Dual transcription of b2a2 and b3a2 BCR-ABL transcripts in chronic myeloid leukaemia is confined to patients with a linked polymorphism within the BCR gene.

Pediatric chronic myeloid leukemia is a unique disease that requires a different approach. Blood (2015) 0.84

Frequencies of BCR-ABL1 fusion transcripts among Sudanese chronic myeloid leukaemia patients. Genet Mol Biol (2010) 0.82

Dual transcripts of BCR-ABL & different polymorphisms in chronic myeloid leukaemia patients. Indian J Med Res (2016) 0.75

Nilotinib versus imatinib for newly diagnosed chronic myeloid leukemia. N Engl J Med (2010) 10.64

BCR-ABL1 lymphoblastic leukaemia is characterized by the deletion of Ikaros. Nature (2008) 10.12

European LeukemiaNet recommendations for the management of chronic myeloid leukemia: 2013. Blood (2013) 8.00

Frequency of major molecular responses to imatinib or interferon alfa plus cytarabine in newly diagnosed chronic myeloid leukemia. N Engl J Med (2003) 6.68

Dynamics of chronic myeloid leukaemia. Nature (2005) 6.63

Lin28 promotes transformation and is associated with advanced human malignancies. Nat Genet (2009) 6.35

Targetable kinase-activating lesions in Ph-like acute lymphoblastic leukemia. N Engl J Med (2014) 5.37

Dasatinib induces notable hematologic and cytogenetic responses in chronic-phase chronic myeloid leukemia after failure of imatinib therapy. Blood (2006) 4.40

Nilotinib versus imatinib for the treatment of patients with newly diagnosed chronic phase, Philadelphia chromosome-positive, chronic myeloid leukaemia: 24-month minimum follow-up of the phase 3 randomised ENESTnd trial. Lancet Oncol (2011) 4.10

Sequential ABL kinase inhibitor therapy selects for compound drug-resistant BCR-ABL mutations with altered oncogenic potency. J Clin Invest (2007) 4.07

High frequency of point mutations clustered within the adenosine triphosphate-binding region of BCR/ABL in patients with chronic myeloid leukemia or Ph-positive acute lymphoblastic leukemia who develop imatinib (STI571) resistance. Blood (2002) 3.93

Detection of BCR-ABL mutations in patients with CML treated with imatinib is virtually always accompanied by clinical resistance, and mutations in the ATP phosphate-binding loop (P-loop) are associated with a poor prognosis. Blood (2003) 3.61

Safety and efficacy of imatinib cessation for CML patients with stable undetectable minimal residual disease: results from the TWISTER study. Blood (2013) 3.23

Nilotinib is effective in patients with chronic myeloid leukemia in chronic phase after imatinib resistance or intolerance: 24-month follow-up results. Blood (2010) 3.15

Dasatinib treatment of chronic-phase chronic myeloid leukemia: analysis of responses according to preexisting BCR-ABL mutations. Blood (2009) 2.87

Desirable performance characteristics for BCR-ABL measurement on an international reporting scale to allow consistent interpretation of individual patient response and comparison of response rates between clinical trials. Blood (2008) 2.80

Juxtamembrane mutant V560GKit is more sensitive to Imatinib (STI571) compared with wild-type c-kit whereas the kinase domain mutant D816VKit is resistant. Mol Cancer Ther (2002) 2.68

Phase III, randomized, open-label study of daily imatinib mesylate 400 mg versus 800 mg in patients with newly diagnosed, previously untreated chronic myeloid leukemia in chronic phase using molecular end points: tyrosine kinase inhibitor optimization and selectivity study. J Clin Oncol (2009) 2.64

OCT-1-mediated influx is a key determinant of the intracellular uptake of imatinib but not nilotinib (AMN107): reduced OCT-1 activity is the cause of low in vitro sensitivity to imatinib. Blood (2006) 2.29

The PARP inhibitor olaparib induces significant killing of ATM-deficient lymphoid tumor cells in vitro and in vivo. Blood (2010) 2.09

Nilotinib is associated with a reduced incidence of BCR-ABL mutations vs imatinib in patients with newly diagnosed chronic myeloid leukemia in chronic phase. Blood (2013) 2.03

