cells. Tretinoin does not produce DIC but produces another complication called the retinoic acid syndrome. Occurring within the first 3 weeks of treatment, it is characterized by fever, dyspnea, chest pain, pulmonary infiltrates, pleural and pericardial effusions, and hypoxia.

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  • The hematologic toxicity of high-dose cytarabine-based induction regimens has typically been greater than that associated with 7 and 3 regimens. Toxicity with high-dose cytarabine includes myelosuppression, pulmonary toxicity, and significant and occasionally irreversible cerebellar toxicity. All patients treated with high-dose cytarabine must be closely monitored for cerebellar toxicity. Full cerebellar testing should be performed before each dose, and further high-dose cytarabine should be withheld if evidence of cerebellar toxicity develops.

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  • Tuyển tập báo cáo các nghiên cứu khoa học quốc tế ngành y học dành cho các bạn tham khảo đề tài: The research on the immuno-modulatory defect of Mesenchymal Stem Cell from Chronic Myeloid Leukemia patients

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  • Tuyển tập báo cáo các nghiên cứu khoa học quốc tế ngành y học dành cho các bạn tham khảo đề tài:P-loop mutations and novel therapeutic approaches for imatinib failures in chronic myeloid leukemia

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  • Tuyển tập báo cáo các nghiên cứu khoa học quốc tế ngành y học dành cho các bạn tham khảo đề tài:First-line treatment for chronic myeloid leukemia: dasatinib, nilotinib, or imatinib

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