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  1. Fulltext A case of chronic myeloid leukaemia in blast transformation with leukemic ascites
    Mohd Ridzuan MS, Yap E, Wan Fariza WJ, Fadilah SA, Salwati S
    Med J Malaysia, 2016 04;71(2):85-7.
    PMID: 27326952 MyJurnal
    Chronic Myeloid Leukaemia (CML) is a disease characterised by a distinctive marker that is the Philadelphia Chromosome and an ability to transform into blast phase, which confers a poor prognosis. The median survival was reported to be between three to six months in correlation to blast phase. Extramedullary involvement with CML to sites such as pleural, meningeal and bones have been reported. We report a case of 41-year-old man who was diagnosed with CML in blast phase and presented with ascites. Ultrasound of abdomen showed coarse echotexture of liver suggestive leukaemic infiltration to the liver. The liver profile was severely deranged and associated with coagulopathy. Flow cytometry analysis of the peritoneal fluid revealed presence of myeloblasts consistent with CML in blast crisis with leukaemic ascites. Bone marrow biopsy also confirmed disease transformation. He received standard induction chemotherapy for acute myeloid leukaemia with dose modifications based on liver enzymes performance. Our case highlights an unusual presentation of CML in blast crisis with leukaemic ascites and the challenges in managing cytotoxic treatments due to the liver infiltration.
    Matched MeSH terms: Leukemia, Myelogenous, Chronic, BCR-ABL Positive/complications; Leukemia, Myelogenous, Chronic, BCR-ABL Positive/diagnosis*; Leukemia, Myelogenous, Chronic, BCR-ABL Positive/drug therapy
  2. 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, Myelogenous, Chronic, BCR-ABL Positive/diagnosis*; Leukemia, Myelogenous, Chronic, BCR-ABL Positive/genetics; Leukemia, Myelogenous, Chronic, BCR-ABL Positive/therapy
  3. Fulltext Nephrotic syndrome in a patient with relapsed of chronic myeloid leukemia after peripheral blood stem cell transplantation
    Bee PC, Gan GG, Sangkar VJ, Haris AR
    Med J Malaysia, 2008 Mar;63(1):71-2.
    PMID: 18935742 MyJurnal
    Nephrotic syndrome (NS) is a well documented complication after allogeneic peripheral blood stem cell transplantation. It is usually due to autoimmune glomerulonephritis and thought to be a clinical manifestation of graft versus host disease. NS has also been reported to be associated with other hematological malignancies. We report a case of nephrotic syndrome in a patient who relapsed after allogeneic peripheral blood stem cell transplantation (PBSCT) for chronic myeloid leukemia (CML). The renal biopsy was suggestive of minimal change disease. There was no other evidence of graft versus host disease. He was treated with high dose prednisolone, with no response and finally succumbed to the underlying disease.
    Matched MeSH terms: Leukemia, Myelogenous, Chronic, BCR-ABL Positive/complications*; Leukemia, Myelogenous, Chronic, BCR-ABL Positive/therapy*
  4. Systematic Review of Normal Subjects Harbouring BCR-ABL1 Fusion Gene
    Kuan JW, Su AT, Leong CF, Osato M, Sashida G
    Acta Haematol., 2020;143(2):96-111.
    PMID: 31401626 DOI: 10.1159/000501146
    The treatment of chronic myeloid leukaemia (CML) requires quantitative polymerase chain reaction (qPCR) to monitor BCR-ABL1 in International Scale (IS). Some normal subjects were found to harbour BCR-ABL1. We performed a systematic review on normal subjects harbouring BCR-ABL1. A literature search was done on July 16, 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 the modified Appraisal Tool for Cross-Sectional Studies independently. The outcomes were prevalence, level of BCR-ABL1IS, proportion, and time of progression to CML. The initial search returned 4,770 studies. Eleven studies, all having used convenient sampling, were included, with total of 1,360 subjects. Ten studies used qualitative PCR and one used qPCR (not IS). The mean prevalence of M-BCR was 5.9, 15.5, and 15.9% in cord blood/newborns/infants (CB/NB/I) (n = 170), children (n = 90), and adults (n = 454), respectively, while m-BCR was 15, 26.9, and 23.1% in CB/NB/I (n = 786), children (n = 67), and adults (n = 208), respectively. No study reported the proportion and time of progression to CML. Nine studies were graded as moderate quality, one study as poor quality, and one study as unacceptable. The result of the studies could neither be inferred to the general normal population nor compared. Follow-up data were scarce.
