D. White

发表

BCR–ABL1 lymphoblastic leukaemia is characterized by the deletion of Ikaros

Christopher B. Miller, J. Downing, S. Shurtleff, 2008, Nature.

Xenograft-directed personalized therapy for a patient with post-transplant relapse of ALL

E. Nievergall, T. Révész, S. Heatley, 2016, Bone Marrow Transplantation.

Exploring the oncogenic and therapeutic target potential of the MYB-TYK2 fusion gene in B-cell acute lymphoblastic leukemia

S. Heatley, D. White, Maxime Francois, 2022, Cancer Gene Therapy.

HMGN1 plays a significant role in CRLF2 driven Down Syndrome leukemia and provides a potential therapeutic target in this high-risk cohort

S. Heatley, C. D. de Bock, D. White, 2021, Oncogene.

Constitutive JAK/STAT signaling is the primary mechanism of resistance to JAKi in TYK2-rearranged acute lymphoblastic leukemia.

S. Heatley, J. Bruning, D. White, 2021, Cancer letters.

Precision medicine approaches may be the future for CRLF2 rearranged Down Syndrome Acute Lymphoblastic Leukaemia patients.

S. Heatley, D. White, Paul Q Thomas, 2018, Cancer letters.

Acute Sensitivity of Ph-like Acute Lymphoblastic Leukemia to the SMAC-Mimetic Birinapant.

P. Houghton, D. Beck, J. Pimanda, 2016, Cancer research.

Characterization of leukemias with ETV6-ABL1 fusion

M. Loh, J. Stuchly, C. Mullighan, 2015, Haematologica.

Direct analysis of FACS-sorted hemopoietic cell fractions using FISH.

C. J. Hutchins, L. To, D. White, 1995, BioTechniques.

Lineage of measurable residual disease in patients with chronic myeloid leukemia in treatment-free remission

D. White, T. Hughes, C. Kok, 2019, Leukemia.

MLLT10 rearranged acute leukemia: Incidence, prognosis, and possible therapeutic strategies

D. White, D. Yeung, L. Eadie, 2020, Genes, chromosomes & cancer.

Contrasting effects of diclofenac and ibuprofen on active imatinib uptake into leukaemic cells

R. D'Andrea, A. Somogyi, D. White, 2012, British Journal of Cancer.

Proton pump inhibitors significantly increase the intracellular concentration of nilotinib, but not imatinib in target CML cells

D. White, T. Hughes, L. Eadie, 2013, Leukemia.

CML patients with deep molecular responses to TKI have restored immune effectors and decreased PD-1 and immune suppressors.

D. White, T. Hughes, Amy Hughes, 2017, Blood.

Guidelines for whole genome bisulphite sequencing of intact and FFPET DNA on the Illumina HiSeq X Ten

J. Kench, J. Rasko, G. Chenevix-Trench, 2018, Epigenetics & Chromatin.

A Method for Next-Generation Sequencing of Paired Diagnostic and Remission Samples to Detect Mitochondrial DNA Mutations Associated with Leukemia.

S. Heatley, A. Schwarer, C. Hahn, 2017, The Journal of molecular diagnostics : JMD.

Interaction of the Efflux Transporters ABCB1 and ABCG2 With Imatinib, Nilotinib, and Dasatinib

T. P. Hughes, D. White, L. Eadie, 2014, Clinical pharmacology and therapeutics.

Monoclonal antibody targeting of IL-3 receptor α with CSL362 effectively depletes CML progenitor and stem cells.

E. Nievergall, Angel F. Lopez, H. Ramshaw, 2014, Blood.

depletes CML progenitor and stem cells with CSL362 effectively α Monoclonal antibody targeting of IL-3 receptor

E. Nievergall, Angel F. Lopez, H. Ramshaw, 2014 .

Lenalidomide maintenance treatment after imatinib discontinuation: results of a phase 1 clinical trial in chronic myeloid leukaemia

J. Reynolds, D. White, T. Hughes, 2019, British journal of haematology.

Functional activity of the OCT-1 protein is predictive of long-term outcome in patients with chronic-phase chronic myeloid leukemia treated with imatinib.

