Chronic Myeloid Leukemia (CML)



Information Patients and the Public (17 links)
Chronic Myelogenous Leukemia Treatment
National Cancer InstitutePDQ summaries are written and frequently updated by editorial boards of experts Further info.
Macmillan Cancer SupportContent is developed by a team of information development nurses and content editors, and reviewed by health professionals. Further info.
Chronic myeloid leukaemia (CML)
Cancer Research UKCancerHelp information is examined by both expert and lay reviewers. Content is reviewed every 12 to 18 months. Further info.
NHS ChoicesNHS Choices information is quality assured by experts and content is reviewed at least every 2 years. Further info.
Leukemia - Chronic Myeloid - CML
Cancer.NetContent is peer reviewed and Cancer.Net has an Editorial Board of experts and advocates. Content is reviewed annually or as needed. Further info.
NCMLS
The Society, founded in 2007, was created by and for patients and their families in order to provide a centralized hub of information for this rare form of leukemia. The site includes Ask the Experts, FAQ, and support information.
Symptoms and Treatment of Chronic Myeloid Leukemia
Medicshow
Animation: Educational video about Symptoms and Treatment of Chronic Myeloid Leukemia
Chronic Myelogenous Leukemia Society of Canada
CML Society of Canada
Established in 2006, Society provides support, education and information on CML, current and emerging treatments and research initiatives for people living with CML and their families in Canada.
Chronic Myeloid Leukaemia (CML)
Leukaemia Care
Detailed guide providing an overview of CML with sections on signs and symptoms, diagnosis, treatment, horizon drugs and support.
Leukemia & Lymphoma Society
Information about CML, causes, risk factors, diagnosis, treatment and other topics.
CML - Stop - Русский - Translate to English
A Russian language forum for patients with CML, their families, physicians and other experts on topical issues.
A worldwide network of non-profit organisations supporting patients with CML and their relatives by sharing knowledge and best practice, supporting campaigns, and educating advocates how to build and grow patient groups. The network is solely run by volunteers who are CML patients themselves.
Gleevecs Effects onTyrosine Kinase
Nelson Caetano
Animation by a Pharmacy student. It begins by introducing the Philadelphia Chromosome, and mentions Gleevec, the first in a class of drugs that specifically target and competively inhibit the ATP binding site on BCR-ABL tyrosine kinase.(2007)
CancerCouncil NSW
Information about CML, diagnosis and symptoms, treatment, living with CML, risk factors, and research.
Leukemia--Chronic Myeloid (Myelogenous)
American Cancer Society
Detailed guide.
Journey of Chronic Myeloid Leukemia (CML)
Novartis / European Hematological Association
Video: the story of a fatal cancer that has been transformed into a chronic condition. CML is now considered the model for targeted therapy in hematology and oncology. This video was originally displayed at the 17th Annual Congress of the European Hematological Association (EHA) in Amsterdam, 2012.
Information for Health Professionals / Researchers (8 links)
- PubMed search for publications about Chronic Myelogenous Leukemia - Limit search to: [Reviews]
PubMed Central search for free-access publications about Chronic Myelogenous Leukemia
MeSH term: Leukemia, Myelogenous, Chronic, BCR-ABL PositiveUS National Library of Medicine
PubMed has over 22 million citations for biomedical literature from MEDLINE, life science journals, and online books. Constantly updated.
Chronic Myelogenous Leukemia Treatment
National Cancer InstitutePDQ summaries are written and frequently updated by editorial boards of experts Further info.
Patient UKPatientUK content is peer reviewed. Content is reviewed by a team led by a Clinical Editor to reflect new or updated guidance and publications. Further info.
What is Chronic Myeloid Leukemia (CML)?
http://www.hemonc101.com/
Dr. Tony Talebi discusses "What is Chronic Myelocytic Leukemia (CML)?" with Dr. Javier Pinilla from the Lee Moffitt Cancer Center.
ABL1 (v-abl Abelson murine leukemia viral oncogene homolog 1)
Atlas of Genetics and Cytogenetics in Oncology and Haematology
An Evening with the CML Experts (2011)
National CML Society
Speaker Dr. Michael Mauro, Prof. of Medicine at OSHU. 1 hr video.
BCR-ABL1 in Chronic Myeloid Leukemia
Medscape
Detailed referenced article by Emmanuel Besa, MD.
