Displaying publications 41 - 60 of 111 in total

Abstract:
Sort:
  1. Ankathil R, Azlan H, Dzarr AA, Baba AA
    Pharmacogenomics, 2018 04;19(5):475-393.
    PMID: 29569526 DOI: 10.2217/pgs-2017-0193
    Despite the excellent efficacy and improved clinical responses obtained with imatinib mesylate (IM), development of resistance in a significant proportion of chronic myeloid leukemia (CML) patients on IM therapy have emerged as a challenging problem in clinical practice. Resistance to imatinib can be due to heterogeneous array of factors involving BCR/ABL-dependent and BCR/ABL-independent pathways. Although BCR/ABL mutation is the major contributory factor for IM resistance, reduced bio-availability of IM in leukemic cells is also an important pharmacokinetic factor that contributes to development of resistance to IM in CML patients. The contribution of polymorphisms of the pharmacogenes in relation to IM disposition and treatment outcomes have been studied by various research groups in numerous population cohorts. However, the conclusions arising from these studies have been highly inconsistent. This review encompasses an updated insight into the impact of pharmacogenetic variability on treatment response of IM in CML patients.
    Matched MeSH terms: Leukemia, Myeloid, Acute/drug therapy*; Leukemia, Myeloid, Acute/genetics*
  2. Norhaya MR, Cheong SK, Hamidah NH, Ainoon O
    Singapore Med J, 1996 Jun;37(3):320-2.
    PMID: 8942241
    A 45-year-old Malay lady developed brisk vesicular, plaque-like reaction to a Mantoux test concomitant with a diagnosis of acute myeloid leukaemia (AML). The lesion resolved one month after chemotherapy. Similar lesions developed later after she was bitten by mosquitoes on the forearms. She also had the lesions over her cheek. A skin biopsy showed infiltration of the dermis with neutrophils and some monocytoid cells. The lesion resolved one week after prednisolone therapy.
    Matched MeSH terms: Leukemia, Myeloid, Acute/complications; Leukemia, Myeloid, Acute/diagnosis*
  3. Lum SH, Choong SS, Krishnan S, Mohamed Z, Ariffin H
    Singapore Med J, 2016 Jun;57(6):320-4.
    PMID: 27353457 DOI: 10.11622/smedj.2016106
    INTRODUCTION: Children with Down syndrome (DS) are at increased risk of developing distinctive clonal myeloid disorders, including transient abnormal myelopoiesis (TAM) and myeloid leukaemia of DS (ML-DS). TAM connotes a spontaneously resolving congenital myeloproliferative state observed in 10%-20% of DS newborns. Following varying intervals of apparent remission, a proportion of children with TAM progress to develop ML-DS in early childhood. Therefore, TAM and ML-DS represent a biological continuum. Both disorders are characterised by recurring truncating somatic mutations of the GATA1 gene, which are considered key pathogenetic events.

    METHODS: We herein report, to our knowledge, the first observation on the frequency and nature of GATA1 gene mutations in a cohort of Malaysian children with DS-associated TAM (n = 9) and ML-DS (n = 24) encountered successively over a period of five years at a national referral centre.

    RESULTS: Of the 29 patients who underwent GATA1 analysis, GATA1 mutations were observed in 15 (51.7%) patients, including 6 (75.0%) out of 8 patients with TAM, and 9 (42.9%) of 21 patients with ML-DS. All identified mutations were located in exon 2 and the majority were sequence-terminating insertions or deletions (66.7%), including several hitherto unreported mutations (12 out of 15).

    CONCLUSION: The low frequency of GATA1 mutations in ML-DS patients is unusual and potentially indicates distinctive genomic events in our patient cohort.