P. Manley, D. White, T. Hughes, 2010, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.

Measurement of in vivo BCR-ABL kinase inhibition to monitor imatinib-induced target blockade and predict response in chronic myeloid leukemia.

L. To, D. White, T. Hughes, 2007, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.

Simvastatin enhances the efficacy of nilotinib in chronic myeloid leukaemia by post-translational modification and drug transporter modulation

B. Ng, C. Chuah, D. White, 2021, Anti-cancer drugs.

BCR-ABL1 expression, RT-qPCR and treatment decisions in chronic myeloid leukaemia

A. Morley, E. Hughes, D. White, 2016, Journal of Clinical Pathology.

Tyrosine kinase inhibitor resistance in chronic myeloid leukemia cell lines: investigating resistance pathways

D. White, T. Hughes, S. Moore, 2011, Leukemia & lymphoma.

JAK2 Alterations in Acute Lymphoblastic Leukemia: Molecular Insights for Superior Precision Medicine Strategies

S. Heatley, J. Bruning, D. White, 2022, Frontiers in Cell and Developmental Biology.

Acquired JAK2 mutations confer resistance to JAK inhibitors in cell models of acute lymphoblastic leukemia

J. Bruning, D. White, D. Yeung, 2021, npj Precision Oncology.

In-vitro modeling of TKI resistance in the high-risk B-cell acute lymphoblastic leukemia fusion gene RANBP2-ABL1 - implications for targeted therapy

S. Heatley, D. White, T. Hughes, 2021, Leukemia & lymphoma.

Relapse of BCR-ABL1-like ALL mediated by the ABL1 kinase domain mutation T315I following initial response to dasatinib treatment

D. J. Moulton, E. Nievergall, C. Mullighan, 2014, Leukemia.

A common novel splice variant of SLC22A1 (OCT1) is associated with impaired responses to imatinib in patients with chronic myeloid leukaemia

R. Clark, D. Marin, J. Goldman, 2013, British journal of haematology.

KMT2A rearranged acute lymphoblastic leukaemia: unravelling the genomic complexity and heterogeneity of this high-risk disease.

D. White, D. Yeung, L. Eadie, 2019, Cancer letters.

Apoptosis regulatory gene NEDD2 maps to human chromosome segment 7q34–35, a region frequently affected in haematological neoplasms

S. Takai, Sharad Kumar, D. White, 1995, Human Genetics.

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?

K. Vandyke, S. Fitter, C. Schultz, 2010, The Journal of clinical endocrinology and metabolism.

A novel somatic JAK2 kinase-domain mutation in pediatric acute lymphoblastic leukemia with rapid on-treatment development of LOH.

S. Heatley, D. Ziegler, D. White, 2017, Cancer genetics.

Reduced CD62L Expression on T Cells and Increased Soluble CD62L Levels Predict Molecular Response to Tyrosine Kinase Inhibitor Therapy in Early Chronic-Phase Chronic Myelogenous Leukemia.

S. Mustjoki, Z. Trajanoski, F. Giles, 2017, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.

OCT-1 function varies with cell lineage but is not influenced by BCR-ABL

J. Rasko, A. Zannettino, C. Bailey, 2011, Haematologica.

Chronic Myeloid Leukemia CD34+ cells have reduced uptake of imatinib due to low OCT-1 Activity

A. Zannettino, A. Zannettino, D. White, 2010, Leukemia.

Dasatinib Cellular Uptake and Efflux in Chronic Myeloid Leukemia Cells: Therapeutic Implications

J. Melo, L. To, Sharad Kumar, 2008, Clinical Cancer Research.

Dasatinib targets chronic myeloid leukemia-CD34+ progenitors as effectively as it targets mature cells

