Cml Quotes

Today when I see a patient with CML, I tell them that the disease is an indolent leukemia with an excellent prognosis, that they will usually live their functional life span provided they take an oral medicine, Gleevec, for the rest of their lives.

Terminology and classification Leukaemias are traditionally classified into four main groups: • acute lymphoblastic leukaemia (ALL) • acute myeloid leukaemia (AML) • chronic lymphocytic leukaemia (CLL) • chronic myeloid leukaemia (CML). In acute leukaemia there is proliferation of primitive stem cells leading to an accumulation of blasts, predominantly in the bone marrow, which causes bone marrow failure. In chronic leukaemia the malignant clone is able to differentiate, resulting in an accumulation of more mature cells. Lymphocytic and lymphoblastic cells are those derived from the lymphoid stem cell (B cells and T cells). Myeloid refers to the other lineages, i.e. precursors of red cells, granulocytes, monocytes and platelets (see Fig. 24.2, p. 989). The diagnosis of leukaemia is usually suspected from an abnormal blood count, often a raised white count, and is confirmed by examination of the bone marrow. This includes the morphology of the abnormal cells, analysis of cell surface markers (immunophenotyping), clone-specific chromosome abnormalities and molecular changes. These results are incorporated in the World Health Organization (WHO) classification of tumours of haematopoietic and lymphoid tissues; the subclassification of acute leukaemias is shown in Box 24.47. The features in the bone marrow not only provide an accurate diagnosis but also give valuable prognostic information, allowing therapy to be tailored to the patient’s disease.

The incidence of CML remains unchanged from the past: only a few thousand patients are diagnosed with this form of leukemia every year. "But the prevalence of CML---the number of patients presently alive with the disease---has dramatically changed with the introduction of Gleevec.  As of 2009, CML patients treated with Gleevec survive an average of thirty years after their initial diagnosis.  Based on that survival figure, Hagop Kantarjian estimates that within the next decade, 250,000 people will be living with CML in America, all of them on targeted therapy.  Druker's drug will alter the national physiognomy of cancer, converting a once-rare disease into a relatively common one.  (Druker jokes that he has achieved the perfect inverstion of the golas of cancer medicine: his drug has increased the prevalence of cancer in the world.)

A man named George Daley, yet another member of the Baltimore lab, had finally accomplished this remaining feat. Daley took one group of mice and filled their marrow with the mutant bcr/abl gene present in the Philadelphia chromosome. Next, he destroyed the bone marrow of a second group of mice with radiation. He injected the second group of mice with the marrow from the first group, and the second group of mice developed CML. The experiment established the mutant chromosome, and therefore its protein product, Bcr/Abl, as the sole cause of CML. The proof bolstered Lydon’s belief that the kinase program at Ciba-Geigy should make Abl its top priority. Despite his and Druker’s conviction that Bcr/Abl was the best target for proving the principle of kinase inhibition, the program had

It’s called CML for short.” “Chronic myeloid leukemia.