    Matched MeSH terms: Leukemia, Myelogenous, Chronic, BCR-ABL Positive/genetics; Leukemia, Myelogenous, Chronic, BCR-ABL Positive/pathology*
  5. Fulltext Molecular rearrangements of chromosome 22 in chronic myeloid leukemia in a multi-ethnic Malaysian population
    Bosco JJ, Dyck JA
    Singapore Med J, 1989 Aug;30(4):363-7.
    PMID: 2814539
    Rearrangements in the DNA of chronic myelogenous leukemia patients of Chinese, Malay and Indian origin were detected in the breakpoint cluster region of chromosome 22 using molecular techniques. The DNA of fifty patients was examined using a 1.2 kb DNA probe. Rearrangements were detected in 46/50 patients. Karyotypic data were available in nine patients, all of whom were Philadelphia chromosome positive and exhibited DNA rearrangement. Detection of the Philadelphia translocation by molecular methods, at this institution, where cytogenetics is not routinely performed, confirms its diagnostic value. The rearrangement data obtained in this study is consistent with molecular features of chronic myelogenous leukemia patients of Western countries.
    Matched MeSH terms: Leukemia, Myelogenous, Chronic, BCR-ABL Positive/ethnology; Leukemia, Myelogenous, Chronic, BCR-ABL Positive/genetics*
  6. A man with concomitant polycythaemia vera and chronic myeloid leukemia: the dynamics of the two disorders
    Bee PC, Gan GG, Nadarajan VS, Latiff NA, Menaka N
    Int J Hematol, 2010 Jan;91(1):136-9.
    PMID: 20047097 DOI: 10.1007/s12185-009-0471-6
    The co-occurrence of JAK2 V617F mutation with BCR-ABL reciprocal translocation is uncommon. We report a 60-year-old man who initially presented with phenotype of polycythemia vera (PV), which evolved into chronic myeloid leukemia and back to PV once treatment with imatinib was commenced. JAK2 V617F mutation and BCR-ABL fusion transcripts were detected in the initial sample. However, JAK2 V617F alleles diminished when BCR-ABL mRNA burden increased and reappeared once the patient was commenced on imatinib. The dynamic interaction between JAK2 V617F and BCR-ABL implies that two independent clones exist with the JAK2 V617F clone only achieving clonal dominance when BCR-ABL positive clones are suppressed by imatinib.
    Matched MeSH terms: Leukemia, Myelogenous, Chronic, BCR-ABL Positive/complications*; Leukemia, Myelogenous, Chronic, BCR-ABL Positive/drug therapy; Leukemia, Myelogenous, Chronic, BCR-ABL Positive/genetics*
  7. Fulltext HOXA4 gene promoter hypermethylation as an epigenetic mechanism mediating resistance to imatinib mesylate in chronic myeloid leukemia patients
    Elias MH, Baba AA, Husin A, Sulong S, Hassan R, Sim GA, et al.
    Biomed Res Int, 2013;2013:129715.
    PMID: 23484077 DOI: 10.1155/2013/129715
    Development of resistance to imatinib mesylate (IM) in chronic myeloid leukemia (CML) patients has emerged as a significant clinical problem. The observation that increased epigenetic silencing of potential tumor suppressor genes correlates with disease progression in some CML patients treated with IM suggests a relationship between epigenetic silencing and resistance development. We hypothesize that promoter hypermethylation of HOXA4 could be an epigenetic mechanism mediating IM resistance in CML patients. Thus a study was undertaken to investigate the promoter hypermethylation status of HOXA4 in CML patients on IM treatment and to determine its role in mediating resistance to IM. Genomic DNA was extracted from peripheral blood samples of 95 CML patients (38 good responders and 57 resistant) and 12 normal controls. All samples were bisulfite treated and analysed by methylation-specific high-resolution melt analysis. Compared to the good responders, the HOXA4 hypermethylation level was significantly higher (P = 0.002) in IM-resistant CML patients. On comparing the risk, HOXA4 hypermethylation was associated with a higher risk for IM resistance (OR 4.658; 95% CI, 1.673-12.971; P = 0.003). Thus, it is reasonable to suggest that promoter hypermethylation of HOXA4 gene could be an epigenetic mechanism mediating IM resistance in CML patients.
