T. Hughes

T. Hughes, A. Grigg, T. Hughes, 2006, Biology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation.

Mutation screening of the c‐MYB negative regulatory domain in acute and chronic myeloid leukaemia

T. Gonda, R. Keough, T. Hughes, 2001, British journal of haematology.

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.

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

R. Herrmann, P. Browett, A. Schwarer, 2012 .

Monitoring Disease Response

T. Hughes, S. Branford, T. Hughes, 2007 .

Molecular monitoring of BCR-ABL as a guide to clinical management in chronic myeloid leukaemia.

T. Hughes, S. Branford, T. Hughes, 2006, Blood reviews.

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.

R. Herrmann, P. Browett, A. Schwarer, 2004, Blood.

Dasatinib treatment of chronic-phase chronic myeloid leukemia: analysis of responses according to preexisting BCR-ABL mutations.

Martin C. Müller, J. Radich, L. Ploughman, 2009, Blood.

Chronic myeloid leukemia: an update of concepts and management recommendations of European LeukemiaNet.

J. Radich, R. Larson, M. Baccarani, 2009, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.

Dasatinib or high-dose imatinib for chronic-phase chronic myeloid leukemia after failure of first-line imatinib: a randomized phase 2 trial.

J. Radich, H. Kantarjian, A. Countouriotis, 2007, Blood.

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.

Moving treatment-free remission into mainstream clinical practice in CML.

T. Hughes, D. Ross, T. Hughes, 2016, Blood.

chronic myeloid leukemia: 2013 European LeukemiaNet recommendations for the management of

Martin C. Müller, J. Radich, R. Larson, 2013 .

Ponatinib efficacy and safety in Philadelphia chromosome-positive leukemia: final 5-year results of the phase 2 PACE trial.

Martin C. Müller, M. Baccarani, H. Kantarjian, 2018, 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.

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.

I. Flinn, R. Larson, H. Kantarjian, 2011, The Lancet. Oncology.

Long-term prognostic significance of early molecular response to imatinib in newly diagnosed chronic myeloid leukemia: an analysis from the International Randomized Study of Interferon and STI571 (IRIS).

Martin C. Müller, J. Radich, R. Larson, 2010, Blood.

ENESTnd Update: Continued Superiority of Nilotinib Versus Imatinib In Patients with Newly Diagnosed Chronic Myeloid Leukemia In Chronic Phase (CML-CP)

R. Larson, R. Clark, H. Kantarjian, 2010 .

24 Months Update of the TOPS Study: a Phase III, Randomized, Open-Label Study of 400mg/d (SD-IM) Versus 800mg/d (HD-IM) of Imatinib Mesylate (IM) in Patients (Pts) with Newly Diagnosed, Previously Untreated Chronic Myeloid Leukemia in Chronic Phase (CML-CP).

J. Radich, M. Baccarani, B. Druker, 2009 .

International randomized study of interferon Vs STI571 (IRIS) 8-year follow up: Sustained survival and low risk for progression or events in patients with newly diagnosed chronic myeloid leukemia in chronic phase (CML-CP) treated with imatinib

J. Radich, R. Larson, B. Druker, 2009 .

Six-year follow-up of patients receiving imatinib for the first-line treatment of chronic myeloid leukemia

J. Radich, R. Larson, B. Druker, 2010, Leukemia.

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

J. Radich, R. Larson, M. Baccarani, 2011, Blood.

Deep molecular responses achieved in patients with CML-CP who are switched to nilotinib after long-term imatinib.

B. Leber, J. Lipton, A. Schwarer, 2014, Blood.

Low incidence of peripheral arterial disease in patients receiving dasatinib in clinical trials

J. Cortes, F. Mahon, N. Shah, 2015, Leukemia.

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.

Population pharmacokinetic and exposure-response analysis of nilotinib in patients with newly diagnosed Ph+ chronic myeloid leukemia in chronic phase

R. Larson, R. Clark, H. Kantarjian, 2011, European Journal of Clinical Pharmacology.

Potential mechanisms of disease progression and management of advanced-phase chronic myeloid leukemia

H. Kantarjian, J. Cortes, E. Jabbour, 2014, Leukemia & lymphoma.

Clinical strategies to achieve an early and successful response to tyrosine kinase inhibitor therapy.

A. Hochhaus, T. Hughes, T. Hughes, 2009, Seminars in hematology.

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 .

Rapid initial decline in BCR-ABL1 is associated with superior responses to second-line nilotinib in patients with chronic-phase chronic myeloid leukemia

Martin C. Müller, L. Beppu, J. Radich, 2013, BMC Cancer.

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.

An imatinib-only window followed by imatinib and chemotherapy for Philadelphia chromosome-positive acute leukemia: long-term results of the CMLALL1 trial

J. Szer, A. Boyd, T. Hughes, 2015, Leukemia & lymphoma.

Imatinib-induced gastric antral vascular ectasia in three patients with chronic myeloid leukaemia

H. Nandurkar, T. Hughes, D. Yeung, 2015, International Journal of Hematology.

Front-line and salvage therapies with tyrosine kinase inhibitors and other treatments in chronic myeloid leukemia.

H. Kantarjian, J. Cortes, A. Hochhaus, 2011, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.

Managing imatinib resistance in chronic myeloid leukaemia

T. Hughes, M. Osborn, T. Hughes, 2010, Current opinion in 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.

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

Z. Rudzki, J. Seymour, T. Hughes, 2007, Clinical Cancer Research.

Efficacy and safety of imatinib in patients with chronic myeloid leukemia and complete or near‐complete cytogenetic response to interferon‐α

A. Schwarer, T. Hughes, S. Branford, 2007 .

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.

Detection of BCR-ABL mutations and resistance to imatinib mesylate.

T. Hughes, S. Branford, T. Hughes, 2006, Methods in molecular medicine.

Imatinib produces significantly superior molecular responses compared to interferon alfa plus cytarabine in patients with newly diagnosed chronic myeloid leukemia in chronic phase

P. Browett, A. Schwarer, I. Gathmann, 2003, Leukemia.

Molecular monitoring of chronic myeloid leukemia.

T. Hughes, S. Branford, T. Hughes, 2003, Seminars in hematology.

Challenges of Treatment: Tyrosine Kinase Inhibitor-Resistant Chronic Myeloid Leukemia

J. Melo, T. Hughes, D. Ross, 2014 .

Handbook of Chronic Myeloid Leukemia

J. Melo, T. Hughes, D. Ross, 2014 .

Dasatinib suppresses in vitro natural killer cell cytotoxicity.

J. Hayball, T. Hughes, S. Blake, 2008, Blood.

Long-term treatment-free remission in patients with chronic myeloid leukemia after second-line nilotinib: ENESTop 5-year update

J. Lipton, N. Takahashi, F. Mahon, 2021, Leukemia.

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

R. Larson, H. Kantarjian, G. Rosti, 2013, Blood.

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

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

Early molecular response predicts outcomes in patients with chronic myeloid leukemia in chronic phase treated with frontline nilotinib or imatinib.

R. Larson, H. Kantarjian, G. Rosti, 2014, Blood.

Plasma exposure of imatinib and its correlation with clinical response in the Tyrosine Kinase Inhibitor Optimization and Selectivity Trial

M. Baccarani, B. Druker, J. Cortes, 2012, Haematologica.

Bone marrow fibrosis associated with long-term imatinib therapy: resolution after switching to a second-generation TKI.

T. Hughes, S. Branford, D. Hiwase, 2019, Blood advances.

Interferon-α-2b and oral cytarabine ocfosfate for newly diagnosed chronic myeloid leukaemia

R. Herrmann, P. Browett, A. Schwarer, 2004 .

Chronic myeloid leukemia.