    Matched MeSH terms: Leukemia, Myeloid/complications; Leukemia, Myeloid/genetics*
  4. Jackson N, Reddy SC, Hishamuddin M, Low HC
    Clin Lab Haematol, 1996 Jun;18(2):105-9.
    PMID: 8866143
    The associations between retinal findings and haematological parameters in acute leukaemia are controversial. Sixty-three newly-diagnosed acute leukaemia patients, aged 12-77 years, were studied prospectively for the presence of intra-retinal haemorrhages (IRH), white-centred haemorrhages (WCH), cotton wool spots (CWS) and macular haemorrhages (MH), Thirty-three patients (52.4%) showed at least one retinal abnormality. The prevalence of individual findings was: IRH (30 cases), WCH (20 cases), CWS (5 cases), MH (11 cases). In contrast to previous studies, there was no association between any of these retinal findings and the haemoglobin level or the platelet count. There was a higher median WBC in patients with IRH (68 x 10(9)/l) than in those without IRH (15.4 x 10(9)/l), P = 0.037. When the acute myeloblastic leukaemia cases were considered separately, an association was also found between higher WBC and the presence of WCH and CWS. There was no association between retinal findings and FAB type in the AML cases. We conclude that a high WBC may be at least as important as anaemia and thrombocytopenia in the pathogenesis of the retinopathy of acute leukaemia.
    Matched MeSH terms: Leukemia, Myeloid/blood; Leukemia, Myeloid/complications; Leukemia, Myeloid/pathology
  5. Reddy SC, Jackson N
    Acta Ophthalmol Scand, 2004 Feb;82(1):81-5.
    PMID: 14738490
    PURPOSE: To determine the prevalence of retinal changes in newly diagnosed acute leukaemia patients, and to establish the relationship between retinal lesions and haematological parameters in these patients.

    METHODS: A total of 127 patients with acute leukaemia (myeloid and lymphoid), of both genders, aged between 13 and 77 years, were examined by an ophthalmologist for retinal changes using direct/indirect ophthalmoscopy within 2 days of diagnosis before starting chemotherapy.

    RESULTS: Retinal lesions were seen in 62 cases (49%), with intraretinal haemorrhages being the most common lesion (42%). A high white blood cell count was significantly associated with intraretinal haemorrhages (p = 0.04) and white-centred haemorrhages (p = 0.001), while a low platelet count was significantly associated with intraretinal haemorrhages (p = 0.03) in acute myeloid leukaemia patients.

    CONCLUSIONS: A high white blood cell count may be considered as important as a low platelet count in the pathogenesis of leukaemic retinopathy.