    Matched MeSH terms: Leukemia, Myelogenous, Chronic, BCR-ABL Positive/drug therapy; Leukemia, Myelogenous, Chronic, BCR-ABL Positive/metabolism*; Leukemia, Myelogenous, Chronic, BCR-ABL Positive/pathology
  8. 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, Myelogenous, Chronic, BCR-ABL Positive
  9. Fulltext Chronic myeloid leukaemia presenting as priapism - how should we treat these?
    Htun, T.H., Dublin, N., Parameswaran, M., Razack, A.H., Chua, C.B.
    JUMMEC, 2008;11(1):27-29.
    MyJurnal
    Priapism is a urological emergency. The treatment for ischaemic priapism is usually cavernosal aspiration with or without cavernosal irrigation. Some patients may need surgical intervention -the various shunt procedures. We report a 21-year-old man with priapism secondary to chronic myeloid leukemia who needed a combined medical and surgical management. He underwent a spongiocavernosal shunt as well as cytoreductive chemotherapy to achieve complete detumescence. Therefore, cytoreductive chemotherapy is an adjunct in difficult cult to treat priapism associated with chronic myeloid leukemia.
    Matched MeSH terms: Leukemia, Myelogenous, Chronic, BCR-ABL Positive
  10. Fulltext Medication-related issues associated with adherence to long-term tyrosine kinase inhibitors for controlling chronic myeloid leukemia: a qualitative study
    Tan BK, Tan SB, Chen LC, Chang KM, Chua SS, Balashanker S, et al.
    Patient Prefer Adherence, 2017;11:1027-1034.
    PMID: 28652712 DOI: 10.2147/PPA.S132894
    PURPOSE: Poor adherence to tyrosine kinase inhibitors (TKIs) could compromise the control of chronic myeloid leukemia (CML) and contributes to poorer survival. Little is known about how medication-related issues affect CML patients' adherence to TKI therapy in Malaysia. This qualitative study aimed to explore these issues.

    PATIENTS AND METHODS: Individual face-to-face, semistructured interviews were conducted at the hematology outpatient clinics of two medical centers in Malaysia from August 2015 to January 2016. CML patients aged ≥18 years who were prescribed a TKI were invited to participate in the study. Interviews were audio-recorded, transcribed verbatim, and thematically analyzed.

    RESULTS: Four themes were identified from 18 interviews: 1) concerns about adverse reactions to TKIs, 2) personal beliefs regarding the use of TKIs, 3) mismanagement of TKIs in daily lives, and 4) financial burden in accessing treatment. Participants skipped their TKIs due to ineffective emesis control measures and perceived wastage of medication from vomiting. Participants also modified their TKI therapy due to fear of potential harm from long-term use, and stopped taking their TKIs based on belief in curative claims of traditional medicines and misconception about therapeutic effects of TKIs. Difficulty in integrating the dosing requirements of TKIs into daily lives led to unintentional skipping of doses, as well as the risk of toxicities from inappropriate dosing intervals or food interactions. Furthermore, financial constraints also resulted in delayed initiation of TKIs, missed clinic appointments, and treatment interruptions.

    CONCLUSION: Malaysian CML patients encountered a range of medication-related issues leading to a complex pattern of nonadherence to TKI therapy. Further studies should investigate whether regular contact with patients to improve understanding of treatment rationale, to elicit and address patients' concerns about adverse reactions, and to empower patients with skills to self-manage their medications might promote better adherence to TKIs and improve CML patients' outcome.

    Study site: hematology outpatient clinics of Ampang Hospital (AH) and University Malaya Medical Centre (UMMC) in Malaysia
    Matched MeSH terms: Leukemia, Myelogenous, Chronic, BCR-ABL Positive
  11. Fulltext Nilotinib dose-optimization in newly diagnosed chronic myeloid leukaemia in chronic phase: final results from ENESTxtnd
    Hughes TP, Munhoz E, Aurelio Salvino M, Ong TC, Elhaddad A, Shortt J, et al.
    Br J Haematol, 2017 10;179(2):219-228.