J. Melo, T. Hughes, J. Apperley, 2003, Hematology. American Society of Hematology. Education Program.

Counterpoint: There is a best duration of deep molecular response for treatment‐free remission, but it is patient‐specific, and that is the challenge

T. Hughes, D. Ross, T. Hughes, 2020, British journal of haematology.

Sudden blast crisis in chronic myeloid leukemia treated with tyrosine kinase inhibitors

T. Hughes, D. Hiwase, T. Hughes, 2012, Leukemia & lymphoma.

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

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

Dasatinib treatment for Philadelphia chromosome‐positive leukemias

J. Cortes, H. Khoury, F. Guilhot, 2009, Cancer.

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.

Allogeneic Bone Marrow Transplantation for Chronic Myeloid Leukemia Using Sibling and Volunteer Unrelated Donors: A Comparison of Complications in the First 2 Years

A. Barrett, J. Goldman, A. Schwarer, 1993, Annals of Internal Medicine.

Diagnosis and monitoring of chronic myeloid leukemia by qualitative and quantitative RT-PCR.

T. Hughes, S. Branford, T. Hughes, 2006, Methods in molecular medicine.

Treatment-Free Remission After Second-Line Nilotinib Treatment

T. Hughes, Franois-Xavier Mahon, 2018, Annals of Internal Medicine.

Imatinib as a potential antiresorptive therapy for bone disease.

A. Zannettino, B. Vernon‐roberts, M. Condina, 2006, Blood.

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.

False-positive results with PCR to detect leukaemia-specific transcript

P. Martiat, J. Goldman, E. Gluckman, 1990, The Lancet.

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.

Dasatinib inhibits the secretion of TNF-alpha following TLR stimulation in vitro and in vivo.

J. Hayball, T. Hughes, K. Diener, 2009, Experimental hematology.

Nilotinib inhibits the Src-family kinase LCK and T-cell function in vitro

A. B. Lyons, T. Hughes, S. Blake, 2009, Journal of cellular and molecular medicine.

The GM-CSF receptor family: Mechanism of activation and implications for disease

R. D'Andrea, Angel F. Lopez, P. Ekert, 2012, Growth factors.

progenitors genomic instability in chronic myeloid leukemia stem cells and primitive mitochondrial respiratory chain complex III-generated ROS cause - Rac2

David A. Williams, C. Eaves, T. Holyoake, 2012 .

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.

Clonal hematopoiesis: a “CHIP” off the old block

T. Hughes, Timothy Hughes, 2015 .

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.

Prediction of graft versus host disease by frequency analysis of cytotoxic T cells after unrelated donor bone marrow transplantation.

S. Mackinnon, J. Goldman, T. Hughes, 1989, Transplantation.

TARGET: a survey of real‐world management of chronic myeloid leukaemia across 33 countries

V. Mathews, Jianxiang Wang, G. Saydam, 2020, British journal of haematology.

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

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

Incidence, outcomes, and risk factors of pleural effusion in patients receiving dasatinib therapy for Philadelphia chromosome-positive leukemia

J. Cortes, J. Lipton, P. Rousselot, 2018, Haematologica.

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

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

Detection of residual leukemia after bone marrow transplant for chronic myeloid leukemia: role of polymerase chain reaction in predicting relapse.

G. Morgan, P. Martiat, J. Goldman, 1991, Blood.

Mannose-binding lectin gene polymorphisms are associated with major infection following allogeneic hemopoietic stem cell transplantation.

C. Mullighan, J. Szer, S. Heatley, 2002, Blood.

Predicting the response of CML patients to tyrosine kinase inhibitor therapy

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

Asciminib in Chronic Myeloid Leukemia after ABL Kinase Inhibitor Failure.

B. Druker, M. Heinrich, J. Cortes, 2019, The New England journal of medicine.

Ponatinib Efficacy and Safety in Patients with the T315I Mutation: Long-Term Follow-up of Phase 1 and Phase 2 (PACE) Trials

I. Flinn, T. Clackson, M. Baccarani, 2014 .

Efficacy and Safety of Nilotinib (NIL) vs Imatinib (IM) in Patients (pts) With Newly Diagnosed Chronic Myeloid Leukemia in Chronic Phase (CML-CP): Long-Term Follow-Up (f/u) of ENESTnd

I. Flinn, R. Larson, R. Clark, 2014 .

Ponatinib (PON) in patients (pts) with Philadelphia chromosome-positive (Ph+) leukemias resistant or intolerant to dasatinib or nilotinib, or with the T315I mutation: Longer-term follow up of the PACE trial.

M. Baccarani, J. Dipersio, H. Kantarjian, 2014 .

Peripheral Arterial Occlusive Disease (PAOD) In Patients (Pts) Receiving Dasatinib: Experience Across Multiple Clinical Trials

J. Cortes, F. Mahon, N. Shah, 2013 .

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.

Intermittent target inhibition with dasatinib 100 mg once daily preserves efficacy and improves tolerability in imatinib-resistant and -intolerant chronic-phase chronic myeloid leukemia.

Andreas Hochhaus, R. Collins, H. Kantarjian, 2008, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.

Ponatinib versus imatinib for newly diagnosed chronic myeloid leukaemia: an international, randomised, open-label, phase 3 trial.

T. Clackson, M. Baccarani, R. Clark, 2016, The Lancet. Oncology.

Nilotinib in imatinib-resistant or imatinib-intolerant patients with chronic myeloid leukemia in chronic phase: 48-month follow-up results of a phase II study

J. Radich, R. Larson, M. Baccarani, 2013, Leukemia.

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.

Dasatinib-associated major molecular responses in patients with chronic myeloid leukemia in chronic phase following imatinib failure: response dynamics and predictive value

J. Radich, H. Kantarjian, J. Lipton, 2009, 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.

Long-term imatinib therapy promotes bone formation in CML patients.

S. Fitter, B. Vernon‐roberts, L. To, 2008, Blood.

Efficacy and safety of nilotinib 300 mg twice daily in patients with chronic myeloid leukemia in chronic phase who are intolerant to prior tyrosine kinase inhibitors: Results from the Phase IIIb ENESTswift study.

Matthew P Wright, T. Hughes, O. Gervásio, 2018, Leukemia research : a Forum for Studies on Leukemia and Normal Hemopoiesis.

Discontinuation of Therapy and Treatment-Free Remission in CML

T. Hughes, D. Ross, T. Hughes, 2016 .

Management of Patients with Chronic Myeloid Leukemia

J. Melo, T. Hughes, D. Ross, 2014 .

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.

Safety and efficacy of pulsed imatinib with or without G‐CSF versus continuous imatinib in chronic phase chronic myeloid leukaemia patients at 5 years follow‐up

F. Michor, T. Holyoake, F. Nicolini, 2013, British journal of haematology.

A pilot study of continuous imatinib vs pulsed imatinib with or without G-CSF in CML patients who have achieved a complete cytogenetic response

R. Clark, T. Holyoake, R. Clark, 2009, Leukemia.

BCR-ABL Levels Continue To Decrease up to 42 Months after Commencement of Standard Dose Imatinib in Patients with Newly Diagnosed Chronic Phase CML Who Achieve a Major Molecular Response.

P. Browett, A. Schwarer, Z. Rudzki, 2004 .

Long-Term Follow-up of Ponatinib Efficacy and Safety in the Phase 2 PACE Trial

Martin C. Müller, T. Clackson, M. Baccarani, 2014 .

Accumulation of JAK activation loop phosphorylation is linked to type I JAK inhibitor withdrawal syndrome in myelofibrosis

R. Majeti, M. Dottore, Angel F. Lopez, 2018, Science Advances.

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.

Hematologic and Cytogenetic Response Dynamics to Nilotinib (AMN107) Depend on the Type of BCR-ABL Mutations in Patients with Chronic Myelogeneous Leukemia (CML) after Imatinib Failure.

J. Radich, M. Baccarani, G. Martinelli, 2006 .

Improved results with PCR for chronic myeloid leukaemia

J. Goldman, T. Hughes, 1990, The Lancet.

POLYMERASE CHAIN REACTION FOR DETECTION OF RESIDUAL LEUKAEMIA

G. Morgan, J. Goldman, L. Wiedemann, 1989, The Lancet.

Inhibition of granulocyte-macrophage colony-stimulating factor prevents dissemination and induces remission of juvenile myelomonocytic leukemia in engrafted immunodeficient mice.

