Pathophysiology

Some tumors can progress to acute myeloid leukemia . It is a part of the disorders myeloproliferative chronic myeloid leukemia who became therapy radical phase of chronic development first , and syndromes other disorders myeloproliferative (fibrosis pure , thrombocythemia basic , polycythemia polyglobuli) in rare cases , LAM necessarily often cancer acute myeloid leukemia in the absence of the lymphatic system. This is another part of the myeloid dysplasia , anemia, especially with the heat resistance excess blasts (RAEB) or chronic leukemia sometimes Vahidi (CMML).
 Pathophysiology
AML of myeloid progenitor cells that can develop either pluripotent or already engaged in the granulocyte line as studies of clonality and marrow cultures shown . The mechanism of leukemogenesis would be "multi -step" with successive mutations of genes such as oncogenes or tumor suppressor genes leading to a leukemic phenotype.
Molecular analysis of structural changes in many genes identified karyotype may be involved in leukemogenesis . Some of these genes are oncogenes ( such as RAS or MYC ) or anti -oncogenes (such as RB or P53 ) is also involved in solid tumors , they do not seem to play an important role in leukemogenesis . Other genes are in particular in a specific type of LA .

Cancer chemotherapy

An updated work has been known bleaching of gasoline for many years due to the increased frequency of LA in chronic occupational exposure .

Is documented well the role of ionizing radiation , both in atomic bomb survivors than in patients who are exposed professionally. Similarly, patients with radiation therapy or isotope products treated at an increased risk for AML , and then classified as a so - called anti-money laundering and secondary .

For more than 20 years, and we also know that cancer chemotherapy by types of acute leukemia secondary AML can be complicated . There are two main types of anti-money laundering and secondary . (Table 2) is to combat money laundering and classic . Following the use of alkylating agents as described after treatment for Hodgkin's disease when they are associated with the type of treatment ( MOP ) and a number of applications. They are characterized by a delay in the emergence of 5-7 years , the incidence of dysplasia stage introductions myelogenous leukemia often indiscriminate nature and association with cytogenetic abnormalities of chromosomes 5 and / or 7 they are often chemoresistant and poor prognosis . Recently , it was reported prevents secondary AML with modes topoisomerase II : epipodophylotoxines (VP16 and VM 26 ) and Antrasiklin. This is described in the majority of solid tumors after treatment. They are characterized by the shorter time for the beginning ( 2-3 years) , similar to those observed in de novo acute myeloid leukemia is characterized by the absence of pre- leukemia, and association with abnormalities cytogenetic specific : the transfer sites AML with the band 11q23, and epipodophylotoxines to use and t (8, 21), T (15, 17) and inv (16 ) to combat money laundering , and use Antrasiklin . In combination , these anomalies classic This page has blamed himself and the same clinical diagnosis of de novo AML. The prognosis is more conservative in complex anomalies .

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Epidemiology

AML is all clinical and biological weapons , unlike immunohistochemistry and prognostic . It is also the task of the epidemiological criteria :

 AML with a nearly 3 per 100,000 people per year in France for the majority of adult diseases ;

 Incidence increases steadily with age ;

 The median age was 65 years , which reflects the pace in the elderly, and the earth where they are treated and are usually used because of the toxicity of chemotherapy.

LAM origin is unknown. However, identified a number of risk factors of blood cancer .

Acute myeloid leukemia (AML)

Acute myeloid leukemia (AML) is a clonal proliferation of acute or subacute , from hematopoietic precursors ( explosions ) of myeloid , erythroid or genealogy Alnoaouat , and developed in all stages of maturation of these precursors.

This disease usually develops in the bone marrow :
 Their presence prevents the formation of naturally in the blood , bone marrow failure syndrome characterized by cytopenias ( anemia , neutropenia, and thrombocytopenia ) , the clinical consequences of the principal means to detect the disease

 The disease can also spread to the blood with the advent of explosions dissemination or other devices hematopoietic (spleen , lymph nodes and liver ... ) or non- hematopoietic (skin , gums, and the central nervous system , ...), which, however , tumor syndrome common acute lymphoblastic leukemia (ALL).

Marrow derived from the post at least 30 % of explosions leukemia clone is essential for the diagnosis :
 This invasion by cellular examination by sternal bone marrow puncture or pelvic ( bone marrow) , which is estimated to get a central element in the diagnosis ;
 The accumulation of leukemia cells do not necessarily come from greater proliferative capacity , but the loss of the ability to accomplish differentiate into mature cells so that cancer cells feature survive with the escape of the rules associated with programmed cell death (apoptosis ).
This loss of differentiation of leukemia cells clone -derived cells leads to the accumulation of a single shape, although it can sometimes be in a certain spontaneous maturation of the leukemia clone .

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