Latest Research Publications
This list of publications is regularly updated (Source: PubMed).
Chronic Myeloid Leukemia as Secondary Malignancy Following the Treatment of Hodgkin Lymphoma: A Case Series.
Anticancer Res. 2019; 39(8):4333-4335 [PubMed] Related Publications
Quinacrine Depletes BCR-ABL and Suppresses Ph-Positive Leukemia Cells.
Cancer Invest. 2019; 37(6):242-252 [PubMed] Related Publications
Efficacy of Dasatinib in a Very Elderly CML Patient Expressing a Rare E13a3
Anticancer Res. 2019; 39(7):3949-3954 [PubMed] Related Publications
Efficacy of Nilotinib in a CML Patient Expressing the Three-way Complex Variant Translocation t(2;9;22).
Anticancer Res. 2019; 39(7):3893-3899 [PubMed] Related Publications
CASE REPORT: We report the three-way complex variant translocation t(2;9;22) in a CP-CML patient. Conventional cytogenetic analysis was employed to identify the ACA. Multiplex reverse transcription-PCR was used to identify the BCR-ABL1 transcript and its levels were measured using quantitative real-time-PCR. This rare ACA t(2;9;22) in our young patient displayed primary resistance to IM, but was responsive to second-line treatment with nilotinib.
CONCLUSION: CP-CML patients exhibiting this rare aberration at diagnosis may benefit from a 2G-TKI therapy compared to IM.
Significance of apoptosis and autophagy of leukemic blasts for the outcomes of acute myeloid leukemia patients.
Adv Clin Exp Med. 2019; 28(7):861-869 [PubMed] Related Publications
OBJECTIVES: The study aimed to investigate the predictive and prognostic significance of autophagy and apoptosis in patients with acute myeloid leukemia (AML).
MATERIAL AND METHODS: The study included 38 patients. Blood was collected before and 12-24 h after the start of treatment, since at that time point, the appropriate blast cell count was still available. Autophagy was measured with the expression of the ATG5, MAP1L3, LC3-I, and LC3-II proteins. The percentage of mononuclear cells in early and late apoptosis was evaluated with flow cytometry, using the annexin V and propidium iodide (PI) binding assay.
RESULTS: The percentage of apoptotic blast cells before treatment was not associated with the response. However, in the remission group, the overall percentage of apoptotic cells measured 12-24 h after the start of treatment was higher than in non-remission patients, which was statistically significant. In neither group we found any difference in the level of autophagy before and 12-24 h after the start of treatment. Nevertheless, we observed an increasing tendency of the MAP1LC3 protein expression (not statistically significant) in the remission group 12-24 h after the start of treatment. Patients with a higher percentage of blast cells in apoptosis and with a higher expression of MAP1LC3 protein measured 12-24 h after the start of the therapy had longer overall survival (OS).
CONCLUSIONS: A higher percentage of apoptotic as well as autophagic blast cells measured 12-24 h after the start of the chemotherapy is an independent factor associated with better outcomes.
Contribution of Chronic Myeloid Leukaemia (CML) as a Disease Model to Define and Study Clonal Heterogeneity.
Adv Exp Med Biol. 2019; 1139:171-185 [PubMed] Related Publications
Lipid nanoparticle-mediated siRNA delivery for safe targeting of human CML in vivo.
Ann Hematol. 2019; 98(8):1905-1918 [PubMed] Related Publications
Assessment of chronic renal injury in patients with chronic myeloid leukemia in the chronic phase receiving tyrosine kinase inhibitors.
Ann Hematol. 2019; 98(7):1627-1640 [PubMed] Related Publications
Ten-year outcome of chronic-phase chronic myeloid leukemia patients treated with imatinib in real life.
Ann Hematol. 2019; 98(8):1891-1904 [PubMed] Related Publications
Detecting the stable point of therapeutic effect of chronic myeloid leukemia based on dynamic network biomarkers.
BMC Bioinformatics. 2019; 20(Suppl 7):202 [PubMed] Free Access to Full Article Related Publications
RESULTS: A therapeutic effect recognition strategy based on dynamic network biomarkers (DNB) is provided for CML patients' gene expression data. With the DNB criteria, the DNB with 250 genes is selected and the therapeutic effect index (TEI) is constructed for the detection of individual disease. The pre-stable state before the disease condition becomes stable is 1 month. Through functional analysis for the DNB, some genes are confirmed as key genes to affect the progress of CML patients' condition.