P. Iversen, I. Lewis, C. Niemeyer, 1997, 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.

Measuring minimal residual disease in chronic myeloid leukemia: fluorescence in situ hybridization and polymerase chain reaction.

T. Hughes, S. Branford, T. Hughes, 2009, Clinical lymphoma & myeloma.

Ph+ ALL: resistance seeds sown early

T. Hughes, S. Branford, T. Hughes, 2007 .

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 .

Monitoring Response to Treatment

J. Melo, T. Hughes, D. Ross, 2014 .

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.

T. Hughes, S. Branford, D. Ross, 2008, Clinical chemistry.

Competitive polymerase chain reaction to estimate the number of BCR-ABL transcripts in chronic myeloid leukemia patients after bone marrow transplantation.

A. Chase, N. Cross, T. Hughes, 1993, Blood.

Persistence of BCR/ABL transcripts after BMT for CML detected by PCR reflects a high risk of relapse.

P. Martiat, J. Goldman, T. Hughes, 1991, Bone marrow transplantation.

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.

Autologous stem cell collection and autograft for patients with chronic myeloid leukemia in the era of ABL kinase inhibitors: Back to the bench

T. Hughes, C. Hui, 2006, Leukemia & lymphoma.

Aberrant RAG-mediated recombination contributes to multiple structural rearrangements in lymphoid blast crisis of chronic myeloid leukemia

Paul P. S. Wang, M. Dinger, D. Thomson, 2020, Leukemia.

A senescence stress secretome is a hallmark of therapy-related myeloid neoplasm stromal tissue occurring soon after cytotoxic exposure

S. Gronthos, S. Paton, T. Hughes, 2022, Leukemia.

Clinical value of PCR in diagnosis and follow-up of leukaemia and lymphoma: report of the third Workshop of the Molecular Biology/BMT study group.

G. Cimino, F. Frassoni, V. Barbu, 1991, Leukemia.

Comment on "KB004, a first in class monoclonal antibody targeting the receptor tyrosine kinase EphA3, in patients with advanced hematologic malignancies: Results from a phase 1 study".

M. Brown, Wenbo Yu, Angel F. Lopez, 2017, Leukemia research : a Forum for Studies on Leukemia and Normal Hemopoiesis.

Bone marrow transplantation for chronic myeloid leukemia: the use of histocompatible unrelated volunteer donors.

S. Mackinnon, D. Catovsky, J. Goldman, 1990, Experimental hematology.

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.

Martin C. Müller, J. Radich, H. Kantarjian, 2012, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.

leukemia after failure of first-line imatinib: a randomized phase 2 trial Dasatinib or high-dose imatinib for chronic-phase chronic myeloid

J. Radich, P. Rousselot, T. Robak, 2008 .

Higher-Dose Imatinib (600 mg/Day) with Selective Intensification in Newly Diagnosed CML Patients in Chronic Phase; Cytogenetic Response Rates at 12 Months Are Superior to IRIS.

J. Reynolds, A. Schwarer, Z. Rudzki, 2004 .

Long‐Term Outcomes of Imatinib Treatment for Chronic Myeloid Leukemia

Francisco Cervantes, Susan Branford, Andreas Hochhaus, 2017, The New England journal of medicine.

Molecular monitoring in CML: how deep? How often? How should it influence therapy?

T. Hughes, N. Shanmuganathan, T. Hughes, 2018, Hematology. American Society of Hematology. Education Program.

Molecular monitoring in CML: how deep? How often? How should it influence therapy?

T. Hughes, N. Shanmuganathan, T. Hughes, 2018, 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.

Treatment-Free Remission After Second-Line Nilotinib Treatment in Patients With Chronic Myeloid Leukemia in Chronic Phase

J. Lipton, N. Takahashi, Dong-Wook Kim, 2018, Annals of Internal Medicine.

Impact of Treatment with Frontline Nilotinib (NIL) vs Imatinib (IM) on Sustained Deep Molecular Response (MR) in Patients (pts) with Newly Diagnosed Chronic Myeloid Leukemia in Chronic Phase (CML-CP)

R. Larson, H. Kantarjian, G. Saglio, 2015 .

Is drug treatment superior to allografting as first-line therapy in chronic myeloid leukemia?

T. Hughes, T. Hughes, 2008, Nature Clinical Practice Oncology.

Imatinib compared with interferon and low-dose cytarabine for newly diagnosed chronic-phase chronic myeloid leukemia.

Francisco Cervantes, Klaus Lechner, Thomas Fischer, 2003, The New England journal of medicine.

Nilotinib dose‐optimization in newly diagnosed chronic myeloid leukaemia in chronic phase: final results from ENESTxtnd

L. Shih, J. Lipton, J. Shortt, 2017, British journal of haematology.

The impact of multiple low-level BCR-ABL1 mutations on response to ponatinib.

J. Hodgson, V. Rivera, S. Lustgarten, 2016, Blood.

Early molecular and cytogenetic response is predictive for long-term progression-free and overall survival in chronic myeloid leukemia (CML)

H. Einsele, J. Hasford, K. Spiekermann, 2012, Leukemia.

Clinical Trials and Observations

R. A. Larson, Martin C. Müller, J. Radich, 2022 .

accelerated-phase chronic myelogenous leukemia inhibitor, is active in patients with imatinib-resistant or -intolerant Nilotinib (formerly AMN107), a highly selective BCR-ABL tyrosine kinase

J. Radich, R. Larson, M. Gobbi, 2008 .

Nilotinib ( formerly AMN 107 ) , a highly selective BCR-ABL tyrosine kinase inhibitor , is active in patients with imatinib-resistant or-intolerant accelerated-phase chronic myelogenous leukemia

J. Radich, R. Larson, M. Gobbi, 2008 .

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 .

Monitoring of minimal residual disease in chronic myeloid leukemia.

S. Faderl, A. Hochhaus, T. Hughes, 2004, Hematology/oncology clinics of North America.

Continuing Reduction in Level of Residual Disease after 4 Years in Patients with CML in Chronic Phase Responding to First-Line Imatinib (IM) in the IRIS Study.

J. Goldman, A. Hochhaus, I. Gathmann, 2005 .

Maintenance of Imatinib Dose Intensity in the First Six Months of Therapy for Newly Diagnosed Patients with CML Is Predictive of Molecular Response, Independent of the Ability To Increase Dose at a Later Point.

J. Reynolds, A. Schwarer, J. Seymour, 2005 .

Gene Expression Signatures Associated with Treatment and Resistance to Imatinib Mesylate in Chronic Myeloid Leukemia Patients.

P. Linsley, C. Sawyers, E. Pogosova-Agadjanyan, 2005 .

Impact of baseline BCR-ABL mutations on response to nilotinib in patients with chronic myeloid leukemia in chronic phase.

Martin C. Müller, L. Beppu, J. Radich, 2009, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.

Dasatinib inhibits recombinant viral antigen-specific murine CD4+ and CD8+ T-cell responses and NK-cell cytolytic activity in vitro and in vivo.

A. B. Lyons, M. Brown, J. Hayball, 2009, Experimental hematology.

The Most Common Dasatinib-Resistant BCR-ABL Kinase Domain Mutations in Patients with Chronic Myeloid Leukemia Are Sensitive to VX-680: Rationale for Early Combination Kinase Inhibitor Therapy.

C. Sawyers, R. Paquette, N. Shah, 2006 .

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.

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

Dong-Wook Kim, T. Hughes, S. Branford, 2012, Blood.

Five-year follow-up of patients receiving imatinib for chronic myeloid leukemia.

Francisco Cervantes, Thomas Fischer, Alois Gratwohl, 2006, The New England journal of medicine.

Sustained deep molecular responses in patients switched to nilotinib due to persistent BCR-ABL1 on imatinib: final ENESTcmr randomized trial results

B. Leber, S. Kamel‐Reid, J. Lipton, 2017, Leukemia.

Long Term Follow up of Patients with CML in Chronic Phase Treated with First-Line Imatinib Suggests That Earlier Achievement of a Major Molecular Response Leads to Greater Stability of Response.