E. Nievergall, D. Ross, D. White, 2013, Haematologica.

Predicting the response of CML patients to tyrosine kinase inhibitor therapy

D. White, T. Hughes, T. Hughes, 2009, Current hematologic malignancy reports.

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

J. Melo, A. Schwarer, J. Seymour, 2013, Blood.

Blocking cytokine signaling along with intense Bcr-Abl kinase inhibition induces apoptosis in primary CML progenitors

J. Melo, R. D'Andrea, Angel F. Lopez, 2010, Leukemia.

Short-term intense Bcr–Abl kinase inhibition with nilotinib is adequate to trigger cell death in BCR-ABL+ cells

J. Melo, D. White, T. Hughes, 2009, Leukemia.

Which TKI? An embarrassment of riches for chronic myeloid leukemia patients.

D. White, T. Hughes, T. Hughes, 2013, Hematology. American Society of Hematology. Education Program.

with for

Christopher, C. Tam, A. Schwarer, 2014 .

Optimizing the selection of kinase inhibitors for chronic myeloid leukemia patients

D. White, D. Yeung, D. Hiwase, 2011, Expert review of hematology.

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

J. Radich, J. Melo, G. Martinelli, 2011, Blood.

OCT-1 activity measurement provides a superior imatinib response predictor than screening for single-nucleotide polymorphisms of OCT-1

D. White, T. Hughes, P. Dang, 2010, Leukemia.

Long-term treatment-free remission of chronic myeloid leukemia with falling levels of residual leukemic cells

A. Schwarer, J. Seymour, D. White, 2018, Leukemia.

Running head: Imatinib Cessation After Stable UMRD in CML

J. Melo, A. Schwarer, J. Seymour, 2017 .

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.

A. Zannettino, D. White, T. Hughes, 2010, Blood.

Patients with low OCT-1 activity and high ABCB1 fold rise have poor long-term outcomes in response to tyrosine kinase inhibitor therapy

D. White, T. Hughes, L. Eadie, 2018, Leukemia.

In-vitro sensitivity to imatinib-induced inhibition of ABL kinase activity is predictive of molecular response in de-novo CML patients.

A. B. Lyons, L. To, D. White, 2005 .

B‐cell acute lymphoblastic leukaemia: recent discoveries in molecular pathology, their prognostic significance, and a review of the current classification

D. White, D. Yeung, M. Osborn, 2021, British journal of haematology.

Sustained inhibition of STAT5, but not JAK2, is essential for TKI-induced cell death in chronic myeloid leukemia

E. Nievergall, D. White, T. Hughes, 2014, Leukemia.

Is telomerase a player in chronic phase chronic myeloid leukemia, disease progression and imatinib resistance?

D. White, 2008, Leukemia & lymphoma.

The Expression of shp-1 and SHP-2: A Novel Powerful Predictor of Major Molecular Response (MMR) Achievement in Chronic Myeloid Leukemia Gleevec-Treated Patients Enrolled into the TOPS Clinical Trial.

J. Radich, M. Thornquist, G. Martinelli, 2008 .

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

J. Radich, G. Martinelli, P. Manley, 2012, Haematologica.

Nilotinib does not significantly reduce imatinib OCT-1 activity in either cell lines or primary CML cells

D. White, T. Hughes, L. Eadie, 2010, Leukemia.

Nilotinib-mediated inhibition of ABCB1 increases intracellular concentration of dasatinib in CML cells: implications for combination TKI therapy

J. Melo, D. White, T. Hughes, 2010, Leukemia.

Identification of a novel GOLGA4–JAK2 fusion gene in B‐cell acute lymphoblastic leukaemia

S. Heatley, D. White, D. Yeung, 2021, British Journal of Haematology.

Pre-B acute lymphoblastic leukaemia recurrent fusion, EP300-ZNF384, is associated with a distinct gene expression

S. Heatley, R. Lock, Jiyuan An, 2018, British Journal of Cancer.

Selected CD34 blood cell allografts for older patients: low transplant-related mortality, graft failure and acute GvHD.