    Matched MeSH terms: Leukemia, Myeloid/blood; Leukemia, Myeloid/diagnosis*; Leukemia, Myeloid/drug therapy
  6. Abbaspour Babaei M, Kamalidehghan B, Saleem M, Huri HZ, Ahmadipour F
    Drug Des Devel Ther, 2016;10:2443-59.
    PMID: 27536065 DOI: 10.2147/DDDT.S89114
    c-Kit, a receptor tyrosine kinase, is involved in intracellular signaling, and the mutated form of c-Kit plays a crucial role in occurrence of some cancers. The function of c-Kit has led to the concept that inhibiting c-Kit kinase activity can be a target for cancer therapy. The promising results of inhibition of c-Kit for treatment of cancers have been observed in some cancers such as gastrointestinal stromal tumor, acute myeloid leukemia, melanoma, and other tumors, and these results have encouraged attempts toward improvement of using c-Kit as a capable target for cancer therapy. This paper presents the findings of previous studies regarding c-Kit as a receptor tyrosine kinase and an oncogene, as well as its gene targets and signaling pathways in normal and cancer cells. The c-Kit gene location, protein structure, and the role of c-Kit in normal cell have been discussed. Comprehending the molecular mechanism underlying c-Kit-mediated tumorogenesis is consequently essential and may lead to the identification of future novel drug targets. The potential mechanisms by which c-Kit induces cellular transformation have been described. This study aims to elucidate the function of c-Kit for future cancer therapy. In addition, it has c-Kit inhibitor drug properties and their functions have been listed in tables and demonstrated in schematic pictures. This review also has collected previous studies that targeted c-Kit as a novel strategy for cancer therapy. This paper further emphasizes the advantages of this approach, as well as the limitations that must be addressed in the future. Finally, although c-Kit is an attractive target for cancer therapy, based on the outcomes of treatment of patients with c-Kit inhibitors, it is unlikely that Kit inhibitors alone can lead to cure. It seems that c-Kit mutations alone are not sufficient for tumorogenesis, but do play a crucial role in cancer occurrence.
    Matched MeSH terms: Leukemia, Myeloid, Acute/drug therapy*; Leukemia, Myeloid, Acute/genetics; Leukemia, Myeloid, Acute/metabolism
  7. Mohd Khairi Zahry, Ankathil, Ravindran
    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
  8. Wong KK, Lawrie CH, Green TM
    Biomark Insights, 2019;14:1177271919846454.
    PMID: 31105426 DOI: 10.1177/1177271919846454
    Epigenetic alteration has been proposed to give rise to numerous classic hallmarks of cancer. Impaired DNA methylation plays a central role in the onset and progression of several types of malignancies, and DNA methylation is mediated by DNA methyltransferases (DNMTs) consisting of DNMT1, DNMT3A, and DNMT3B. DNMTs are frequently implicated in the pathogenesis and aggressiveness of acute myeloid leukaemia (AML) patients. In this review, we describe and discuss the oncogenic roles of DNMT1, DNMT3A, and DNMT3B in AML. The clinical response predictive roles of DNMTs in clinical trials utilising hypomethylating agents (azacitidine and decitabine) in AML patients are presented. Novel hypomethylating agent (guadecitabine) and experimental DNMT inhibitors in AML are also discussed. In summary, hypermethylation of tumour suppressors mediated by DNMT1 or DNMT3B contributes to the progression and severity of AML (except MLL-AF9 and inv(16)(p13;q22) AML for DNMT3B), while mutation affecting DNMT3A represents an early genetic lesion in the pathogenesis of AML. In clinical trials of AML patients, expression of DNMTs is downregulated by hypomethylating agents while the clinical response predictive roles of DNMT biomarkers remain unresolved. Finally, nucleoside hypomethylating agents have continued to show enhanced responses in clinical trials of AML patients, and novel non-nucleoside DNMT inhibitors have demonstrated cytotoxicity against AML cells in pre-clinical settings.
    Matched MeSH terms: Leukemia, Myeloid, Acute
  9. Sutiman N, Nwe MS, Ni Lai EE, Lee DK, Chan MY, Eng-Juh Yeoh A, et al.
    Clin Lymphoma Myeloma Leuk, 2021 03;21(3):e290-e300.
    PMID: 33384264 DOI: 10.1016/j.clml.2020.11.016
    PURPOSE: To determine the prognostic factors in pediatric patients with acute myeloid leukemia (AML) and to assess whether their outcomes have improved over time.

    PATIENTS AND METHODS: Sixty-two patients with AML excluding acute promyelocytic leukemia were retrospectively analyzed. Patients in the earlier cohort (n = 36) were treated on the Medical Research Council (MRC) AML12 protocol, whereas those in the recent cohort (n = 26) were treated on the Malaysia-Singapore AML protocol (MASPORE 2006), which differed in terms of risk group stratification, cumulative anthracycline dose, and timing of hematopoietic stem-cell transplantation for high-risk patients.

    RESULTS: Significant improvements in 10-year overall survival and event-free survival were observed in patients treated with the recent MASPORE 2006 protocol compared to the earlier MRC AML12 protocol (overall survival: 88.0% ± 6.5% vs 50.1% ± 8.6%, P = .002; event-free survival: 72.1% ± 9.0 vs 50.1% ± 8.6%, P = .045). In univariate analysis, patients in the recent cohort had significantly lower intensive care unit admission rate (11.5% vs 47.2%, P = .005) and numerically lower relapse rate (26.9% vs 50.0%, P = .068) compared to the earlier cohort. Multivariate analysis showed that treatment protocol was the only independent predictive factor for overall survival (hazard ratio = 0.21; 95% confidence interval, 0.06-0.73, P = .014).

    CONCLUSION: Outcomes of pediatric AML patients have improved over time. The more recent MASPORE 2006 protocol led to significant improvement in long-term survival rates and reduction in intensive care unit admission rate.

