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  1. Fulltext Cytogenetics and molecular genetic tests for the diagnosis and treatment of chronic myeloid leukemia
    Mohd Khairi Zahry, Ankathil, Ravindran
    Buletin Persatuan Genetik Malaysia, 2008;14(1):9-11.
    MyJurnal
    Chronic Myeloid Leukemia (CML) is a clonal disorder thought to originate in a single abnormal haematopoietic stem cell. This myeloproliferative fatal stem cell disorder comprises
    approximately 14% of all leukemias. In most cases, CML runs a triphasic course, which includes an initial chronic phase that transforms eventually into a blastic phase resembling acute leukemia. In 60%- 80% of patients, an intermediate or accelerated phase precedes the terminal blastic phase. Accelerated phase and blastic phase sometimes are lumped together and considered to be
    advanced phase CML. The entire continuum from chronic phase to blastic phase lasts a median of 3 to 5 years . This time period can be broken down in to the chronic phase which if untreated,
    lasts for 2 to 5 years and finally the fatal blastic phase, which lasts from 3 to 6 months. A patient can present in any of these 3 stages.
    Matched MeSH terms: Leukemia, Myeloid, Chronic-Phase
  2. Identification of copy number alterations by array comparative genomic hybridization in patients with late chronic or accelerated phase chronic myeloid leukemia treated with imatinib mesylate
    Nadarajan VS, Phan CL, Ang CH, Liang KL, Gan GG, Bee PC, et al.
    Int J Hematol, 2011 Apr;93(4):465-473.
    PMID: 21387093 DOI: 10.1007/s12185-011-0796-9
    The outcome of treating chronic myeloid leukemia (CML) with imatinib mesylate (IM) is inferior when therapy is commenced in late chronic or accelerated phase as compared to early chronic phase. This may be attributed to additional genomic alterations that accumulate during disease progression. We sought to identify such lesions in patients showing suboptimal response to IM by performing array-CGH analysis on 39 sequential samples from 15 CML patients. Seventy-four cumulative copy number alterations (CNAs) consisting of 35 losses and 39 gains were identified. Alterations flanking the ABL1 and BCR genes on chromosomes 9 and 22, respectively, were the most common identified lesions with 5 patients losing variable portions of 9q34.11 proximal to ABL1. Losses involving 1p36, 5q31, 17q25, Y and gains of 3q21, 8q24, 22q11, Xp11 were among other recurrent lesions identified. Aberrations were also observed in individual patients, involving regions containing known leukemia-associated genes; CDKN2A/2B, IKZF1, RB1, TLX1, AFF4. CML patients in late stages of their disease, harbor pre-existing and evolving sub-microscopic CNAs that may influence disease progression and IM response.
    Matched MeSH terms: Leukemia, Myeloid, Chronic-Phase/drug therapy; Leukemia, Myeloid, Chronic-Phase/genetics
  3. Systematic review of pre-clinical chronic myeloid leukaemia
    Kuan JW, Su AT, Leong CF, Osato M, Sashida G
    Int J Hematol, 2018 Nov;108(5):465-484.
    PMID: 30218276 DOI: 10.1007/s12185-018-2528-x
    BACKGROUND: Studies of a provisional entity pre-clinical chronic myeloid leukaemia (CML), which precedes chronic phase (CP) without leucocytosis or blood/marrow feature of CML CP, has been increasing.

    OBJECTIVE: To perform a systematic review of pre-clinical CML and analysis the data relevant to disease progression to CML CP.

    METHOD: We performed a literature search on 16 July 2017 using EBSCOhost Research Databases interface and Western Pacific Region Index Medicus. Two authors selected the studies, extracted the data and evaluated the quality of studies using an 8-item tool, independently. The outcomes were percentage of Philadelphia chromosome in the number of metaphases examined (Ph%), correlation between Ph% and blood count and time progress to CML.

    RESULT: Our initial search returned 4770 studies. A total of 10 studies with a total 17 subjects were included. The lowest Ph%, which eventually progresses to CML, was 10%. Absolute basophil count seemed to correlate better with Ph% compared to total white cell and absolute eosinophil count. The time from the first documented pre-clinical CML to CML ranged from 12 to 48 months. The overall quality of the included studies was average.

    CONCLUSION: This is the first systematic review on pre-clinical CML. This entity requires additional large-scale studies.

    Matched MeSH terms: Leukemia, Myeloid, Chronic-Phase
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