L. To, D. White, C. Hui, 2003, Cytotherapy.

Low GFI1 expression in white blood cells of CP–CML patients at diagnosis is strongly associated with subsequent blastic transformation

R. D'Andrea, D. White, T. Hughes, 2013, Leukemia.

NPM1 mutations occur rarely or not at all in chronic myeloid leukaemia patients in chronic phase or blast crisis

R. D'Andrea, D. White, T. Hughes, 2013, Leukemia.

Unraveling the "known unknowns": lessons and reflections from the new directions in leukemia research 2012 conference.

Anna L. Brown, R. D'Andrea, D. White, 2012, Cancer research.

Modelling ponatinib resistance in tyrosine kinase inhibitor-naïve and dasatinib resistant BCR-ABL1+ cell lines

D. White, T. Hughes, C. Kok, 2018, Oncotarget.

Targetable kinase-activating lesions in Ph-like acute lymphoblastic leukemia.

Heather L. Mulder, Erin K. Hedlund, Michael C. Rusch, 2014, The New England journal of medicine.

Measurable residual disease analysis in paediatric acute lymphoblastic leukaemia patients with ABL-class fusions

M. Cowley, S. Heatley, J. Zuna, 2022, British Journal of Cancer.

Two novel cases of NUTM1‐rearranged B‐cell acute lymphoblastic leukaemia presenting with high‐risk features

S. Heatley, D. White, S. Khaw, 2021, British journal of haematology.

Integrative genomic analysis reveals cancer-associated mutations at diagnosis of CML in patients with high-risk disease.

Anna L. Brown, Paul P. S. Wang, D. Thomson, 2018, Blood.

The Role of Wnt/β -Catenin Signaling in Normal and Malignant Hematopoiesis, Hemostasis

D. White, T. Sadras, R. D’Andrea, 2017 .

Association between imatinib transporters and metabolizing enzymes genotype and response in newly diagnosed chronic myeloid leukemia patients receiving imatinib therapy

J. Radich, M. Baccarani, M. Thornquist, 2013, Haematologica.

Successful peripheral blood stem cell mobilisation with filgrastim in patients with chronic myeloid leukaemia achieving complete cytogenetic response with imatinib, without increasing disease burden as measured by quantitative real-time PCR

L. To, A. Trickett, D. Ma, 2003, Leukemia.

The effect of co-occurring lesions on leukaemogenesis and drug response in T-ALL and ETP-ALL

S. Heatley, D. White, T. Hughes, 2019, British Journal of Cancer.

Guidelines for whole genome bisulphite sequencing of intact and FFPET DNA on the Illumina HiSeq X Ten

J. Kench, J. Rasko, G. Chenevix-Trench, 2018, Epigenetics & Chromatin.

ABCB1 Overexpression Is a Key Initiator of Resistance to Tyrosine Kinase Inhibitors in CML Cell Lines

D. White, T. Hughes, L. Eadie, 2016, PloS one.

COBL is a novel hotspot for IKZF1 deletions in childhood acute lymphoblastic leukemia

R. Marschalek, S. Heatley, C. Meyer, 2016, Oncotarget.

In vitro sensitivity to imatinib-induced inhibition of ABL kinase activity is predictive of molecular response in patients with de novo CML.

A. B. Lyons, L. To, D. White, 2005, Blood.

DUX Hunting—Clinical Features and Diagnostic Challenges Associated with DUX4-Rearranged Leukaemia

M. O’Connor, D. White, D. Yeung, 2020, Cancers.

High prevalence of relapse in children with Philadelphia-like acute lymphoblastic leukemia despite risk-adapted treatment

E. Nievergall, C. Mullighan, T. Révész, 2017, Haematologica.

Relapses and treatment-related events contributed equally to poor prognosis in children with ABL-class fusion positive B-cell acute lymphoblastic leukemia treated according to AIEOP-BFM protocols

D. Steinemann, T. Révész, O. Haas, 2019, Haematologica.

Most CML patients who have a suboptimal response to imatinib have low OCT-1 activity: higher doses of imatinib may overcome the negative impact of low OCT-1 activity.