    Matched MeSH terms: Leukemia, Myeloid, Acute/diagnosis; Leukemia, Myeloid, Acute/mortality*; Leukemia, Myeloid, Acute/therapy*
  10. Aziz H, Ping CY, Alias H, Ab Mutalib NS, Jamal R
    Front Pharmacol, 2017;8:897.
    PMID: 29270125 DOI: 10.3389/fphar.2017.00897
    It is believed that there are key differences in the genomic profile between adult and childhood acute myeloid leukemia (AML). Relapse is the significant contributor of mortality in patients with AML and remains as the leading cause of cancer death among children, posing great challenges in the treatment of AML. The knowledge about the genomic lesions in childhood AML is still premature as most genomic events defined in children were derived from adult cohorts. However, the emerging technologies of next generation sequencing have narrowed the gap of knowledge in the biology of AML by the detection of gene mutations for each sub-type which have led to the improvement in terms of prognostication as well as the use of targeted therapies. In this review, we describe the recent understanding of the genomic landscape including the prevalence of mutation, prognostic impact, and targeted therapies that will provide an insight into the pathogenesis of AML relapse in both adult and childhood cases.
    Matched MeSH terms: Leukemia, Myeloid, Acute
  11. RamaChandran S, Ariffin H
    Pediatr Blood Cancer, 2009 Sep;53(3):488-90.
    PMID: 19434733 DOI: 10.1002/pbc.22063
    Haemophagocytic lymphohistiocytosis (HLH) is an uncommon disease with a high fatality rate. Etoposide is an important component of current HLH treatment regimes. Two patients with HLH developed etoposide-related secondary acute myeloid leukemia (sAML) following therapy for HLH. Etoposide, an epipodophyllotoxin, is a topoisomerase II inhibitor that interacts with DNA to potentiate leukaemogenesis. The risk of developing sAML is estimated to be between 1% and 5%, 2-20 years after exposure to etoposide but may also be related to cumulative drug doses, treatment schedules, host factors and co-administration of other antineoplastic agents.
    Matched MeSH terms: Leukemia, Myeloid, Acute/chemically induced*
  12. Chong LA, Josephine P, Ariffin H
    Med J Malaysia, 2006 Jun;61(2):236-8.
    PMID: 16898320 MyJurnal
    We report a case of a child with severe congenital neutropenia (Kostmann's syndrome) who was treated with daily prophylactic subcutaneous granulocyte colony-stimulating factor (G-CSF) from the age of eight to sixteen years before being discontinued for poor haematological and clinical response. She did not have a HLA-matched sibling to enable bone marrow transplantation. She subsequently developed acute megakaryoblastic leukemia at the age of 17 years and succumbed during induction chemotherapy. The role of G-CSF in the pathogenesis of her malignant transformation to AML is complicated as this disorder has a propensity for myelodysplasia or AML as part of its natural history.
    Matched MeSH terms: Leukemia, Myeloid/pathology*
  13. Ng KP, Soo-Hoo TS, Na SL, Gan GG, Sangkar JV, Teh AKH
    Med J Malaysia, 2003 Oct;58(4):608-12.
    PMID: 15190640
    Scopulariopsis brevicaulis is a soil fungus normally associated with onychomycosis. It causes subcutaneous infection in immunocompromised patients and is rarely isolated from blood. A case of systemic Scopulariopsis brevicaulis infection was reported in a patient with acute myeloid leukemia. The patient developed persistent fever that did not respond to wide spectrum antibiotics and amphotericin B. Scopulariopsis brevicaulis was the only pathogen isolated from blood cultures. The fever subsided with itraconazole and there was no recurrence of fungal infection with prolonged maintenance of oral itraconazole.
    Matched MeSH terms: Leukemia, Myeloid/complications*
  14. S-Abdul-Wahid F, Soon-Keng C
    Br J Haematol, 2002 Mar;116(4):731.
    PMID: 11886374
    Matched MeSH terms: Leukemia, Myeloid/pathology*
  15. Esa E, Hashim AK, Mohamed EHM, Zakaria Z, Abu Hassan AN, Mat Yusoff Y, et al.
    Genet Test Mol Biomarkers, 2021 Mar;25(3):199-210.
    PMID: 33734890 DOI: 10.1089/gtmb.2020.0182
    Background: The association between dysregulated microRNAs (miRNAs) and acute myeloid leukemia (AML) is well known. However, our understanding of the regulatory role of miRNAs in the cytogenetically normal AML (CN-AML) subtype pathway is still poor. The current study integrated miRNA and mRNA profiles to explore novel miRNA-mRNA interactions that affect the regulatory patterns of de novo CN-AML. Methods: We utilized a multiplexed nanoString nCounter platform to profile both miRNAs and mRNAs using similar sets of patient samples (n = 24). Correlations were assessed, and an miRNA-mRNA network was constructed. The underlying biological functions of the mRNAs were predicted by gene enrichment. Finally, the interacting pairs were assessed using TargetScan and microT-CDS. We identified 637 significant negative correlations (false discovery rate <0.05). Results: Network analysis revealed a cluster of 12 miRNAs representing the majority of mRNA targets. Within the cluster, five miRNAs (miR-495-3p, miR-185-5p, let-7i-5p, miR-409-3p, and miR-127-3p) were posited to play a pivotal role in the regulation of CN-AML, as they are associated with the negative regulation of myeloid leukocyte differentiation, negative regulation of myeloid cell differentiation, and positive regulation of hematopoiesis. Conclusion: Three novel interactions in CN-AML were predicted as let-7i-5p:HOXA9, miR-495-3p:PIK3R1, and miR-495-3p:CDK6 may be responsible for regulating myeloid cell differentiation in CN-AML.