CONCLUSIONS: The results provide a certain theoretical direction and theoretical basis for medical personnel in the treatment of CML patients, and find new therapeutic targets in the future. The biomarkers of CML can help patients to be treated promptly and minimize drug resistance, treatment failure and relapse, which reduce the mortality of CML significantly.
HDAC1,2 Knock-Out and HDACi Induced Cell Apoptosis in Imatinib-Resistant K562 Cells.
Int J Mol Sci. 2019; 20(9) [PubMed] Free Access to Full Article Related Publications
Clinical Implications of Discordant Early Molecular Responses in CML Patients Treated with Imatinib.
Int J Mol Sci. 2019; 20(9) [PubMed] Free Access to Full Article Related Publications
Downregulation of the histone methyltransferase SETD2 promotes imatinib resistance in chronic myeloid leukaemia cells.
Cell Prolif. 2019; 52(4):e12611 [PubMed] Related Publications
MATERIALS AND METHODS: The level of SETD2 in imatinib-sensitive and imatinib-resistant chronic myeloid leukaemia (CML) cells was examined by immunoblotting and quantitative real-time PCR. We analysed CD34
RESULTS: SETD2 was found to act as a tumour suppressor in CML. The novel oncogenic targets MYCN and ERG were shown to be the direct downstream targets of SETD2, where their overexpression induced by SETD2 knockdown caused imatinib insensitivity and leukaemic stem cell enrichment in CML cell lines. Treatment with JIB-04, an inhibitor that restores H3K36me3 levels through blockade of its demethylation, successfully improved the cell imatinib sensitivity and enhanced the chemotherapeutic effect.
CONCLUSIONS: Our study not only emphasizes the regulatory mechanism of SETD2 in CML, but also provides promising therapeutic strategies for overcoming the imatinib resistance in patients with CML.
One-step discrimination of BCR/ABL
Anal Chim Acta. 2019; 1067:129-136 [PubMed] Related Publications
Incidence and evaluation of predisposition to cardiovascular toxicity in chronic myeloid leukemia patients treated with bosutinib in the real-life practice.
Ann Hematol. 2019; 98(8):1885-1890 [PubMed] Related Publications
Effect of low-level BCR-ABL1 kinase domain mutations identified by next-generation sequencing in patients with chronic myeloid leukaemia: a population-based study.
Lancet Haematol. 2019; 6(5):e276-e284 [PubMed] Related Publications
METHODS: In this population-based study, we included consecutive patients newly diagnosed with chronic myeloid leukaemia treated with first-line tyrosine kinase inhibitors, and patients identified at the time of resistance to first-line treatment with imatinib at six institutions (teaching hospitals and district hospitals) in southeast England. We screened patients for BCR-ABL1 kinase domain mutations using NGS, irrespective of patient response to tyrosine kinase inhibitor therapy. When we detected a mutation with NGS, we retrospectively analysed all previous samples to establish the date of first occurrence and subsequent kinetics of the mutant subclone (or subclones). The primary endpoints of this study were progression-free and event-free survival at 5 years.
FINDINGS: Between Feb 1, 2007, and Dec 31, 2014, we screened 121 patients with chronic myeloid leukaemia for BCR-ABL1 kinase domain mutation. 99 consecutive patients were newly diagnosed, with available sequential RNA stored. The remaining 22 patients were diagnosed between June 1, 1999, and June 30, 2006, and were screened at the time of resistance to first-line treatment with imatinib. Imatinib was the first-line treatment for 111 patients, nilotinib for seven patients, and dasatinib for three patients. We detected a kinase domain mutation in 25 (21%) of 121 patients. Low-level kinase domain mutations were first identified in 17 (68%) of 25 patients with mutation. For patients with a complete cytogenetic response, 13 (14%) of 93 patients screened had a mutation. Five (71%) of the seven patients with a clinically relevant mutation lost complete cytogenetic response compared with 15 (17%) of 86 patients without a clinically relevant mutation (80 patients without mutation and six patients with a tyrosine kinase inhibitor-sensitive mutation, p=0·0031). Patients harbouring a mutant clone had poorer 5-year progression-free survival (65·3% [95% CI 40·5-81·8] vs 86·9% [75·8-93·2]; p=0·0161) and poorer 5-year event-free survival (22·2% [CI 5·6-45·9] vs 62·0% [50·4-71·6]; p<0·0001) than did patients without a mutation. We identified a kinase domain mutation in four (10%) of 41 patients with samples available at 3 months after starting first-line tyrosine kinase inhibitor treatment; all four subsequently progressed to accelerated phase disease compared with only three (8%) of 37 without a mutation (p<0·0001).