P. Manley, A. Zannettino, D. White, 2007, Blood.

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.

P. Manley, A. Zannettino, D. White, 2006, Blood.

Demethylating therapy increases anti-CD123 CAR T cell cytotoxicity against acute myeloid leukemia

M. Brown, Angel F. Lopez, C. Miething, 2021, Nature Communications.

TGF-α and IL-6 plasma levels selectively identify CML patients who fail to achieve an early molecular response or progress in the first year of therapy

E. Nievergall, J. Reynolds, W. Erber, 2016, Leukemia.

ABCC6 plays a significant role in the transport of nilotinib and dasatinib, and contributes to TKI resistance in vitro, in both cell lines and primary patient mononuclear cells

D. White, T. Hughes, P. Dang, 2018, PloS one.

Quantitative phosphotyrosine profiling of patient-derived xenografts identifies therapeutic targets in pediatric leukemia.

D. Teachey, T. Révész, P. Houghton, 2016, Cancer research.

QuantitativePhosphotyrosinePro fi lingof Patient-DerivedXenografts Identi fi esTherapeuticTargets in Pediatric Leukemia

D. Teachey, T. Révész, P. Houghton, 2016 .

The new allosteric inhibitor asciminib is susceptible to resistance mediated by ABCB1 and ABCG2 overexpression in vitro

D. White, T. Hughes, S. Branford, 2018, Oncotarget.

Impact of early dose intensity on cytogenetic and molecular responses in chronic- phase CML patients receiving 600 mg/day of imatinib as initial therapy.

Deborah L White, Simon Durrant, Susan Branford, 2008, Blood.

Solute Carrier Family 29A1 Mediates In Vitro Resistance to Azacitidine in Acute Myeloid Leukemia Cell Lines

D. White, C. Kok, D. Hiwase, 2023, International journal of molecular sciences.

BCR-ABL1 genomic DNA PCR response kinetics during first-line imatinib treatment of chronic myeloid leukemia

D. White, T. Hughes, S. Branford, 2018, Haematologica.

TIDEL-II: first-line use of imatinib in CML with early switch to nilotinib for failure to achieve time-dependent molecular targets.

C. Tam, A. Schwarer, D. White, 2015, Blood.

KIR2DL5B genotype predicts outcomes in CML patients treated with response-directed sequential imatinib/nilotinib strategy.

Deborah L White, Susan Branford, D. White, 2015, Blood.

The immunotoxicity, but not anti-tumor efficacy, of anti-CD40 and anti-CD137 immunotherapies is dependent on the gut microbiota

D. Lynn, Anastasia Sribnaia, F. Ryan, 2021, Cell reports. Medicine.

THE EXPRESSION OF MATURE MYELOID CELL DIFFERENTIATION MARKERS IN ACUTE LEUKEMIA

L. Ashman, D. White, R. Kimber, 1987, Pathology.

Successful treatment‐free remission in chronic myeloid leukaemia and its association with reduced immune suppressors and increased natural killer cells

D. White, T. Hughes, C. Kok, 2020, British journal of haematology.

Widespread Aberrant Alternative Splicing despite Molecular Remission in Chronic Myeloid Leukaemia Patients

U. Schmitz, J. Rasko, S. Clark, 2020, medRxiv.

A DNA real-time quantitative PCR method suitable for routine monitoring of low levels of minimal residual disease in chronic myeloid leukemia.