    Matched MeSH terms: Leukemia, Myeloid, Acute/genetics*
  16. Banerjee AK
    Med J Malaya, 1971 Mar;25(3):187-92.
    PMID: 4253245
    Matched MeSH terms: Leukemia, Myeloid, Acute/complications*
  17. Amini R, Azizi Jalilian F, Veerakumarasivam A, Abdullah S, Abdulamir AS, Nadali F, et al.
    Biomed Res Int, 2013;2013:752603.
    PMID: 23509773 DOI: 10.1155/2013/752603
    Vascular endothelial growth factor (VEGF) is a potent angiogenic factor involved in angiogenesis-mediated progression of acute myeloid leukemia (AML). Studies have reported the role of soluble form of fms-like tyrosine kinase (sFlT-1) delivery as an antitumor agent by inhibiting VEGF. This study investigates the outcome of delivery of a VEGF165 antagonist, soluble vascular endothelial growth factor receptor, namely sFLT-1, mediating lipofectamine 2000 in acute myeloid leukemic cells. A recombinant plasmid expressing sFLT-1 was constructed and transfected into the K562 and HL60 cells using lipofectamine 2000 transfection reagent. sFLT-1 expression/secretion in pVAX-sFLT-1 transfected cells was verified by RT-PCR and western blot. MTS assay was carried out to evaluate the effect of sFLT-1 on human umbilical vein endothelial cells and K562 and HL60 cells in vitro. Treatment with pVAX-sFLT-1 showed no association between sFLT-1 and proliferation of infected K562 and HL60 cells, while it demonstrated a significant inhibitory impact on the proliferation of HUVECs. The results of the current study imply that the combination of nonviral gene carrier and sFLT-1 possesses the potential to provide efficient tool for the antiangiogenic gene therapy of AML.
    Matched MeSH terms: Leukemia, Myeloid, Acute/genetics*; Leukemia, Myeloid, Acute/therapy
  18. Tan YF, Sim GC, Habsah A, Leong CF, Cheong SK
    Malays J Pathol, 2008 Dec;30(2):73-9.
    PMID: 19291915 MyJurnal
    Dendritic cells (DC) are professional antigen presenting cells of the immune system. Through the use of DC vaccines (DC after exposure to tumour antigens), cryopreserved in single-use aliquots, an attractive and novel immunotherapeutic strategy is available as an option for treatment. In this paper we describe an in vitro attempt to scale-up production of clinical-grade DC vaccines from leukemic cells. Blast cells of two relapsed AML patients were harvested for DC generation in serum-free culture medium containing clinical-grade cytokines GM-CSF, IL-4 and TNF-alpha. Cells from patient 1 were cultured in a bag and those from patient 2 were cultured in a flask. The numbers of seeding cells were 2.24 x 10(8) and 0.8 x 10(8), respectively. DC yields were 10 x 10(6) and 29.8 x 10(6) cells, giving a conversion rate of 4.7% and 37%, respectively. These DC vaccines were then cryopreserved in approximately one million cells per vial with 20% fresh frozen group AB plasma and 10% DMSO. At 12 months and 21 months post cryopreservation, these DC vaccines were thawed, and their sterility, viability, phenotype and functionality were studied. DC vaccines remained sterile up to 21 months of storage. Viability of the cryopreserved DC in the culture bag and flask was found to be 50% and 70% at 12 months post cryopreservation respectively; and 48% and 67% at 21 months post cryopreservation respectively. These DC vaccines exhibited mature DC surface phenotypic markers of CD83, CD86 and HLA-DR, and negative for haemopoietic markers. Mixed lymphocyte reaction (MLR) study showed functional DC vaccines. These experiments demonstrated that it is possible to produce clinical-grade DC vaccines in vitro from blast cells of leukemic patients, which could be cryopreserved up to 21 months for use if repeated vaccinations are required in the course of therapy.
    Matched MeSH terms: Leukemia, Myeloid, Acute/immunology*; Leukemia, Myeloid, Acute/therapy
  19. Abdul Rahman HI, Shah SA, Alias H, Ibrahim HM
    Asian Pac J Cancer Prev, 2008 Oct-Dec;9(4):649-52.
    PMID: 19256754
    BACKGROUND: In Malaysia, acute leukemia is the most common cancer among children below the age of 15. A case-control study was here conducted for cases from the Klang Valley, Malaysia, who received treatment at the National University of Malaysia Hospital (HUKM) and Kuala Lumpur General Hospital (GHKL). The main objective was to determine any association with environmental factors.

