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Nowadays, many people are affected by different types of cancer, including chronic myeloid leukemia. In 2001, imatinib mesylate, an effective treatment for this pathology, was introduced on the market. This tyrosine kinase inhibitor has proved its effectiveness following the IRIS study. That is why it has been considered the only first-line treatment for a long time. However, over the years, this medication has encountered numerous resistances resulting in loss of hematological, cytogenic or molecular responses in patients. The question that arises is the following: what are the resistance mechanisms to imatinib and what are the solutions? My dissertation focused on several points to answer this question. After analyzing the resistances, the mutations, representing 40 to 60 % of the whole, were discussed. Among them, T315I, F317L and Y253H have been studied in order to discover solutions. Second – and third-generation tyrosine kinase inhibitors are effective. It is from these results that the practitioner chooses the most appropriate treatment but it is not the only element to consider: it is important to take into account the adverse effects. These are binding for patients and therefore a source of non-compliance. Studies on the minimum duration of treatment are under way and could better manage the disadvantages. De nos jours, nombreuses sont les personnes touches par différents types de cancers, notamment la leucémie myéloïde chronique. En 2001, l’imatinib mésylate, traitement efficace de cette pathologie, a été introduit sur le marché. Cet inhibiteur de tyrosine kinase a prouvé son efficacité suite à l’étude IRIS. C’est pourquoi, il a été longtemps considéré comme l’unique traitement de première ligne. Toutefois, avec les années, cette médication a rencontré de nombreuses résistances entraînant des pertes de réponses hématologiques, cytogéniques ou encore moléculaires chez les patients. La question qui en découle est donc la suivante : quelles sont les mécanismes de résistances à l’imatinib ainsi que les solutions y apportés ? Mon mémoire s’est articulé autour de plusieurs points afin de répondre à cette interrogation. Après avoir analysé les différentes résistances, les mutations, représentant 40 à 60 %, de l’ensemble, ont été abordées. Parmi celles-ci, T315I, F317L et Y253H ont été étudiées de manière à découvrir des solutions. Ce sont les inhibiteurs de tyrosine kinase de deuxième et troisième génération qui ont démontré leur efficacité. C’est à partir de ces résultats que le praticien choisira le traitement le plus approprié mais ce n’est pas le seul élément à considérer : il est important de prendre en compte les effets indésirables. Ces derniers sont contraignants pour les patients et donc une source de non-compliance. Des études sur la durée minimale du traitement sont en cours et permettraient de mieux gérer les inconvénients.

Imatinib Mesylate --- Leukemia, Myelogenous, Chronic, BCR-ABL Positive

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Leukemia, Myelogenous, Chronic, BCR-ABL Positive --- Hematopoietic Stem Cells --- Leukemia, Myeloid, Chronic-Phase --- metabolism --- pathology

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Cytotoxicity, Immunologic --- Leukemia, Myelogenous, Chronic, BCR-ABL Positive --- Antigens, CD34 --- Hematopoietic Stem Cell Transplantation --- therapy --- metabolism --- immunology

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Molecular Pathogenesis and Treatment of Chronic Myelogenous Leukemia provides a comprehensive understanding of the recent molecular genetics of Chronic Myelogenous Leukemia (CML) and a characterization of the molecular targets for drug development. Included are therapeutic implications, diagnosis, and prognosis for understanding and facilitating daily practice in the management of patients with CML. Understanding of the pathogenesis and therapy of hematological malignancies such as CML has grown significantly in recent years. This development owe much to the progress in molecular biology and now makes a major contribution to diagnosis and to treatment that pharmacologically targets the molecular events of CML. Molecular targeting therapy with newly developed agents such as small molecules and antibodies for hematological malignancies are being discovered after years of research. Some of these, including tyrosine kinase inhibitors such as imatinib, nilotinib, and dasatinib, lead to increased survival rates and improved therapies. With the opinion leaders of basic and clinical research in the field as authors, this book reviews recent advances in the biology of CML.