A. Schwarer, Z. Rudzki, J. Seymour, 2008 .

Expanded Phase 1 Study of ABL001, a Potent, Allosteric Inhibitor of BCR-ABL, Reveals Significant and Durable Responses in Patients with CML-Chronic Phase with Failure of Prior TKI Therapy

M. Heinrich, J. Cortes, D. DeAngelo, 2016 .

4-year results of the ponatinib phase II PACE trial in patients (pts) with heavily pretreated leukemia.

M. Baccarani, H. Kantarjian, F. Haluska, 2016 .

Efficacy and Safety of Ponatinib in Patients with Accelerated Phase or Blast Phase Chronic Myeloid Leukemia (AP-CML or BP-CML) or Philadelphia Chromosome-Positive Acute Lymphoblastic Leukemia (Ph+ ALL): 12-Month Follow-up of the PACE Trial

Martin C. Müller, T. Clackson, M. Baccarani, 2012 .

Molecular Analysis of Dasatinib Resistance Mechanisms in CML Patients Identifies Novel BCR-ABL Mutations Predicted To Retain Sensitivity to Imatinib: Rationale for Combination Tyrosine Kinase Inhibitor Therapy.

C. Sawyers, F. Huang, R. Paquette, 2005 .

Compound mutations in BCR-ABL1 are not major drivers of primary or secondary resistance to ponatinib in CP-CML patients.

Martin C. Müller, J. Hodgson, T. Clackson, 2016, Blood.

A phase 2 study of MK-0457 in patients with BCR-ABL T315I mutant chronic myelogenous leukemia and philadelphia chromosome-positive acute lymphoblastic leukemia

A. Nagler, I. Dufva, G. Martinelli, 2014, Blood Cancer Journal.

Update On Imatinib-Resistant Chronic Myeloid Leukemia Patients in Chronic Phase (CML-CP) On Nilotinib Therapy at 24 Months: Clinical Response, Safety, and Long-Term Outcomes.

J. Radich, R. Larson, M. Baccarani, 2009 .

Nilotinib Demonstrates Superior Efficacy Compared with Imatinib in Patients with Newly Diagnosed Chronic Myeloid Leukemia in Chronic Phase: Results From the International Randomized Phase III ENESTnd Trial

R. Larson, R. Clark, H. Kantarjian, 2009 .

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.

Outcome of Patients with Chronic Myeloid Leukemia in Chronic Phase (CML-CP) Based On Early Molecular Response and Factors Associated with Early Response: 4-Year Follow-up Data From Enestnd (Evaluating Nilotinib Efficacy and Safety in Clinical Trials Newly Diagnosed Patients)

R. Larson, H. Kantarjian, G. Saglio, 2012 .

A Pivotal Phase 2 Trial of Ponatinib in Patients with Chronic Myeloid Leukemia (CML) and Philadelphia Chromosome-Positive Acute Lymphoblastic Leukemia (Ph+ALL) Resistant or Intolerant to Dasatinib or Nilotinib, or with the T315I BCR-ABL Mutation: 12-Month Follow-up of the PACE Trial

Martin C. Müller, T. Clackson, M. Baccarani, 2012 .

Nilotinib vs imatinib in patients with newly diagnosed Philadelphia chromosome-positive chronic myeloid leukemia in chronic phase: ENESTnd 3-year follow-up

I. Flinn, R. Larson, R. Clark, 2012, Leukemia.

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

H. Scott, T. Hughes, S. Branford, 2012, Blood.

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.

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.

Dasatinib Efficacy in Patients with Chronic Myeloid Leukemia in Chronic Phase (CML-CP) and Pre-Existing BCR-ABL Mutations

Martin C. Müller, L. Ploughman, B. Druker, 2008 .

Nilotinib Efficacy According to Baseline BCR-ABL Mutations in Patients with Imatinib-Resistant Chronic Myeloid Leukemia in Chronic Phase (CML-CP)

Martin C. Müller, J. Radich, G. Martinelli, 2008 .

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

Franziska Michor, Mithat Gonen, Susan Branford, 2011, Blood.

The Majority of Chronic Myeloid Leukaemia Patients Who Cease Imatinib after Achieving a Sustained Complete Molecular Response (CMR) Remain in CMR, and Any Relapses Occur Early.

J. Reynolds, A. Schwarer, J. Seymour, 2008 .

BCR-ABL1 kinase domain mutations may persist at very low levels for many years and lead to subsequent TKI resistance

H. Scott, T. Hughes, S. Branford, 2013, British Journal of Cancer.

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.

Stem cell factor as a single agent induces selective proliferation of the Philadelphia chromosome positive fraction of chronic myeloid leukemia CD34(+) cells.

L. To, J. Lévesque, P. Simmons, 1998, Blood.

chronic phase vs imatinib in patients with newly diagnosed chronic myeloid leukemia

R. Larson, H. Kantarjian, G. Rosti, 2013 .

A senescence stress secretome is a hallmark of therapy-related myeloid neoplasm stromal tissue occurring soon after cytotoxic exposure

Sharad Kumar, S. Gronthos, S. Paton, 2022, 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.

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

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

Efficacy and Safety Of Ponatinib Following Failure Of Dasatinib In Patients (pts) With Chronic Phase Chronic Myeloid Leukemia (CP-CML) In The PACE Trial

Martin C. Müller, T. Clackson, M. Baccarani, 2013 .

Mutational analysis in chronic myeloid leukemia: when and what to do?

T. Hughes, S. Branford, T. Hughes, 2011, Current opinion in hematology.

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.

Renal toxicity after total body irradiation.

T. Hughes, M. Borg, N. Horvath, 2001, International journal of radiation oncology, biology, physics.

Donor leukocyte infusions for chronic myeloid leukemia in relapse after allogeneic bone marrow transplantation [letter]

A. Barrett, A. Schwarer, T. Hughes, 1992 .

Establishment of the first World Health Organization International Genetic Reference Panel for quantitation of BCR-ABL mRNA.

Paul Metcalfe, Helen E White, Susan Branford, 2010, Blood.

Factors affecting the outcome of allogeneic bone marrow transplantation for adult patients with refractory or relapsed acute leukaemia

R. Herrmann, J. Szer, J. Matthews, 1999, British journal of haematology.

First Approved Kinase Inhibitor for AML

J. Rasko, T. Hughes, T. Hughes, 2017, Cell.

Mobilization of predominantly Philadelphia chromosome‐negative blood progenitors using cyclophosphamide and rHUG‐CSF in early chronic‐phase chronic myeloid leukaemia: correlation with Sokal prognostic index and haematological control

R. Herrmann, J. Szer, A. Schwarer, 1997, British journal of haematology.

Dasatinib in the treatment of chronic myeloid leukemia in accelerated phase after imatinib failure: the START a trial.

R. Larson, G. Rosti, J. Cortes, 2009, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.

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 allosteric inhibitor ABL001 enables dual targeting of BCR–ABL1

Hans Bitter, Franco Lombardo, Joseph Schoepfer, 2017, Nature.

European LeukemiaNet 2020 recommendations for treating chronic myeloid leukemia

C. Schiffer, R. Larson, M. Baccarani, 2020, Leukemia.

European LeukemiaNet recommendations for the management of chronic myeloid leukemia: 2013.

Francisco Cervantes, Simona Soverini, Giovanni Martinelli, 2013, Blood.

Nilotinib versus imatinib for newly diagnosed chronic myeloid leukemia.

Ricardo Pasquini, Giuseppe Saglio, Andreas Hochhaus, 2010, The New England journal of medicine.

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.

Martin C. Müller, J. Radich, S. Kamel‐Reid, 2008, Blood.

Monitoring CML patients responding to treatment with tyrosine kinase inhibitors: review and recommendations for harmonizing current methodology for detecting BCR-ABL transcripts and kinase domain mutations and for expressing results.