    METHODS: Case subjects were children aged below 15 years and diagnosed with acute leukemia in HUKM and GHKL between January 1, 2001 and May 30, 2007. Control subjects were children aged below 15 years who were diagnosed with any non-cancerous acute illnesses in these hospitals. A total of 128 case subjects and 128 control subjects were enrolled in this study. The information was collected using a structured questionnaire and a global positioning system (GPS) device. All factors were analyzed using unmatched logistic regression.

    RESULTS: The analysis showed that the occurrence of acute leukemia among children was strongly determined by the following factors: family income (odds ratio (OR) 0.19, 95% confidence interval (CI): 0.09-0.42), father with higher social contact (OR 7.61, 95% CI: 3.78-15.4), number of elder siblings (OR 0.36, 95% CI: 0.18-0.77), father who smokes (OR 2.78, 95% CI: 1.49-5.16), and the distance of the house from a power line (OR 2.30, 95% CI: 1.18-4.49).

    CONCLUSIONS: Some socioeconomic, demographic, and environmental factors are strong predictors of the occurrence of acute leukemia among children in Klang Valley, Malaysia. In terms of environmental factors, it is recommended that future housing areas should be developed at least 200 m away from power lines.
    Matched MeSH terms: Leukemia, Myeloid, Acute/epidemiology*; Leukemia, Myeloid, Acute/therapy
  20. Maha A, Cheong SK, Leong CF, Seow HF
    Hematology, 2008 Feb;13(1):13-20.
    PMID: 18534060 DOI: 10.1179/102453308X315762
    Despite the advances in understanding the pathophysiology of acute myeloid leukaemia (AML), the cure rate for acute myeloid leukaemia patients remains low. Cytogenetic abnormalities and age are the prognostic factors that guide treatment decisions. However, many AML patients still die. The biological factors that influence treatment outcome are largely unknown. Thus, the objective of our study was to use the in vitro viability test to correlate with treatment outcome. Acute myeloid leukaemia blasts demonstrated differing ability to survive in culture. Our examination of blast phenotype at various days in culture showed two possible growth directions. First, cells underwent maturation by increased expression of CD16 and down-regulated CD34 (a haemopoietic stem cell marker). These cells also appeared to have undergone apoptosis. Alternatively, cells continued to survive in culture and maintained high expression of CD34. An MTT assay was carried out to determine viability after three days of culture. Lower optical density values were obtained for samples that underwent apoptosis and higher values were obtained for samples that survived in culture. Apoptosis was measured by Annexin V/propidium iodide staining. A comparison between results of MTT assay and duration of disease free survival revealed that a higher viability in vitro correlated significantly with shorter survival duration in the patient (R -0.761, p=0.002, n=13). Thus, this study further supports the hypothesis that AML patients with poor survival may be related to having blasts with a biologically more immature or stem cell-like nature.
    Matched MeSH terms: Leukemia, Myeloid, Acute/drug therapy; Leukemia, Myeloid, Acute/pathology*
Filters
Contact Us

Please provide feedback to Administrator (afdal@afpm.org.my)

External Links