Chronic myeloid leukemia --- Pathology --- Protein Kinase Inhibitors --- Genetics --- Antineoplastic Agents --- Drug Therapy --- Leukemia, Myelogenous, Chronic, BCR-ABL Positive --- Leukemia, Myeloid --- Medicine --- Therapeutics --- Enzyme Inhibitors --- Therapeutic Uses --- Biology --- Analytical, Diagnostic and Therapeutic Techniques and Equipment --- Health Occupations --- Molecular Mechanisms of Pharmacological Action --- Biological Science Disciplines --- Pharmacologic Actions --- Leukemia --- Disciplines and Occupations --- Natural Science Disciplines --- Neoplasms by Histologic Type --- Chemical Actions and Uses --- Neoplasms --- Chemicals and Drugs --- Diseases --- Health & Biological Sciences --- Molecular aspects --- Molecular aspects. --- Treatment. --- Leucaemia --- Leucemia --- Leucocythaemia --- Leucocythemia --- Leucosis --- Leukaemia --- Leukosis --- Chronic granulocytic leukemia --- Chronic myelocytic leukemia --- Chronic myelogenous leukemia --- CML (Disease) --- Anemia --- Cancer --- Leucocytosis --- Preleukemia --- Chronic leukemia --- Myeloid leukemia --- Hematology. --- Oncology  . --- Oncology. --- Tumors --- Haematology --- Internal medicine --- Blood

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This book, written by a team of leading experts, provides a comprehensive overview of acute myeloid leukemia (AML), the most frequent acute leukemia in adults. The opening chapters present current knowledge of epidemiology, etiologic factors, and the pathogenesis and molecular development of AML. Detailed guidance is offered on laboratory and clinical diagnostic workup and disease classification, and the patient- and disease-related factors that determine prognosis and treatment allocation are identified. On the basis of these general considerations, initial treatments in patients considered fit for intensive treatment and in older and co-morbid patients are reviewed, and the available relapse treatment strategies, explained. For all clinical scenarios, the most recent data on the optimal use of newly approved agents in different AML subgroups are presented. Separate chapters address the treatment of acute promyelocytic leukemia, current practice of allogeneic stem cell transplantation, and special clinical situations. Finally, promising approaches in drug development, current standards and challenges in assessment of measurable residual disease, immune approaches, and ideas for innovative trial designs are considered.

Hematology. --- Haematology --- Internal medicine --- Blood --- Diseases --- Acute myeloid leukemia. --- Acute myelogenous leukemia --- Acute myeloid granulocytic leukemia --- Acute myelocytic leukemia --- AML (Disease) --- Acute leukemia --- Myeloid leukemia --- Leukemia, Myeloid, Acute. --- ANLL --- Acute Myelogenous Leukemia --- Acute Myeloid Leukemia --- Acute Myeloid Leukemia with Maturation --- Acute Myeloid Leukemia without Maturation --- Leukemia, Acute Myelogenous --- Leukemia, Acute Myeloid --- Leukemia, Myeloblastic, Acute --- Leukemia, Myelocytic, Acute --- Leukemia, Myeloid, Acute, M1 --- Leukemia, Myeloid, Acute, M2 --- Leukemia, Nonlymphoblastic, Acute --- Myeloblastic Leukemia, Acute --- Myelocytic Leukemia, Acute --- Myelogenous Leukemia, Acute --- Myeloid Leukemia, Acute, M1 --- Myeloid Leukemia, Acute, M2 --- Nonlymphoblastic Leukemia, Acute --- Leukemia, Myelogenous, Acute --- Leukemia, Nonlymphocytic, Acute --- Myeloid Leukemia, Acute --- Nonlymphocytic Leukemia, Acute --- Acute Myeloblastic Leukemia --- Acute Myeloblastic Leukemias --- Acute Myelocytic Leukemia --- Acute Myelocytic Leukemias --- Acute Myelogenous Leukemias --- Acute Myeloid Leukemias --- Acute Nonlymphoblastic Leukemia --- Acute Nonlymphoblastic Leukemias --- Acute Nonlymphocytic Leukemia --- Acute Nonlymphocytic Leukemias --- Leukemia, Acute Myeloblastic --- Leukemia, Acute Myelocytic --- Leukemia, Acute Nonlymphoblastic --- Leukemia, Acute Nonlymphocytic --- Leukemias, Acute Myeloblastic --- Leukemias, Acute Myelocytic --- Leukemias, Acute Myelogenous --- Leukemias, Acute Myeloid --- Leukemias, Acute Nonlymphoblastic --- Leukemias, Acute Nonlymphocytic --- Myeloblastic Leukemias, Acute --- Myelocytic Leukemias, Acute --- Myelogenous Leukemias, Acute --- Myeloid Leukemias, Acute --- Nonlymphoblastic Leukemias, Acute --- Nonlymphocytic Leukemias, Acute --- Leucèmia mieloide --- Leucèmia granulocítica --- Leucèmia mielocítica --- Leucèmia mielògena --- Leucèmia --- Trastorns mieloproliferatius