INTERPRETATION: NGS reliably and consistently detected early appearance of kinase domain mutations that would not otherwise be detected by Sanger sequencing. For the first time, to our knowledge, we report the presence of kinase domain mutations after only 3 months of therapy, which could have substantial clinical implications. NGS will allow early clinical intervention and our findings will contribute to the establishment of new recommendations on the frequency of kinase domain mutation analysis to improve patient clinical care.
FUNDING: None.
Chronic myeloid leukemia manifested as myeloid sarcoma: Review of literature and case report.
J Clin Neurosci. 2019; 64:269-276 [PubMed] Related Publications
Efficacy and Safety of Imatinib in Paediatric CML - A Single Centre Study.
In Vivo. 2019 May-Jun; 33(3):869-875 [PubMed] Free Access to Full Article Related Publications
PATIENTS AND METHODS: Our cohort comprised 14 CML patients who were treated with imatinib between July 2010 and September 2018. The European Leukaemia Net (ELN) standard milestones of response criteria were used to evaluate its therapeutic effectiveness.
RESULTS: Complete haematological remission and partial cytogenetic response were achieved in all patients. Complete cytogenetic response was achieved in seven patients. Major molecular response was achieved in six patients. Two patients underwent haematopoietic stem cell transplantation due to unsatisfactory response to imatinib.
CONCLUSION: Imatinib is effective in treating paediatric CML and limits the progression to advanced stages, however, the quality of life still needs to be optimised.
Monitoring and Analysis of Chinese Chronic Myeloid Leukemia Patients Who Have Stopped Tyrosine Kinase Inhibitor Therapy.
Curr Med Sci. 2019; 39(2):211-216 [PubMed] Related Publications
Imatinib independent aberrant methylation of NOV/CCN3 in chronic myelogenous leukemia patients: a mechanism upstream of BCR-ABL1 function?
Cell Commun Signal. 2019; 17(1):38 [PubMed] Free Access to Full Article Related Publications
METHODS: To address this issue, we applied bisulfite-sequencing technique as a high-resolution method to study the regulatory segment of the CCN3 gene. The results were analyzed in newly diagnosed CML patients as well as following imatinib therapy. We also evaluated the correlation of CCN3 promoter methylation with BCR-ABL1 levels.
RESULTS: Our findings revealed that the methylation occurs frequently in the promoter region of CML patients showing a significant increase of the methylated percentage at the CpG sites compared to normal individuals. Interestingly, this hypermethylation was indicated to be independent of BCR-ABL1 titers in both groups, which might suggest a mechanism beyond the BCR-ABL1 function.
CONCLUSION: Despite suggesting that the CCN3 hypermethylation acts as a molecular mechanism independent of BCR-ABL1 function in CML patients, this scenario requires further validation by complementary experiments. In the case of acting upstream of BCR-ABL1 signaling, the methylation marker can provide early detection and a novel platform for targeted epigenetic modifiers for efficient treatment in imatinib resistant patients.
Patient-reported outcomes in the phase 3 BFORE trial of bosutinib versus imatinib for newly diagnosed chronic phase chronic myeloid leukemia.
J Cancer Res Clin Oncol. 2019; 145(6):1589-1599 [PubMed] Related Publications
METHODS: Patients with newly diagnosed CP CML were randomized 1:1 to receive once-daily bosutinib 400 mg or imatinib 400 mg as first-line therapy. Patients completed the Functional Assessment of Cancer Therapy-Leukemia (FACT-Leu) and EuroQoL-5 Dimensions (EQ-5D) questionnaires at baseline, every 3 months for the first 24 months of treatment, every 6 months thereafter, and at treatment completion. We report PRO results at month 12 in the mITT population (bosutinib: n = 246; imatinib: n = 241).