Simona Soverini, Giovanni Martinelli, Susan Branford, 2006, Blood.

Inhibition of c-fms by Imatinib: Expanding the Spectrum of Treatment

A. B. Lyons, A. Zannettino, T. Hughes, 2005, Cell cycle.

Lin28 Enhances Tumorigenesis and is Associated With Advanced Human Malignancies

John T. Powers, T. Golub, M. Meyerson, 2009, Nature Genetics.

Prognosis for patients with CML and >10% BCR-ABL1 after 3 months of imatinib depends on the rate of BCR-ABL1 decline.

Nicola D. Roberts, J. Seymour, T. Hughes, 2014, Blood.

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.

BCR–ABL Transcript Dynamics Support the Hypothesis That Leukemic Stem Cells Are Reduced during Imatinib Treatment

Susan Branford, Andrew M. Stein, Dean Bottino, 2011, Clinical Cancer Research.

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.

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.

R. Herrmann, Z. Rudzki, T. Hughes, 2002, Blood.

p53 in chronic myeloid leukemia cell lines.

S. Bi, J. Goldman, A. Chase, 1992, Leukemia.

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.

Susan Branford, Richard Herrmann, R. Herrmann, 2003, Blood.

Chronic myeloid leukemia: reminiscences and dreams

G. Daley, J. Radich, J. Cortes, 2016, Haematologica.

chronic-phase chronic myeloid leukemia after failure of imatinib therapy Dasatinib induces notable hematologic and cytogenetic responses in

Martin C. Müller, M. Baccarani, H. Kantarjian, 2013 .

Dasatinib or high‐dose imatinib for chronic‐phase chronic myeloid leukemia resistant to imatinib at a dose of 400 to 600 milligrams daily

H. Kantarjian, J. Cortes, N. Shah, 2009, Cancer.

Dasatinib induces notable hematologic and cytogenetic responses in chronic-phase chronic myeloid leukemia after failure of imatinib therapy.

M. Baccarani, H. Kantarjian, B. Druker, 2007, Blood.

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.

Significance of residual leukaemia transcripts after bone marrow transplant for CML

C. Sawyers, P. Martiat, J. Goldman, 1990, The Lancet.

Dysregulation of bone remodeling by imatinib mesylate.

K. Vandyke, S. Fitter, A. Zannettino, 2010, Blood.

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.

Six-year follow-up of patients receiving imatinib for the first-line treatment of chronic myeloid leukemia

J. Radich, R. Larson, B. Druker, 2009, Leukemia.

Signalling by the βc family of cytokines.

J. Sandow, Angel F. Lopez, P. Ekert, 2013, Cytokine & growth factor reviews.

Monitoring disease response to tyrosine kinase inhibitor therapy in CML.

T. Hughes, S. Branford, T. Hughes, 2009, Hematology. American Society of Hematology. Education Program.

Overall survival with ponatinib versus allogeneic stem cell transplantation in Philadelphia chromosome‐positive leukemias with the T315I mutation

H. Kantarjian, G. Martinelli, J. Cortes, 2017, Cancer.

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.

Practical considerations for monitoring patients with chronic myeloid leukemia.

T. Hughes, S. Branford, T. Hughes, 2010, Seminars in hematology.

Dynamics of chronic myeloid leukemia response to dasatinib, nilotinib, and high-dose imatinib

Franziska Michor, Mithat Gonen, Susan Branford, 2014, Haematologica.

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

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

BCR-ABL1-positive CML and BCR-ABL1-negative chronic myeloproliferative disorders: some common and contrasting features

G. Daley, A. Green, W. Vainchenker, 2008, Leukemia.

Optimizing outcomes for patients with advanced disease in chronic myelogenous leukemia.

J. Radich, M. Baccarani, J. Cortes, 2008, Seminars in oncology.

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.

Polycomb Factor PHF19 Controls Cell Growth and Differentiation Toward Erythroid Pathway in Chronic Myeloid Leukemia Cells

E. Blanco, P. Vizán, C. Ballaré, 2021, Frontiers in Cell and Developmental Biology.

The role of alternative splicing patterns of BCR/ABL transcripts in the generation of the blast crisis of chronic myeloid leukaemia

P. Martiat, L. Chan, T. Hughes, 1990, British journal of haematology.

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.

Nilotinib (formerly AMN107), a highly selective BCR-ABL tyrosine kinase inhibitor, is active in patients with imatinib-resistant or -intolerant accelerated-phase chronic myelogenous leukemia.

J. Radich, R. Larson, M. Gobbi, 2008, Blood.

The price of drugs for chronic myeloid leukemia (CML) is a reflection of the unsustainable prices of cancer drugs: from the perspective of a large group of CML experts.

Francisco Cervantes, Ryuzo Ohno, Richard E. Clark, 2013, Blood.

Dasatinib alters the metastatic phenotype of B16-OVA melanoma in vivo

M. Brown, J. Hayball, T. Hughes, 2010, Cancer biology & therapy.

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

J. Melo, T. Hughes, S. Branford, 2009, Blood.

Prospective histomorphometric and DXA evaluation of bone remodeling in imatinib-treated CML patients: evidence for site-specific skeletal effects.

K. Vandyke, S. Fitter, C. Schultz, 2013, The Journal of clinical endocrinology and metabolism.

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.

A phase 2 trial of ponatinib in Philadelphia chromosome-positive leukemias.

T. Clackson, M. Baccarani, J. Dipersio, 2013, The New England journal of medicine.

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.

Sequential Kinase Inhibitor Therapy in CML Patients Can Select for Cells Harboring Compound BCR-ABL Kinase Domain Mutations with Increased Oncogenic Potency: Rationale for Early Combination Therapy of ABL Kinase Inhibitors.

C. Sawyers, R. Paquette, N. Shah, 2006 .

Many BCR-ABL1 compound mutations reported in chronic myeloid leukemia patients may actually be artifacts due to PCR-mediated recombination.

H. Scott, T. Hughes, S. Branford, 2014, Blood.

Sensitive detection of BCR-ABL1 mutations in patients with chronic myeloid leukemia after imatinib resistance is predictive of outcome during subsequent therapy.

H. Scott, T. Hughes, S. Branford, 2011, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.

Sequential ABL kinase inhibitor therapy selects for compound drug-resistant BCR-ABL mutations with altered oncogenic potency.

C. Sawyers, R. Paquette, N. Shah, 2007, The Journal of clinical investigation.

Limited clinical value of regular bone marrow cytogenetic analysis in imatinib-treated chronic phase CML patients monitored by RQ-PCR for BCR-ABL

T. Hughes, S. Branford, D. Ross, 2006, Leukemia.

Efficacy and Safety of Nilotinib In Chronic Phase (CP) Chronic Myeloid Leukemia (CML) Patients (Pts) with Type 2 Diabetes In the ENESTnd Trial.

R. Larson, D. Marin, H. Kantarjian, 2010 .

Nilotinib vs imatinib in patients with newly diagnosed Philadelphia chromosome-positive chronic myeloid leukemia in chronic phase: ENESTnd 3-year follow-up

I. Flinn, R. Larson, R. Clark, 2012, Leukemia.

Treatment-free remission in patients with chronic myeloid leukaemia

T. Hughes, D. Ross, T. Hughes, 2020, Nature Reviews Clinical Oncology.

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.

Establishment and validation of analytical reference panels for the standardization of quantitative BCR-ABL1 measurements on the international scale.

Helen E White, Dong-Wook Kim, Timothy Hughes, 2013, Clinical chemistry.

Suboptimal Responses in Chronic Myeloid Leukemia

H. Kantarjian, E. Jabbour, G. Saglio, 2011, Cancer.

International standardisation of quantitative real-time RT-PCR for BCR-ABL.

J. Goldman, N. Cross, A. Hochhaus, 2008, Leukemia research.

Response: Reliability of PCR for BCR-ABL transcripts

J. Goldman, T. Hughes, S. Branford, 2007 .

Comparison of "Log Reduction from Median Pretherapeutic Value" vs Ratio BCR-ABL/ABL to Express the Therapeutic Response in CML Patients.