    PMID: 28699641 DOI: 10.1111/bjh.14829
    The Evaluating Nilotinib Efficacy and Safety in Clinical Trials-Extending Molecular Responses (ENESTxtnd) study was conducted to evaluate the kinetics of molecular response to nilotinib in patients with newly diagnosed chronic myeloid leukaemia in chronic phase and the impact of novel dose-optimization strategies on patient outcomes. The ENESTxtnd protocol allowed nilotinib dose escalation (from 300 to 400 mg twice daily) in the case of suboptimal response or treatment failure as well as dose re-escalation for patients with nilotinib dose reductions due to adverse events. Among 421 patients enrolled in ENESTxtnd, 70·8% (95% confidence interval, 66·2-75·1%) achieved major molecular response (BCR-ABL1 ≤ 0·1% on the International Scale) by 12 months (primary endpoint). By 24 months, 81·0% of patients achieved major molecular response, including 63·6% (56 of 88) of those with dose escalations for lack of efficacy and 74·3% (55 of 74) of those with dose reductions due to adverse events (including 43 of 54 patients with successful re-escalation). The safety profile of nilotinib was consistent with prior studies. The most common non-haematological adverse events were headache, rash, and nausea; cardiovascular events were reported in 4·5% of patients (grade 3/4, 3·1%). The study was registered at clinicaltrials.gov (NCT01254188).
    Matched MeSH terms: Leukemia, Myelogenous, Chronic, BCR-ABL Positive/diagnosis; Leukemia, Myelogenous, Chronic, BCR-ABL Positive/drug therapy*; Leukemia, Myelogenous, Chronic, BCR-ABL Positive/epidemiology
  12. Fulltext Primary imatinib resistance in chronic myeloid leukemia patients in a developing country: BCR-ABL kinase domain mutations or BCR-ABL independent mechanisms?
    Yap E, Tumian NR, Azma RZ, Sharifah NA, Salwati S, Hamidah NH, et al.
    Malays J Pathol, 2017 Aug;39(2):107-113.
    PMID: 28866691 MyJurnal
    Clinical resistance to imatinib (IM) in chronic myeloid leukemia (CML) carries adverse consequences. We investigated 22 CML patients who developed IM-resistance for BCR-ABL kinase domain (KD) mutations. The median follow-up for this study was 101.9 months (range: 22.2 to 176.5 months) and the estimated mean overall survival was 150.87 months (95% CI: 130.0 to 171.0). Five out of 22 patients tested positive for BCR-ABL KD mutations: 2 had T315I, 2 had E255K and 1 had V289F mutations. Of the remaining 17 patients who did not harbor BCR-ABL KD mutations, 11 patients received nilotinib while the rest continued on IM. All 17 achieved haematological remission but only 5 patients achieved complete cytogenetic remission, 4 of whom did so after switching to nilotinib. Our study shows that most of our IM-resistant patients do not test positive for BCR-ABL KD mutations by available testing methods and the role of second generation tyrosine kinase inhibitors remains undetermined. A critical analysis of the BCR-ABL KD mutations and the underlying mechanisms/ pathways of BCR-ABL independent IM-resistance along with potential treatments in the horizon will be discussed.
    Matched MeSH terms: Leukemia, Myelogenous, Chronic, BCR-ABL Positive
  13. Fulltext BCR-ABL positive essential thrombocythaemia: a variant of chronic myelogerous leukaemia or a distinct clinical entity: a special case report
    Fadilah SA, Cheong SK
    Singapore Med J, 2000 Dec;41(12):595-8.
    PMID: 11296785
    A 37-year-old Malay man presented initially with the clinical picture of essential thrombocythaemia (ET) without the extreme leukocytosis, marked splenomegaly and low neutrophil alkaline phosphatase characteristic of chronic myelogenous leukaemia (CML). Bone marrow examination showed massive megakaryocytic hyperplasia; cytogenetic studies showed the presence of Philadelphia chromosome. The patient was treated with hydroxyurea that resulted in reduction in the platelet count. Seventeen months later, he presented with fever associated with tender massive splenomegaly. Bone marrow finding was consistent with chronic phase CML. The presence of a rearrangement involving the major breakpoint cluster region (M-bcr) on chromosome 22 was confirmed by reverse transcriptase-polymerase chain reaction. The clinical importance of finding the Philadelphia chromosome in patients who seem to have ET is in assessing prognosis. ET generally follows a chronic, indolent course. However, this patient who had Philadelphia chromosome underwent clinical transition to chronic phase CML17 months and blast crisis 29 months after presentation.