A. Morley, E. Hughes, D. White, 2015, The Journal of molecular diagnostics : JMD.

Differential expression of MUC4, GPR110 and IL2RA defines two groups of CRLF2-rearranged acute lymphoblastic leukemia patients with distinct secondary lesions.

T. Révész, S. Heatley, A. Moore, 2017, Cancer letters.

Detection of minimal residual disease in an AML patient with trisomy 8 using interphase FISH

C. J. Hutchins, L. To, D. White, 1997, Pathology.

The clinical significance of ABCB1 overexpression in predicting outcome of CML patients undergoing first-line imatinib treatment

D. White, T. Hughes, A. Grigg, 2017, Leukemia.

Increased peroxisome proliferator-activated receptor γ activity reduces imatinib uptake and efficacy in chronic myeloid leukemia mononuclear cells

D. White, T. Hughes, C. Kok, 2017, Haematologica.

Degree of kinase inhibition achieved in vitro by imatinib and nilotinib is decreased by high levels of ABCB1 but not ABCG2

D. White, T. Hughes, L. Eadie, 2013, Leukemia & lymphoma.

OCT1 and imatinib transport in CML: is it clinically relevant?

D. White, T. Hughes, D. Watkins, 2015, Leukemia.

Pre-B acute lymphoblastic leukaemia recurrent fusion, EP300-ZNF384, is associated with a distinct gene expression

S. Heatley, R. Lock, Jiyuan An, 2018, British Journal of Cancer.

Clarithromycin enhances dasatinib-induced cell death in chronic myeloid leukemia cells, by inhibition of late stage autophagy

D. White, T. Hughes, T. Leclercq, 2013, Leukemia & lymphoma.

Imatinib increases the intracellular concentration of nilotinib, which may explain the observed synergy between these drugs.

P. Manley, D. White, T. Hughes, 2007, Blood.

CML Patients with Low OCT-1 Activity Achieve Better Molecular Responses on High Dose Imatinib Than on Standard Dose. Those with High OCT-1 Activity Have Excellent Responses on Either Dose: A TOPS Correlative Study

J. Radich, M. Thornquist, G. Martinelli, 2008 .

Predicting the Response of CML Patients to Tyrosine Kinase Inhibitor Therapy

D. White, T. Hughes, T. Hughes, 2009, Current hematologic malignancy reports.

The Functional Activity of the OCT-1 Protein Is Predictive of Molecular Response and Survival in CP-CML Patients Treated with Imatinib: A 5 Year Update of the TIDEL Trial.

P. Manley, D. White, T. Hughes, 2009 .

In Contrast to Imatinib, OCT-1 Mediated Influx Has Minimal Impact on Cellular Uptake of Dasatinib in CML Patients at Diagnosis.

J. Melo, L. To, D. White, 2007 .

ATP Dependent Efflux Transporters ABCB1 and ABCG2 Are Unlikely to Impact the Efficacy, or Mediate Resistance to the Tyrosine Kinase Inhibitor, Ponatinib

T. Clackson, D. White, T. Hughes, 2011 .

CYP2C8 Genotype Significantly Alters Imatinib Metabolism in Chronic Myeloid Leukaemia Patients

A. Somogyi, D. White, T. Hughes, 2017, Clinical Pharmacokinetics.

Imatinib trough levels in chronic myelogenous leukemia: does one dose fit all?

D. White, D. Yeung, 2011, Leukemia & lymphoma.

Modelling Predictors of Molecular Response to Frontline Imatinib for Patients with Chronic Myeloid Leukaemia

Damith Ranasinghe, Fred Brown, Haneen Banjar, 2017, PloS one.