P. Paschka, R. Hehlmann, A. Hochhaus, 2004 .

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

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

Imatinib inhibits the in vitro development of the monocyte/macrophage lineage from normal human bone marrow progenitors

A. B. Lyons, T. Hughes, K. Doherty, 2003, Leukemia.

after allogeneic bone marrow transplantation (letter) Donor leukocyte infusions for chronic myeloid leukemia in relapse

A. Barrett, T. Hughes, J. Goldman, 2011 .

Donor leukocyte infusions for chronic myeloid leukemia in relapse after allogeneic bone marrow transplantation.

A. Barrett, J. Goldman, A. Schwarer, 1992, Blood.

Laying the foundation for genomically-based risk assessment in chronic myeloid leukemia

S. Mustjoki, B. Druker, J. Cortes, 2019, Leukemia.

HLA‐identical sibling donor bone marrow transplantation for chronic myeloid leukaemia in first chronic phase: influence of GVHD prophylaxis on outcome

A. Barrett, S. Mackinnon, J. Goldman, 1992, British journal of haematology.

Non-HLA immunogenetic polymorphisms and the risk of complications after allogeneic hemopoietic stem-cell transplantation

C. Mullighan, J. Szer, S. Heatley, 2004, Transplantation.

Role of the β Common (βc) Family of Cytokines in Health and Disease.

J. Sandow, Angel F. Lopez, P. Ekert, 2018, Cold Spring Harbor perspectives in biology.

Erratum: Six-year follow-up of patients receiving imatinib for the first-line treatment of chronic myeloid leukemia(Leukemia (2009) 23 (1054-1061) DOI: 10.1038/leu.2009.38)

Martin C. Müller, R. Larson, B. Druker, 2010 .

S. Mackinnon, N. Cross, H. Waldmann, 1993, Bone marrow transplantation.

Early BCR-ABL1 kinetics are predictive of subsequent achievement of treatment-free remission in chronic myeloid leukemia.

Dong-Wook Kim, T. Hughes, S. Branford, 2020, Blood.

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.

Long-term benefits and risks of frontline nilotinib vs imatinib for chronic myeloid leukemia in chronic phase: 5-year update of the randomized ENESTnd trial

I. Flinn, R. Larson, R. Clark, 2016, Leukemia.

Long-term treatment-free remission (TFR) in patients (pts) with chronic myeloid leukemia in chronic phase (CML-CP) after stopping second-line (2L) nilotinib: ENESTop 144-wk results.

J. Lipton, N. Takahashi, F. Mahon, 2018 .

Treatment-free remission (TFR) following nilotinib (NIL) in patients (pts) with chronic myeloid leukemia in chronic phase (CML-CP): ENESTfreedom, ENESTop, ENESTgoal, and ENESTpath.

M. Baccarani, G. Saglio, C. Keir, 2014 .

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

Susan Branford, J. Reynolds, N. Briggs, 2013, Blood.

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

A. B. Lyons, G. Mayrhofer, T. Hughes, 2008, Clinical immunology.

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

Susan Branford, Timothy P. Hughes, Fabrizio Pane, 2014, International Journal of Hematology.

Dasatinib induces durable cytogenetic responses in patients with chronic myelogenous leukemia in chronic phase with resistance or intolerance to imatinib

R M Stone, R. Larson, H. Dombret, 2008, Leukemia.

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.

Dasatinib (SPRYCEL®) vs Escalated Dose of Imatinib (im) in Patients (pts) with Chronic Phase Chronic Myeloid Leukemia (CP-CML) Resistant to Imatinib: Results of the CA180-017 START-R Randomized Study.

B. Druker, A. Countouriotis, P. Rousselot, 2006 .

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

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

Drug-interaction studies evaluating T-cell proliferation reveal distinct activity of dasatinib and imatinib in combination with cyclosporine A.

A. B. Lyons, T. Hughes, Timothy P Hughes, 2012, Experimental hematology.

Any BCR-ABL Reduction Below 10% At 6 Months Of Therapy Significantly Improves Outcome For CML Patients With a Poor Response At 3 Months

Nicola D. Roberts, T. Hughes, D. Yeung, 2013 .

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.

Five-year results of the ponatinib phase II PACE trial in heavily pretreated CP-CML patients (pts).

M. Baccarani, H. Kantarjian, J. Cortes, 2017 .

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

Z. Rudzki, T. Hughes, S. Branford, 2002, British journal of haematology.

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.

Oral versus intravenous ganciclovir for the prophylaxis of cytomegalovirus disease after allogeneic bone marrow transplantation

J. Szer, T. Hughes, S. Durrant, 2004, Internal medicine journal.

marrow transplantation BCR-ABL transcripts in chronic myeloid leukemia patients after bone Competitive polymerase chain reaction to estimate the number of

A. Chase, N. Cross, T. Hughes, 2011 .

following allogeneic hemopoietic stem cell transplantation Mannose-binding lectin gene polymorphisms are associated with major

C. Mullighan, J. Szer, S. Heatley, 2002 .

Biological importance of residual leukaemic cells after BMT for CML: does the polymerase chain reaction help?

J. Goldman, T. Hughes, T. Hughes, 1990, Bone marrow transplantation.

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.

Concurrent use of proton pump inhibitors or H2 blockers did not adversely affect nilotinib efficacy in patients with chronic myeloid leukemia

R. Larson, M. Baccarani, H. Kantarjian, 2012, Cancer Chemotherapy and Pharmacology.

Population pharmacokinetic and exposure-response analysis of nilotinib in patients with newly diagnosed Ph+ chronic myeloid leukemia in chronic phase

R. Larson, R. Clark, H. Kantarjian, 2012, European Journal of Clinical Pharmacology.

Long-term outcomes with frontline nilotinib versus imatinib in newly diagnosed chronic myeloid leukemia in chronic phase: ENESTnd 10-year analysis

I. Flinn, R. Larson, R. Clark, 2021, Leukemia.

A dual role for the N-terminal domain of the IL-3 receptor in cell signalling

M. Dottore, Angel F. Lopez, T. Nero, 2018, Nature Communications.

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

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

Novel Fusion Genes at CML Diagnosis Reveal a Complex Pattern of Genomic Rearrangements and Sequence Inversions Associated with the Philadelphia Chromosome in Patients with Early Blast Crisis

Paul P. S. Wang, H. Scott, A. Schreiber, 2016 .

Epic: A Phase 3 Trial of Ponatinib Compared with Imatinib in Patients with Newly Diagnosed Chronic Myeloid Leukemia in Chronic Phase (CP-CML)

T. Clackson, M. Baccarani, R. Clark, 2014 .

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.

Efficacy of Dasatinib in Patients with Chronic-Phase Chronic Myelogenous Leukemia with Resistance or Intolerance to Imatinib: 2-Year Follow-Up Data from START-C (CA180-013).

M. Baccarani, H. Kantarjian, J. Lipton, 2007 .

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.

What's NEXT for CML-NGS mutation screening.

T. Hughes, N. Shanmuganathan, T. Hughes, 2020, Blood.

Early Management of CML

T. Hughes, N. Shanmuganathan, T. Hughes, 2019, Current Hematologic Malignancy Reports.

Enestnd 4-Year (y) Update: Continued Superiority of Nilotinib Vs Imatinib in Patients (pts) with Newly Diagnosed Philadelphia Chromosome–Positive (Ph+) Chronic Myeloid Leukemia in Chronic Phase (CML-CP)

R. Larson, R. Clark, H. Kantarjian, 2012 .

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 .

A Phase I/II study of nilotinib in Japanese patients with imatinib-resistant or -intolerant Ph+ CML or relapsed/refractory Ph+ ALL

T. Naoe, H. Tanii, J. Ishikawa, 2009, International journal of hematology.

ENESTnd 5-year (y) update: Long-term outcomes of patients (pts) with chronic myeloid leukemia in chronic phase (CML-CP) treated with frontline nilotinib (NIL) versus imatinib (IM).