RESULTS: Mean FACT-Leu combined and subscale scores were similar at baseline in the bosutinib and imatinib arms; at month 12, all scores demonstrated improvement or maintenance of health-related quality of life (HRQoL) in both treatment arms. Repeated-measures mixed-effects models showed no significant difference between bosutinib and imatinib for any FACT-Leu score. Functional health status, as measured by EQ-5D, also demonstrated improvement or maintenance with bosutinib and imatinib at month 12.
CONCLUSIONS: Similar improvements in PROs compared with baseline were seen after 12 months of treatment with first-line bosutinib or imatinib in the BFORE trial. Newly diagnosed patients with CP CML receiving bosutinib or imatinib can preserve or improve HRQoL during treatment, although clinical efficacy was superior with bosutinib.
Predictive value of early molecular response for deep molecular response in chronic phase of chronic myeloid leukemia.
Medicine (Baltimore). 2019; 98(15):e15222 [PubMed] Free Access to Full Article Related Publications
Distribution of common BCR-ABL fusion transcripts and their impact on treatment response in Imatinib treated CML patients: A study from India.
Indian J Pathol Microbiol. 2019 Apr-Jun; 62(2):256-260 [PubMed] Related Publications
Aims/settings and design: We conducted this study on 400 CML-CP patients to look for the distribution of fusion transcripts i.e. b3a2 and b2a2, their clinico-hematological profile and impact on treatment response in patients treated with Imatinib.
Material and Methods: CML-CP was diagnosed by reverse transcriptase PCR (RT-PCR) for the BCR-ABL fusion transcript. Real-time quantitative PCR (RQ-PCR) was performed on peripheral blood every 3-6 monthly to look for treatment response.
Results: The overall frequency of b3a2 transcript was observed in 288 (72%) followed by b2a2 in 104 (26%) and hybrid fusion transcript (b3a2 + b2a2) was seen in 8 (2%) cases. MMR was attained in 198/288 (68.7%) patients with b3a2 transcript and 90/288 (31.3%) patients failed to achieve MMR after 12 months of Imatinib therapy. Among the patients with b2a2 transcript, 44/104 (42.3%) patients achieved MMR and 60/104 (57.7%) patients failed to achieve MMR after 12 months of Imatinib therapy.
Conclusions: In conclusion, the frequency of b3a2 transcript was more as compared to b2a2 transcript. MMR was significantly higher in patients with b3a2 transcript as compared to patients with b2a2.
Novel lncRNA-IUR suppresses Bcr-Abl-induced tumorigenesis through regulation of STAT5-CD71 pathway.
Mol Cancer. 2019; 18(1):84 [PubMed] Free Access to Full Article Related Publications
METHODS: LncRNA cDNA microarray was used to identify novel lncRNAs involved in Bcr-Abl-mediated cellular transformation. To study the functional relevance of novel imatinib-upregulated lncRNA (IUR) family in Abl-induced tumorigenesis, Abl-transformed cell survival and xenografted tumor growth in mice was evaluated. Primary bone marrow transformation and in vivo leukemia transplant using lncRNA-IUR knockdown (KD) transgenic mice were further conducted to corroborate the role of lncRNA-IUR in Abl-induced tumorigenesis. Transcriptome RNA-seq, Western blot, RNA pull down and RNA Immunoprecipitation (RIP) were employed to determine the mechanisms by which lncRNA-IUR-5 regulates Bcr-Abl-mediated tumorigenesis.
RESULTS: We identified a conserved lncRNA-IUR family as a key negative regulator of Bcr-Abl-induced tumorigenesis. Increased expression of lncRNA-IUR was detected in both human and mouse Abl-transformed cells upon imatinib treatment. In contrast, reduced expression of lncRNA-IUR was observed in the peripheral blood lymphocytes derived from Bcr-Abl-positive acute lymphoblastic leukemia (ALL) patients compared to normal subjects. Knockdown of lncRNA-IUR remarkably promoted Abl-transformed leukemic cell survival and xenografted tumor growth in mice, whereas overexpression of lncRNA-IUR had opposite effects. Also, silencing murine lncRNA-IUR promoted Bcr-Abl-mediated primary bone marrow transformation and Abl-transformed leukemia cell survival in vivo. Besides, knockdown of murine lncRNA-IUR in transgenic mice provided a favorable microenvironment for development of Abl-mediated leukemia. Finally, we demonstrated that lncRNA-IUR-5 suppressed Bcr-Abl-mediated tumorigenesis by negatively regulating STAT5-mediated expression of CD71.
