D. White

发表

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

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

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.

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.

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.

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.

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

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

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

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

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.

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

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

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

Amy Hughes, A. Yong, Carine Tang, 2017, Blood.

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.

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.

Optimizing the selection of kinase inhibitors for chronic myeloid leukemia patients

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

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.

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.

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.

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.

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.

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

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

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

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.

Predicting the Response of CML Patients to Tyrosine Kinase Inhibitor Therapy

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

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.

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.

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

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

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.

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 .

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

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

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.

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

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

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.

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.

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

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

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

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

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.

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.

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.

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.

Characterization of leukemias with ETV6-ABL1 fusion

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

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 .

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.

Predicting the response of CML patients to tyrosine kinase inhibitor therapy

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

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.

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.

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

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

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.

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.

A Low Concentration of ABL001 Potentiates In Vitro TKI-Induced Bcr-Abl Kinase Inhibition in CML Cells

D. Yeung, L. Eadie, Liu Lu, 2016 .

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.

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.

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.

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

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

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.

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.

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.

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 .

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.

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

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

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.

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

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

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.

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

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

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

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

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

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

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.

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.

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.

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.

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

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

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

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

CYP2C8 Genotype Significantly Alters Imatinib Metabolism in Chronic Myeloid Leukaemia Patients

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

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.

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.

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

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

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

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

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.