R. Larson, R. Clark, H. Kantarjian, 2014 .

Predicting the Response of CML Patients to Tyrosine Kinase Inhibitor Therapy

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

Asciminib, a Specific Allosteric BCR-ABL1 Inhibitor, in Patients with Chronic Myeloid Leukemia Carrying the T315I Mutation in a Phase 1 Trial

J. Cortes, M. Deininger, D. DeAngelo, 2018, Blood.

Incidence of Hyperglycemia by 3 Years in Patients (Pts) with Newly Diagnosed Chronic Myeloid Leukemia in Chronic Phase (CML-CP) Treated with Nilotinib (NIL) or Imatinib (IM) in ENESTnd

R. Larson, H. Kantarjian, G. Saglio, 2012 .

The Adverse Effect of High Sokal Risk for First Line Imatinib Treated Patients Is Overcome By a Rapid Rate of BCR-ABL Decline Measured As Early As 1 Month of Treatment

J. Seymour, T. Hughes, S. Branford, 2014 .

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 .

Efficacy of dasatinib in chronic phase chronic myelogenous leukemia patients after imatinib failure according to baseline BCR- ABL mutations

P. Erben, A. Hochhaus, N. Shah, 2007 .

Clinical impact of dose modification and dose intensity on response to ponatinib (PON) in patients (pts) with Philadelphia chromosome-positive (Ph+) leukemias.

M. Baccarani, H. Kantarjian, F. Haluska, 2014 .

The Impact of Ponatinib Versus Allogeneic Stem Cell Transplant (SCT) on Outcomes in Patients with Chronic Myeloid Leukemia (CML) or Philadelphia Chromosome-Positive Acute Lymphoblastic Leukemia (Ph+ ALL) with the T315I Mutation

H. Kantarjian, G. Martinelli, J. Cortes, 2015 .

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 .

Imatinib (IM) Pharmacokinetic (PK) Exposure and Its Correlation with Clinical Outcome in Patients with Chronic-Phase Chronic Myeloid Leukemia (CML-CP) for 400 Mg and 800 Mg Daily Doses (Tyrosine Kinase Dose Optimization Study [TOPS])

M. Baccarani, B. Druker, J. Cortes, 2008 .

Asciminib monotherapy in patients with CML-CP without BCR::ABL1 T315I mutations treated with at least two prior TKIs: 4-year phase 1 safety and efficacy results

M. Geyer, M. Heinrich, M. Deininger, 2023, Leukemia.

Ponatinib In Heavily Pretreated Patients With Chronic Phase Chronic Myeloid Leukemia (CP-CML): Management Of Adverse Events (AEs)

Martin C. Müller, M. Baccarani, J. Dipersio, 2013 .

The Incidence of BCR-ABL Mutations and Their Impact on Outcome in Patients with Newly Diagnosed Chronic Myeloid Leukemia in Chronic Phase (CML-CP) Treated with Nilotinib or Imatinib in ENESTnd: 36-Month Follow-up

R. Larson, H. Kantarjian, G. Rosti, 2011 .

Asciminib, a First-in-Class STAMP Inhibitor, Provides Durable Molecular Response in Patients (pts) with Chronic Myeloid Leukemia (CML) Harboring the T315I Mutation: Primary Efficacy and Safety Results from a Phase 1 Trial

M. Heinrich, J. Cortes, M. Deininger, 2020 .

CYP2C8 Genotype Significantly Alters Imatinib Metabolism in Chronic Myeloid Leukaemia Patients

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

Comparison of nilotinib and imatinib in patients (pts) with newly diagnosed chronic myeloid leukemia in chronic phase (CML-CP): ENESTnd 24-month follow-up.

R. Larson, H. Kantarjian, G. Saglio, 2010, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.

DNA-Based Measurement of BCR-ABL in Chronic Myeloid Leukemia (CML).

A. Morley, T. Hughes, D. Ross, 2007 .

Safety and efficacy of switching to nilotinib 400 mg twice daily for patients with chronic myeloid leukemia in chronic phase with suboptimal response or failure on front-line imatinib or nilotinib 300 mg twice daily

R. Larson, H. Kantarjian, G. Rosti, 2014, Haematologica.

Dasatinib-Associated Major Molecular Responses Are Rapidly Achieved in Patients with Chronic Myeloid Leukemia in Chronic Phase (CML-CP) Following Resistance, Suboptimal Response, or Intolerance on Imatinib.

Martin C. Müller, J. Radich, J. Lipton, 2008 .

The Initial Molecular Response of Chronic Phase CML Patients Treated with Second Generation ABL Inhibitor Therapy after Imatinib Failure Can Predict Inadequate Response and Provide Indications for Rational Mutation Screening

Z. Rudzki, T. Hughes, S. Branford, 2008 .

Treatment-Free Remission in Patients with Chronic Myeloid Leukemia in Chronic Phase According to Reasons for Switching from Imatinib to Nilotinib: Subgroup Analysis from ENESTop

J. Lipton, N. Takahashi, F. Mahon, 2016 .

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

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

How complete is “complete” molecular response in imatinib-treated chronic myeloid leukemia?

T. Hughes, D. Ross, T. Hughes, 2008, Leukemia & lymphoma.

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 .

Two Year Data from a Prospective Safety Study Analyzing the Consequences of Imatinib Mesylate Inhibition of Sensitive Kinases Other Than bcr-abl in Patients with Previously Untreated Chronic Phase CML.

J. Reynolds, A. Schwarer, J. Seymour, 2006 .

Responses and Disease Progression in CML-CP Patients Treated with Nilotinib after Imatinib Failure Appear To Be Affected by the BCR-ABL Mutation Status and Types.

J. Radich, G. Martinelli, G. Saglio, 2007 .

therapy reveal treatment effects on leukemic stem cells Dynamics of chronic myeloid leukemia response to long-term targeted

M. Gonen, H. Kantarjian, F. Michor, 2011 .

Cardiac Safety Profile of Imatinib and Nilotinib In Patients (pts) with Newly Diagnosed Chronic Myeloid Leukemia In Chronic Phase (CML-CP): Results From ENESTnd

R. Larson, H. Kantarjian, G. Rosti, 2010 .

Modelling the safe minimum frequency of molecular monitoring for CML patients attempting treatment-free remission.

T. Hughes, S. Branford, D. Yeung, 2019, Blood.

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 .

Treatment-Free Remission (TFR) Eligibility in Patients (pts) with Chronic Myeloid Leukemia in Chronic Phase (CML-CP) and Residual Disease on Long-Term Imatinib (IM) Who Switched to Second-Line Nilotinib (NIL)

B. Leber, J. Lipton, T. Hughes, 2015 .

Response and Outcomes to Nilotinib at 24 Months in Imatinib-Resistant Chronic Myeloid Leukemia Patients in Chronic Phase (CML-CP) and Accelerated Phase (CML-AP) with and without BCR-ABL Mutations.

Martin C. Müller, L. Beppu, J. Radich, 2009 .

Steady-State Imatinib Trough Levels as Well as Dose Interruptions Are Associated with Clinical Response (CCyR and MMR) and Adverse Events (AEs) in Patients with Chronic Myeloid Leukemia (CML) Receiving IM as Frontline Therapy.

J. Nedelman, R. Larson, M. Baccarani, 2009 .

Nilotinib versus imatinib in patients (pts) with newly diagnosed chronic myeloid leukemia in chronic phase (CML-CP): ENESTnd 3-year (yr) follow-up (f/u).

I. Flinn, R. Larson, H. Kantarjian, 2012 .

EPIC: A phase III trial of ponatinib (PON) versus imatinib (IM) in patients (pts) with newly diagnosed CP-CML.