Macrophage colony-stimulating factor receptor c-fms is a novel target of imatinib. Blood (2005) 1.80

A de novo splice donor mutation in the thrombopoietin gene causes hereditary thrombocythemia in a Polish family. Haematologica (2008) 1.63

Dasatinib cellular uptake and efflux in chronic myeloid leukemia cells: therapeutic implications. Clin Cancer Res (2008) 1.62

Real-time quantitative PCR analysis can be used as a primary screen to identify patients with CML treated with imatinib who have BCR-ABL kinase domain mutations. Blood (2004) 1.57

BCR-ABL transcript dynamics support the hypothesis that leukemic stem cells are reduced during imatinib treatment. Clin Cancer Res (2011) 1.56

International standardisation of quantitative real-time RT-PCR for BCR-ABL. Leuk Res (2007) 1.54

BCR-ABL messenger RNA levels continue to decline in patients with chronic phase chronic myeloid leukemia treated with imatinib for more than 5 years and approximately half of all first-line treated patients have stable undetectable BCR-ABL using strict sensitivity criteria. Clin Cancer Res (2007) 1.50

Population pharmacokinetic and exposure-response analysis of nilotinib in patients with newly diagnosed Ph+ chronic myeloid leukemia in chronic phase. Eur J Clin Pharmacol (2011) 1.48

Selecting optimal second-line tyrosine kinase inhibitor therapy for chronic myeloid leukemia patients after imatinib failure: does the BCR-ABL mutation status really matter? Blood (2009) 1.42

How I determine if and when to recommend stopping tyrosine kinase inhibitor treatment for chronic myeloid leukaemia. Br J Haematol (2014) 1.41

Functional activity of the OCT-1 protein is predictive of long-term outcome in patients with chronic-phase chronic myeloid leukemia treated with imatinib. J Clin Oncol (2010) 1.40

Mannose-binding lectin gene polymorphisms are associated with major infection following allogeneic hemopoietic stem cell transplantation. Blood (2002) 1.39

Sensitive detection of BCR-ABL1 mutations in patients with chronic myeloid leukemia after imatinib resistance is predictive of outcome during subsequent therapy. J Clin Oncol (2011) 1.38

Dasatinib in the treatment of chronic myeloid leukemia in accelerated phase after imatinib failure: the START a trial. J Clin Oncol (2009) 1.35

Initial molecular response at 3 months may predict both response and event-free survival at 24 months in imatinib-resistant or -intolerant patients with Philadelphia chromosome-positive chronic myeloid leukemia in chronic phase treated with nilotinib. J Clin Oncol (2012) 1.30

Long-term imatinib therapy promotes bone formation in CML patients. Blood (2007) 1.30

Dysregulation of bone remodeling by imatinib mesylate. Blood (2009) 1.26

The Src/ABL kinase inhibitor dasatinib (BMS-354825) inhibits function of normal human T-lymphocytes in vitro. Clin Immunol (2008) 1.17

Rac2-MRC-cIII-generated ROS cause genomic instability in chronic myeloid leukemia stem cells and primitive progenitors. Blood (2012) 1.16

Early molecular response and female sex strongly predict stable undetectable BCR-ABL1, the criteria for imatinib discontinuation in patients with CML. Blood (2013) 1.15

Poor response to second-line kinase inhibitors in chronic myeloid leukemia patients with multiple low-level mutations, irrespective of their resistance profile. Blood (2011) 1.13

Dasatinib suppresses in vitro natural killer cell cytotoxicity. Blood (2008) 1.13

Chronic myeloid leukemia. Hematology Am Soc Hematol Educ Program (2003) 1.10

Monoclonal antibody targeting of IL-3 receptor α with CSL362 effectively depletes CML progenitor and stem cells. Blood (2013) 1.02

Association between imatinib transporters and metabolizing enzymes genotype and response in newly diagnosed chronic myeloid leukemia patients receiving imatinib therapy. Haematologica (2012) 1.00

Dynamics of chronic myeloid leukemia response to long-term targeted therapy reveal treatment effects on leukemic stem cells. Blood (2011) 0.98

