LEUCEMIE AIGUE MYELOIDE PDF

Only comments seeking to improve the quality and accuracy of information on the Orphanet website are accepted. For all other comments, please send your remarks via contact us. Only comments written in English can be processed. A group of neoplasms arising from precursor cells committed to the myeloid cell-line differentiation. All of them are characterized by clonal expansion of myeloid blasts. They manifest by fever, pallor, anemia, hemorrhages and recurrent infections.

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Only comments seeking to improve the quality and accuracy of information on the Orphanet website are accepted. For all other comments, please send your remarks via contact us. Only comments written in English can be processed. A group of neoplasms arising from precursor cells committed to the myeloid cell-line differentiation.

All of them are characterized by clonal expansion of myeloid blasts. They manifest by fever, pallor, anemia, hemorrhages and recurrent infections.

Although, AML can occur at any age, it is typically a disease affecting elder people, usually more than 65 years. The main clinical picture consists of a short time period with pallor, fatigue, fever, infections and hemorrhages. Presence of all these features is not compulsory.

Central nervous system infiltration is uncommon and mainly related with monocytic variants. Extramedullary accumulation of myeloid blasts in different tissues, mainly skin, can be observed and is known as myeloid sarcoma see this term. Testes are usually not affected. Pathogenesis of AML is still unclear but a two-hit model has been suggested as the probable mechanism for leukemogenesis.

That means that AML could be the consequence of at least 2 different types of gene mutations. Class I mutations resulting in proliferative advantage while the class II mutations alter the normal hematopoietic differentiation. Controversy is also still in the type of cell from which AML arises.

While data supporting progenitor cells committed to specific myeloid cell type has been reported, other studies argue in favor for a more immature stem. Diagnosis relies on laboratory findings showing anemia, thrombocytopenia and leucopenia or leukocytosis which result from disturbed hematopoietic function due to bone marrow and peripheral blood infiltration by immature blast cells.

Diagnosis of AML also relies on bone marrow aspirate or biopsy after the disease has been suspected. After morphological examination, immunophenotyping of leukemic cells, cytogenetic and molecular analysis should be performed.

Differential diagnosis includes megaloblastic anaemia, myelodysplastic syndromes, acute lymphoblastic leukemia, acute biphenotypic leukemia, chronic myeloid leukemia myeloid blast phase , and metastases of tumors such rhabdomyosarcoma and neuroblastoma see these terms. Based on stratification, patients can be treated with chemotherapy consolidation or allogenic hematopoietic stem cell transplantation HSCT.

Refractory or relapsed AML is treated with a second induction course adding new drugs such gemtuzumab ozogamicin to the standard treatment.

Some drugs such as azacitidine or decitabine are available for the treatment of elderly AML patients under specific circumstances. Prognosis varies widely according to cytogenetics, molecular findings, response to induction treatment and age, between others. Prognosis of elder patients is rather poor. Other search option s Alphabetical list.

Suggest an update. Summary and related texts. Related genes. Clinical signs. Check this box if you wish to receive a copy of your message. Disease definition A group of neoplasms arising from precursor cells committed to the myeloid cell-line differentiation. Clinical description Although, AML can occur at any age, it is typically a disease affecting elder people, usually more than 65 years. Etiology Pathogenesis of AML is still unclear but a two-hit model has been suggested as the probable mechanism for leukemogenesis.

Diagnostic methods Diagnosis relies on laboratory findings showing anemia, thrombocytopenia and leucopenia or leukocytosis which result from disturbed hematopoietic function due to bone marrow and peripheral blood infiltration by immature blast cells. Differential diagnosis Differential diagnosis includes megaloblastic anaemia, myelodysplastic syndromes, acute lymphoblastic leukemia, acute biphenotypic leukemia, chronic myeloid leukemia myeloid blast phase , and metastases of tumors such rhabdomyosarcoma and neuroblastoma see these terms.

Prognosis Prognosis varies widely according to cytogenetics, molecular findings, response to induction treatment and age, between others. Detailed information Article for general public Italiano Deutsch Additional information Further information on this disease Classification s 3 Gene s 38 Other website s 2. Health care resources for this disease Expert centres Diagnostic tests Patient organisations 57 Orphan designation s and orphan drug s Specialised Social Services Eurordis directory.

The documents contained in this web site are presented for information purposes only. The material is in no way intended to replace professional medical care by a qualified specialist and should not be used as a basis for diagnosis or treatment.

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Leucémie aiguë promyélocytaire

Celles-ci se nomment chlorome ou sarcome granulocytaire. Les LLA de mauvais pronostic comprennent les translocations t 9;22 chromosome de Philadelphie , t 1;19 et 11 q23 translocation entre le chromosome 11 et plusieurs autres chromosomes. Aapro, P. Rev Med Suisse ; volume 4. Tableau 1. Tableau 2.

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The survival improvement of patients treated with chemotherapy or radiotherapy for malignancies are increasing therapy-related acute myeloid leukemia t-AML. It was thought to be the direct consequence of genetic events induced by such treatments. We here review the mechanisms of specific chemotherapy-related DNA damage inducing the chromosomal or genomic abnormalities characteristic of t-AML. We also focus on how such aberrations could initiate or participate to leukemogenesis. However, only a part of patients exposed to cytotoxic therapy is developing t-AML, suggesting that some genetic predisposition may be involved such as polymorphisms in genes related to DNA repair. Journal page Archives Contents list.

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