T. Clackson, M. Baccarani, H. Kantarjian, 2014 .

Clinical utility of genomic DNA Q-PCR for the monitoring of a patient with atypical e19a2 BCR-ABL1 transcripts in chronic myeloid leukemia

T. Hughes, S. Branford, P. Dang, 2020, Leukemia & lymphoma.

ENESTop 5-Year Update: Durability of Treatment-Free Remission Following Second-Line Nilotinib and Exploratory Analysis of Molecular Response Regain after Nilotinib Re-Initiation in Patients with Chronic Myeloid Leukemia

J. Lipton, N. Takahashi, F. Mahon, 2020 .

ENESTop 192-week results: Treatment-free remission (TFR) in patients (pts) with chronic myeloid leukemia in chronic phase (CML-CP) after stopping second-line (2L) nilotinib (NIL).

J. Lipton, N. Takahashi, F. Mahon, 2019, Journal of Clinical Oncology.

Response dynamics to nilotinib depend on the type of BCR-ABL mutations in patients with chronic myelogenous leukemia (CML) after imatinib failure

M. Baccarani, G. Martinelli, G. Saglio, 2007 .

Efficacy and Safety of Ponatinib in Chronic Phase-Chronic Myeloid Leukemia (CP-CML) According to the Extent of Treatment with Prior Tyrosine Kinase Inhibitors (TKIs): Final (5-Year) Results of the PACE Study

H. Kantarjian, J. Cortes, M. Deininger, 2017 .

myeloid leukemia in chronic phase treated with frontline nilotinib or Early molecular response predicts outcomes in patients with chronic

R. Larson, H. Kantarjian, R. Ribeiro, 2014 .

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 .

S884 COMBINATION OF ASCIMINIB PLUS NILOTINIB (NIL) OR DASATINIB (DAS) IN PATIENTS (PTS) WITH CHRONIC MYELOID LEUKEMIA (CML): RESULTS FROM A PHASE 1 STUDY

J. Cortes, M. Talpaz, M. Mauro, 2019, HemaSphere.

CML-466 Asciminib Provides Durable Molecular Responses in Patients With Chronic Myeloid Leukemia in Chronic Phase (CML-CP) With the T315I Mutation: Updated Efficacy and Safety Data From a Phase I Trial.

M. Talpaz, M. Mauro, A. Hochhaus, 2022, Clinical lymphoma, myeloma & leukemia.

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 .

Therapeutic concentrations of dasatinib inhibit in vitro osteoclastogenesis

A. Zannettino, K. Vandyke, S. Fitter, 2009, Leukemia.

Molecular Response at 3 Months On Nilotinib Therapy Predicts Response and Long-Term Outcomes in Patients with Imatinib-Resistant or -Intolerant Chronic Myeloid Leukemia in Chronic Phase (CML-CP).

Martin C. Müller, L. Beppu, J. Radich, 2009 .

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

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

Management of Pregnancy in Women With Chronic Myeloid Leukemia.

J. Seymour, T. Hughes, K. Burbury, 2018, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.

Arterial Occlusive Events (AOEs) in the Phase 2 Ponatinib PACE Trial: 5-Year Update in Heavily Treated Patients (Pts) with Chronic-Phase Chronic Myeloid Leukemia (CP-CML)

T. Clackson, H. Kantarjian, J. Cortes, 2017 .

COVID-19 in Patients (pts) with Chronic Myeloid Leukemia (CML): Results from the International CML Foundation (iCMLf) CML and COVID-19 (CANDID) Study

J. Cortes, Q. Jiang, M. Mauro, 2020, Blood.

Patient-Reported Quality of Life before and after Stopping Treatment in the ENESTop Trial of Treatment-Free Remission for Patients with Chronic Myeloid Leukemia in Chronic Phase

A. Gnanasakthy, J. Lipton, N. Takahashi, 2016 .

Chronic Myeloid Leukemia Patients with Deep Molecular Responses to Tyrosine Kinase Inhibitors Have Increased Effector Natural Killer and Cytotoxic T Cell Immune Responses to Leukaemia-Associated Antigens and Concomitant Reduced Immune Suppressors

T. Hughes, Amy Hughes, A. Yong, 2015 .

Abstract MP25: Brain Atrophy And White Matter Injury In Relation To Cardiovascular Risk Factors And Race/ethnicity: The Multi-ethnic Study Of Atherosclerosis

L. Chen, P. Greenland, G. Erus, 2021 .

Alloreactive cytotoxic T-cell frequency analysis and HLA matching for bone marrow transplants from HLA matched unrelated donors.

S. Mackinnon, J. Goldman, T. Hughes, 1989, Transplantation proceedings.

Effect of continued imatinib (IM) in pts with detectable BCR-ABL after ≥ 2 years on study on deep molecular responses (MR): 36-month update from ENESTcmr.

B. Leber, S. Kamel‐Reid, J. Lipton, 2014 .

Long-Term Outcomes in Patients with Chronic Myeloid Leukemia in Chronic Phase Receiving Frontline Nilotinib Versus Imatinib: Enestnd 10-Year Analysis

I. Flinn, R. Larson, R. Clark, 2019, Blood.

Clinical Impact Of Dose Modification On Response To Ponatinib In Patients With Chronic Phase Chronic Myeloid Leukemia (CP-CML)

Martin C. Müller, T. Clackson, M. Baccarani, 2013 .

ASXL1 and BIM germ line variants predict response and identify CML patients with the greatest risk of imatinib failure.

Paul P. S. Wang, J. Reynolds, H. Scott, 2017, Blood advances.

Imatinib Dose Interruption in Responding CML Patients Is Associated with Characteristic BCR-ABL Kinetics, Which Could Help to Differentiate Non-Adherence From Drug Resistance

T. Hughes, S. Branford, D. Yeung, 2011 .

Efficacy and Safety of Ponatinib in CP-CML Patients By Number of Prior Tyrosine Kinase Inhibitors: 4-Year Follow-up of the Phase 2 PACE Trial

Martin C. Müller, M. Baccarani, H. Kantarjian, 2015 .

Impact of dose reductions on 5-year efficacy in newly diagnosed patients with chronic myeloid leukemia in chronic phase (CML-CP) from DASISION.

H. Kantarjian, J. Cortes, E. Jabbour, 2017 .

Impact Of Baseline (BL) Mutations, Including Low-Level and Compound Mutations, On Ponatinib Response and End Of Treatment (EOT) Mutation Analysis In Patients (Pts) With Chronic Phase Chronic Myeloid Leukemia (CP-CML)

Martin C. Müller, T. Clackson, M. Baccarani, 2013 .

Production of GM-CSF by CML Cells Can Modulate the Anti-Proliferative and Pro-Apoptotic Effects of Imatinib on CML CD34+ Cells.

A. B. Lyons, T. Hughes, P. Viboonjuntra, 2005 .

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

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

ENESTnd Update: Nilotinib (NIL) Vs Imatinib (IM) In Patients (pts) With Newly Diagnosed Chronic Myeloid Leukemia In Chronic Phase (CML-CP) and The Impact Of Early Molecular Response (EMR) and Sokal Risk At Diagnosis On Long-Term Outcomes

I. Flinn, R. Larson, R. Clark, 2013 .

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 .

Pre-Imatinib Factors Can Be Used To Define the Risk of BCR-ABL Mutations for Patients with CML in Chronic Phase and Identify a Minority Who Should Have Regular Mutation Screening.

Z. Rudzki, T. Hughes, S. Branford, 2005 .

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

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

Cumulative Incidence of Treatment-Free Remission (TFR) for Patients with Chronic Myeloid Leukemia (CML): The Adelaide Experience

T. Hughes, S. Branford, D. Yeung, 2017 .

Molecular Response of ≤10% BCR::ABL1IS Is Predictive of Positive Outcomes in Treatment-Resistant Patients with Chronic Phase Chronic Myeloid Leukemia (CP-CML) Treated with Ponatinib from the Phase 2 Optic Trial

G. Rosti, J. Cortes, M. Deininger, 2022, 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 .

A phase II study of AMN107, a novel inhibitor of Bcr-Abl, administered to imatinib-resistant or intolerant patients (pts) with Ph+ chronic myelogenous leukemia (CML) in blast crisis (BC) or relapsed/refractory Ph+ acute lymphoblastic leukemia (ALL).

R. Larson, M. Baccarani, H. Kantarjian, 2006, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.