    Matched MeSH terms: Leukemia, Myelogenous, Chronic, BCR-ABL Positive/diagnosis*; Leukemia, Myelogenous, Chronic, BCR-ABL Positive/drug therapy; Leukemia, Myelogenous, Chronic, BCR-ABL Positive/genetics
  14. Fulltext The predictive value of early molecular response in chronic myeloid leukaemia patients treated with imatinib in a single real-world medical centre in a developing country
    Bee PC, Sekaran V, Ng RR, Kweh TY, Gan GG
    Singapore Med J, 2017 Mar;58(3):150-154.
    PMID: 27029807 DOI: 10.11622/smedj.2016063
    INTRODUCTION: The prognosis of patients with chronic myeloid leukaemia (CML) has improved since the introduction of imatinib. However, patients who do not achieve complete cytogenetic response (CCyR) and major molecular response (MMR) have poorer prognosis. Recent clinical trials have demonstrated that early and deeper cytogenetic and molecular responses predict a better long-term outcome. This study aimed to analyse the relationship between early molecular response and clinical outcome in a real-life setting.

    METHODS: This retrospective study included all patients with CML, in chronic or accelerated phase, who were treated with imatinib at University of Malaya Medical Centre, Malaysia.

    RESULTS: A total of 70 patients were analysed. The median follow-up duration was 74 months, and the cumulative percentages of patients with CCyR and MMR were 80.0% and 65.7%, respectively. Overall survival (OS) and event-free survival (EFS) at ten years were 94.3% and 92.9%, respectively. Patients who achieved CCyR and MMR had significantly better OS and EFS than those who did not. At six months, patients who had a BCR-ABL level ≤ 10% had significantly better OS and EFS than those who had a BCR-ABL level > 10%. The target milestone of CCyR at 12 months and MMR at 18 months showed no survival advantage in our patients.

    CONCLUSION: Our data showed that imatinib is still useful as first-line therapy. However, vigilant monitoring of patients who have a BCR-ABL level > 10% at six months of treatment should be implemented so that prompt action can be taken to provide the best outcome for these patients.

    Matched MeSH terms: Leukemia, Myelogenous, Chronic, BCR-ABL Positive/diagnosis; Leukemia, Myelogenous, Chronic, BCR-ABL Positive/drug therapy*; Leukemia, Myelogenous, Chronic, BCR-ABL Positive/genetics*
  15. Real-time quantification for BCR-ABL transcripts in chronic myeloid leukaemia patients in UKMMC, Malaysia
    Wong FL, Hamidah NH, Hawa AA, Nurul AN, Leong CF, Saw F, et al.
    Malays J Pathol, 2011 Dec;33(2):107-12.
    PMID: 22299211
    Molecular pathogenesis of chronic myeloid leukemia (CML) is well established and molecular monitoring for patients with CML has become an important practice in the management of patients on imatinib therapy. In the present study, we report the use of RQ-PCR method for detection of BCR-ABL fusion gene for our CML cases. We performed a two-step RQ-PCR on bone marrow aspirates or peripheral blood of 37 CML patients. Quantitative expression of BCR-ABL fusion gene was carried out relative to the expression of a housekeeping gene as endogenous control to compensate for uneven cell numbers, RNA quality, or variations in reverse transcription efficiencies. Twenty-four of these patients were pre-treated with hydroxyurea or alpha interferon prior to the imatinib therapy. Their BCR-ABL fusion gene levels were monitored for 18 months. All samples processed were evaluable. The PCR amplification efficiency of the ABL gene is 90.5% (0.2158) and the BCR-ABL gene, 93.4% (0.1573).
    Matched MeSH terms: Leukemia, Myelogenous, Chronic, BCR-ABL Positive/genetics*
  16. A rare presentation of chronic myeloid leukaemia with priapism treated with corporoglandular shunting
    Huei TJ, Lip HT, Shamsuddin O
    Med J Malaysia, 2018 12;73(6):420-422.
    PMID: 30647220
    Priapism is a rare clinical presentation of a patient with chronic myeloid leukaemia (CML). Herein, we present a young Nepalese man that presented to the emergency department with an acute and painful penile erection for two days. Clinically, he was pale and abdominal examination revealed hepatomegaly. Combined oncologic and initial urological intervention with carvernosal aspiration and intracavernosal phenylephrine failed to achieve detumescence. The patient underwent an emergency corporoglandular shunting eventually. In this case report, we discuss the management compared with previously reported cases.