CONCLUSIONS: The results suggest that lncRNA-IUR may act as a critical tumor suppressor in Bcr-Abl-mediated tumorigenesis by suppressing the STAT5-CD71 pathway. This study provides new insights into functional involvement of lncRNAs in leukemogenesis.
Results of the European survey on the assessment of deep molecular response in chronic phase CML patients during tyrosine kinase inhibitor therapy (EUREKA registry).
J Cancer Res Clin Oncol. 2019; 145(6):1645-1650 [PubMed] Related Publications
METHODS: Data were collected on the standardized assessment of molecular response in the context of real-life practice. BCR-ABL1 transcript levels after > 2 years of TKI therapy were evaluated for DMR by local laboratories as well as standardized EUTOS laboratories. Since standardized molecular monitoring is a prerequisite for treatment discontinuation, central surveillance of the performance of the participating laboratories was carried out.
RESULTS: Between 2014 and 2017, 3377 peripheral blood samples from 1117 CML patients were shipped to 11 standardized reference laboratories in six European countries. BCR-ABL1 transcript types were b3a2 (41.63%), b2a2 (29.99%), b2a2/b3a2 (3.58%) and atypical (0.54%). For 23.72% of the patients, the initial transcript type had not been reported. Response levels (EUTOS laboratory) were: no MMR, n = 197 (6.51%); MMR, n = 496 (16.40%); MR
CONCLUSIONS: Multicenter DMR assessment is feasible in the context of real-life clinical practice in Europe. Information on the BCR-ABL1 transcript type at diagnosis is crucial to accurately monitor patients' molecular response during or after TKI therapy.
Costunolide enhances sensitivity of K562/ADR chronic myeloid leukemia cells to doxorubicin through PI3K/Akt pathway.
Phytother Res. 2019; 33(6):1683-1688 [PubMed] Related Publications
OGG1 rs1052133 Polymorphism and Genetic Susceptibility to Chronic Myelogenous Leukaemia
Asian Pac J Cancer Prev. 2019; 20(3):925-928 [PubMed] Related Publications
Role of natural killer cells for immunotherapy in chronic myeloid leukemia (Review).
Oncol Rep. 2019; 41(5):2625-2635 [PubMed] Related Publications
Sodium butyrate and panobinostat induce apoptosis of chronic myeloid leukemia cells via multiple pathways.
Mol Genet Genomic Med. 2019; 7(5):e613 [PubMed] Free Access to Full Article Related Publications
METHODS: Cell viability was assessed using MTT assay. Cell apoptosis was detected with flow cytometry. Cell cycle analysis and western blot were performed to explore the possible molecules related to HDACIs effects.
RESULTS: The effect of NaBu was more powerful on K562/ADR than on K562 cells. LBH589 triggered apoptosis and inhibited the growth of K562 cells. Both HDACIs inhibited K562 and K562/ADR cells via activation of intrinsic/extrinsic apoptotic pathways and inhibition of AKT-mTOR pathway while NaBu also activated endoplasmic reticulum stress (ERS) mediated apoptotic pathway in K562/ADR cells. LBH589 reduced the expression of drug-resistant related proteins in K562 cells. However, neither NaBu nor LBH589 could significantly influence the expression of the drug-resistant related proteins in K562/ADR cells.
CONCLUSION: The combination of HDACI and other therapeutic strategies are likely required to overcome drug resistance in CML therapy.
Usnea Acid as Multidrug Resistance (MDR) Reversing Agent against Human Chronic Myelogenous Leukemia K562/ADR Cells via an ROS Dependent Apoptosis.
Biomed Res Int. 2019; 2019:8727935 [PubMed] Free Access to Full Article Related Publications
Methods: CCK8 assay was used to measure cell viability rate of K562/ADR. Intracellular reactive oxygen species (ROS) generation, cell cycle distribution, cell apoptosis were measured with flow cytometry, respectively. Proteins related to apoptosis were measured by Western blot. Intracellular Adriamycin accumulation was observed by confocal microscopy and measured by flow cytometry.
Results: In vitro study showed intracellular Adriamycin accumulation was remarkably increased by UA. Cell viability treated with Adr (4
Conclusion: These data provide compelling evidence that UA is a promising agent against MDR in leukemia cell line and suggest a promising therapeutic approach for leukemia.