Chronic phase chronic myeloid leukemia patients with low OCT-1 activity randomized to high-dose imatinib achieve better responses and have lower failure rates than those randomized to standard-dose imatinib. Haematologica (2011) 0.97

Dasatinib inhibits recombinant viral antigen-specific murine CD4+ and CD8+ T-cell responses and NK-cell cytolytic activity in vitro and in vivo. Exp Hematol (2008) 0.96

Dasatinib inhibits the secretion of TNF-alpha following TLR stimulation in vitro and in vivo. Exp Hematol (2009) 0.94

SHP-1 expression accounts for resistance to imatinib treatment in Philadelphia chromosome-positive cells derived from patients with chronic myeloid leukemia. Blood (2011) 0.94

Tyrosine kinase inhibitor resistance in chronic myeloid leukemia cell lines: investigating resistance pathways. Leuk Lymphoma (2011) 0.93

Inhibition of c-fms by imatinib: expanding the spectrum of treatment. Cell Cycle (2005) 0.93

Imatinib as a potential antiresorptive therapy for bone disease. Blood (2006) 0.91

Suboptimal responses in chronic myeloid leukemia: implications and management strategies. Cancer (2011) 0.90

Plasma exposure of imatinib and its correlation with clinical response in the Tyrosine Kinase Inhibitor Optimization and Selectivity Trial. Haematologica (2012) 0.89

Genetic susceptibility to viral exposure may increase the risk of cerebral palsy. Aust N Z J Obstet Gynaecol (2009) 0.89

Imatinib inhibits the functional capacity of cultured human monocytes. Immunol Cell Biol (2005) 0.88

Validation of the multiplex ligation-dependent probe amplification (MLPA) technique for the determination of HER2 gene amplification in breast cancer. Diagn Mol Pathol (2011) 0.87

Generalized crystal-storing histiocytosis as a presentation of multiple myeloma: a case with a possible pro-aggregation defect in the immunoglobulin heavy chain. Virchows Arch (2004) 0.87

Clarithromycin enhances dasatinib-induced cell death in chronic myeloid leukemia cells, by inhibition of late stage autophagy. Leuk Lymphoma (2012) 0.86

Dasatinib treatment for Philadelphia chromosome-positive leukemias: practical considerations. Cancer (2009) 0.85

ABL-kinase domain point mutation as a cause of imatinib (STI571) resistance in CML patient who progress to myeloid blast crisis. Leuk Res (2003) 0.85

Potential mechanisms of disease progression and management of advanced-phase chronic myeloid leukemia. Leuk Lymphoma (2013) 0.85

Classification of patients with chronic myeloid leukemia on basis of BCR-ABL transcript level at 3 months fails to identify patients with low organic cation transporter-1 activity destined to have poor imatinib response. J Clin Oncol (2012) 0.85

Mutational analysis in chronic myeloid leukemia: when and what to do? Curr Opin Hematol (2011) 0.85

Familial occurrence of warts, hypogammaglobulinemia, infections, and myelokathexis (WHIM) syndrome. Arch Immunol Ther Exp (Warsz) (2008) 0.85

Therapeutic targeting of BCR-ABL: prognostic markers of response and resistance mechanism in chronic myeloid leukaemia. Crit Rev Oncog (2012) 0.84

The prevalence of inherited thrombophilias in a Caucasian Australian population. Pathology (2005) 0.84

Familial vasopressin-sensitive ACTH-independent macronodular adrenal hyperplasia (VPs-AIMAH): clinical studies of three kindreds. Clin Endocrinol (Oxf) (2008) 0.84

Imatinib increases the intracellular concentration of nilotinib, which may explain the observed synergy between these drugs. Blood (2007) 0.84

BCR-ABL1 doubling times more reliably assess the dynamics of CML relapse compared with the BCR-ABL1 fold rise: implications for monitoring and management. Blood (2012) 0.84

Nilotinib inhibits the Src-family kinase LCK and T-cell function in vitro. J Cell Mol Med (2009) 0.83

OCT-1 function varies with cell lineage but is not influenced by BCR-ABL. Haematologica (2010) 0.83