    Matched MeSH terms: Leukemia, Myelogenous, Chronic, BCR-ABL Positive/complications*
  17. Hydroxyurea treatment for chronic myeloid leukaemia during pregnancy
    Jackson N, Shukri A, Ali K
    Br J Haematol, 1993 Sep;85(1):203-4.
    PMID: 8251394
    A patient being treated for chronic myeloid leukaemia with hydroxyurea became pregnant. Despite an increase in the dose of hydroxyurea (to 3 g per day) during the pregnancy, her white blood cell count could only be controlled at about 150 x 10(9)/l. A healthy baby girl was born at 37 weeks with normal blood counts and no evidence of congenital abnormality. There are now five reports of the use of hydroxyurea in pregnancy, and where leukapheresis is not available it may be the treatment of choice.
    Matched MeSH terms: Leukemia, Myelogenous, Chronic, BCR-ABL Positive/drug therapy*
  18. Clinical stage of chronic granulocytic leukaemia and BCR breakpoint location in South-East Asian patients
    Dyck JA, Bosco JJ
    Br J Haematol, 1989 May;72(1):64-7.
    PMID: 2736243
    Forty-six Malaysian patients with chronic granulocytic leukaemia were found to be rearranged in the breakpoint cluster region (BCR) of chromosome 22, molecular evidence of Philadelphia chromosome (t9.22) translocation. Through the use of a 1.2 kb 3' BCR probe and two restriction enzyme digests, patients' breakpoints could be localized either to 5' or 3' regions of the BCR. Breakpoint site localization at the time of DNA sampling did not show any positive statistical association to clinical status defined as chronic phase, chronic phase with less than 6 months to blast crisis, accelerated phase and blast crisis. This was in contrast to earlier reports which indicated that patients with breakpoint at 3' site were at a higher biologic risk for entering blast crisis.
    Matched MeSH terms: Leukemia, Myelogenous, Chronic, BCR-ABL Positive/genetics*
  19. Fulltext Pregnancy in a patient receiving busulphan for chronic myeloid leukaemia
    Norhaya MR, Cheong SK, Hamidah NH, Ainoon O
    Singapore Med J, 1994 Feb;35(1):102-3.
    PMID: 8009265
    A 33-year-old Malay lady with chronic myeloid leukaemia (CML) became amenorrhoeic during therapy with busulphan. Pregnancy was diagnosed via a urine pregnancy test and an ultrasound confirmed a viable foetus at 16 weeks. The busulphan was stopped. Her pregnancy was unremarkable and continued till term. She delivered a healthy child.
    Matched MeSH terms: Leukemia, Myelogenous, Chronic, BCR-ABL Positive/drug therapy*
  20. Low level of TERC gene amplification between chronic myeloid leukaemia patients resistant and respond to imatinib mesylate treatment
    Mohamad Ashari ZS, Sulong S, Hassan R, Husin A, Sim GA, Abdul Wahid SF
    Asian Pac J Cancer Prev, 2014;15(4):1863-9.
    PMID: 24641422
    The amplification of telomerase component (TERC) gene could play an important role in generation and treatment of haematological malignancies. This present study was aimed to investigate copy number amplification status of TERC gene in chronic myeloid leukaemia (CML) patients who were being treated with imatinib mesylate (IM). Genomic DNA was extracted from peripheral blood of CML-IM Resistant (n=63), CML-IM Respond (n=63) and healthy individuals (n=30). TERC gene copy number predicted (CNP) and copy number calculated (CNC) were determined based on Taqman® Copy Number Assay. Fluorescence in situ hybridization (FISH) analysis was performed to confirm the normal signal pattern in C4 (calibrator) for TERC gene. Nine of CML patients showed TERC gene amplification (CNP=3), others had 2 CNP. A total of 17 CML patients expressed CNC>2.31 and the rest had 2.31>CNC>1.5. TERC gene CNP value in healthy individuals was 2 and their CNC value showed in range 1.59-2.31. The average CNC TERC gene copy number was 2.07, 1.99 and 1.94 in CML- IM Resistant patients, CML-IM Respond and healthy groups, respectively. No significant difference of TERC gene amplification observed between CML-IM Resistant and CML-IM Respond patients. Low levels of TERC gene amplification might not have a huge impact in haematological disorders especially in terms of resistance towards IM treatment.
    Matched MeSH terms: Leukemia, Myelogenous, Chronic, BCR-ABL Positive/drug therapy; Leukemia, Myelogenous, Chronic, BCR-ABL Positive/genetics*
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