Selective Escalation of Imatinib Therapy and Early Switching to Nilotinib In De Novo Chronic Phase CML Patients: Interim Results From the TIDEL-II Trial

A. Schwarer, D. White, T. Hughes, 2010 .

A 20 Gene Expression Signature That Predicts Early Molecular Response Failure in Chronic Phase CML Patients Treated with Frontline Imatinib

D. White, T. Hughes, C. Kok, 2015 .

Upfront Imatinib Therapy in CML Patients with Rapid Switching to Nilotinib for Failure to Achieve Molecular Targets or Intolerance Achieves High Overall Rates of Molecular Response and a Low Risk of Progression - An Update of the TIDEL-II Trial

A. Schwarer, D. White, T. Hughes, 2011 .

Gene expression signature that predicts early molecular response failure in chronic-phase CML patients on frontline imatinib.

J. Reynolds, D. White, T. Hughes, 2019, Blood advances.

Early Switch to Nilotinib Does Not Overcome the Adverse Outcome for CML Patients Failing to Achieve Early Molecular Response On Imatinib, Despite Excellent Overall Outcomes in the TIDEL II Trial

A. Schwarer, D. White, T. Hughes, 2012 .

Elevated PTPN2 expression is associated with inferior molecular response in de-novo chronic myeloid leukaemia patients

D. White, T. Hughes, C. Kok, 2014, Leukemia.

Outcomes for Australian children with relapsed/refractory acute lymphoblastic leukaemia treated with blinatumomab

R. Marschalek, S. Heatley, C. Meyer, 2021, Pediatric blood & cancer.

CKLF and IL1B transcript levels at diagnosis are predictive of relapse in children with pre‐B‐cell acute lymphoblastic leukaemia

A. Zannettino, S. Fitter, T. Révész, 2021, British journal of haematology.

Ponatinib is not transported by ABCB1, ABCG2 or OCT-1 in CML cells

D. White, T. Hughes, V. Saunders, 2015, Leukemia.

The In-Vivo Level of Imatinib Induced Kinase Inhibition Achieved in De-Novo CML Patients during the First 28 Days of Therapy Is a Powerful Predictor of Molecular Outcome.

L. To, D. White, T. Hughes, 2005 .

Azacytidine Sensitizes AML Cells for Effective Elimination By CD123 CAR T-Cells

M. Brown, Wenbo Yu, Angel F. Lopez, 2019, Blood.

Reduced Activity of the OCT-1 Protein in Primitive CML Cells: A Likely Determinant of Stem Cell Resistance in Imatinib Treated CML Patients

A. Zannettino, D. White, T. Hughes, 2008 .

Most CML patients who have a suboptimal response to imatinib have low OCT-1 activity: higher doses of imatinib may overcome the negative impact of low OCT-1 activity.

P. Manley, A. Zannettino, D. White, 2007, Blood.

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.

D. White, T. Hughes, 2012, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.

Enhancing the Functional Activity of the OCT-1 Influx Pump May Overcome the Negative Impact of Low OCT-1 Activity in Imatinib Treated CML Patients

D. White, C. Kok, P. Dang, 2008 .

Detection of rearrangement within the breakpoint cluster region of chromosome 22 in the diagnosis of chronic myeloid leukemia.

Z. Rudzki, D. White, G. Casey, 1989, Australian and New Zealand journal of medicine.

Adverse outcomes for chronic myeloid leukemia patients with splenomegaly and low in vivo kinase inhibition on imatinib.

D. White, C. Kok, S. Branford, 2023, Blood cancer journal.

The acquisition order of leukemic drug resistance mutations is directed by the selective fitness associated with each resistance mechanism

D. White, C. Kok, D. Yeung, 2023, Scientific reports.

The IC50 Assay Is Predictive of Molecular Response, and Indicative of Optimal Dose in De-Novo CML Patients.

T. Kalebic, D. White, V. Saunders, 2008 .

Response to ‘Overexpression of ABCB1 as prediction marker for CML: How close we are to translation into clinics?’

D. White, L. Eadie, T. Hughes, 2017, Leukemia.

Genome-Wide Analysis of Genetic Alterations in Chronic Myelogenous Leukemia.

J. Downing, S. Shurtleff, I. Radtke, 2008 .