Degree of kinase inhibition achieved in vitro by imatinib and nilotinib is decreased by high levels of ABCB1 but not ABCG2. Leuk Lymphoma (2012) 0.83

Predicting the response of CML patients to tyrosine kinase inhibitor therapy. Curr Hematol Malig Rep (2011) 0.83

Plasma adiponectin levels are markedly elevated in imatinib-treated chronic myeloid leukemia (CML) patients: a mechanism for improved insulin sensitivity in type 2 diabetic CML patients? J Clin Endocrinol Metab (2010) 0.82

Pure red cell aplasia due to treatment with epoietin beta: first case report of PRCA from Poland. Przegl Lek (2006) 0.82

Prospective histomorphometric and DXA evaluation of bone remodeling in imatinib-treated CML patients: evidence for site-specific skeletal effects. J Clin Endocrinol Metab (2012) 0.82

Protein kinase activity of phosphoinositide 3-kinase regulates cytokine-dependent cell survival. PLoS Biol (2013) 0.82

Genomic translocation breakpoint sequences are conserved in BCR-ABL1 cell lines despite the presence of amplification. Cancer Genet Cytogenet (2009) 0.81

Strategies for the treatment of imatinib-resistant chronic myeloid leukemia. Clin Adv Hematol Oncol (2003) 0.81

Dasatinib alters the metastatic phenotype of B16-OVA melanoma in vivo. Cancer Biol Ther (2010) 0.81

Sarcoma and familial retinoblastoma. Clin Experiment Ophthalmol (2003) 0.81

Haemorrhagic colitis caused by dasatinib. Case Rep Hematol (2012) 0.80

Rapid initial decline in BCR-ABL1 is associated with superior responses to second-line nilotinib in patients with chronic-phase chronic myeloid leukemia. BMC Cancer (2013) 0.80

Dasatinib targets chronic myeloid leukemia-CD34+ progenitors as effectively as it targets mature cells. Haematologica (2012) 0.80

Long-term response to imatinib is not affected by the initial dose in patients with Philadelphia chromosome-positive chronic myeloid leukemia in chronic phase: final update from the Tyrosine Kinase Inhibitor Optimization and Selectivity (TOPS) study. Int J Hematol (2014) 0.80

Practical considerations for monitoring patients with chronic myeloid leukemia. Semin Hematol (2010) 0.79

The poor response to imatinib observed in CML patients with low OCT-1 activity is not attributable to lower uptake of imatinib into their CD34+ cells. Blood (2010) 0.79

Preimplantation genetic diagnosis for beta-thalassaemia using sequencing of single cell PCR products to detect mutations and polymorphic loci. Mol Hum Reprod (2002) 0.79

Reverse transcription with random pentadecamer primers improves the detection limit of a quantitative PCR assay for BCR-ABL transcripts in chronic myeloid leukemia: implications for defining sensitivity in minimal residual disease. Clin Chem (2008) 0.79

Autologous stem cell collection and autograft for patients with chronic myeloid leukemia in the era of ABL kinase inhibitors: back to the bench. Leuk Lymphoma (2006) 0.78

Drug-interaction studies evaluating T-cell proliferation reveal distinct activity of dasatinib and imatinib in combination with cyclosporine A. Exp Hematol (2012) 0.78

CDX-2 expression is reduced in colorectal carcinomas with solid growth pattern and proximal location, but is largely independent of MSI status. Pol J Pathol (2004) 0.77

Predicting the response of CML patients to tyrosine kinase inhibitor therapy. Curr Hematol Malig Rep (2009) 0.77

The JAK2 V617F mutation is frequently present in buccal swabs from patients suffering from Philadelphia-negative chronic myeloproliferative disorders, who carry the mutation detected in bone marrow or peripheral blood cells [corrected]. J Clin Pathol (2007) 0.75

Sudden blast crisis in chronic myeloid leukemia treated with tyrosine kinase inhibitors. Leuk Lymphoma (2012) 0.75

How complete is "complete" molecular response in imatinib-treated chronic myeloid leukemia? Leuk Lymphoma (2008) 0.75