S. Branford

发表

Martin A. Nowak, Yoh Iwasa, Franziska Michor, 2005, Nature.

Rationale for the recommendations for harmonizing current methodology for detecting BCR-ABL transcripts in patients with chronic myeloid leukaemia

J. Goldman, N. Cross, G. Saglio, 2006, Leukemia.

Frequency of major molecular responses to imatinib or interferon alfa plus cytarabine in newly diagnosed chronic myeloid leukemia.

Susan Branford, Andreas Hochhaus, Jaspal Kaeda, 2003, The New England journal of medicine.

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

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

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.

Chronic myeloid leukemia: molecular monitoring in clinical practice.

S. Branford, 2007, Hematology. American Society of Hematology. Education Program.

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.

Indirect Sandwich Enzyme-Linked Immunosorbent Assay (ELISA) for Plasma Apolipoprotein E

P. Barter, R. Bais, S. Branford, 1996, Annals of clinical biochemistry.

Monitoring disease response in chronic-phase chronic myeloid leukemia: the age of molecular assays?

S. Branford, D. Yeung, 2012, Hematology. American Society of Hematology. Education Program.

Genomic Mechanisms Influencing Outcome in Chronic Myeloid Leukemia

S. Branford, N. Shanmuganathan, A. Fernandes, 2022, Cancers.

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.

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 .

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.

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.

Clonal evolution and clinical implications of genetic abnormalities in blastic transformation of chronic myeloid leukaemia

S. Miyano, Y. Shiraishi, K. Chiba, 2021, Nature Communications.

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.

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 .

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.

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

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

Practical advice for determining the role of BCR‐ABL mutations in guiding tyrosine kinase inhibitor therapy in patients with chronic myeloid leukemia

H. Kantarjian, J. Cortes, E. Jabbour, 2011, Cancer.

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.

Delayed diagnosis leading to accelerated-phase chronic eosinophilic leukemia due to a cytogenetically cryptic, imatinib-responsive TNIP1–PDFGRB fusion gene

H. Scott, A. Schreiber, J. Geoghegan, 2016, Leukemia.

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.

Sensitive detection and quantification of minimal residual disease in chronic myeloid leukaemia using nested quantitative PCR for BCR‐ABL DNA

A. Morley, S. Branford, D. Ross, 2010, International journal of laboratory hematology.

Optimal Monitoring of CML Treatment: Molecular and Mutation Analysis

S. Branford, D. Yeung, 2016 .

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

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

Paper or plastic? BCR-ABL1 quantitation and mutation detection from dried blood spots.

L. Beppu, J. Radich, Jordan L Smith, 2016, Blood.

Characterization of a reference material for BCR-ABL (M-BCR) mRNA quantitation by real-time amplification assays: towards new standards for gene expression measurements

J. Cayuela, T. Lion, J. Saldanha, 2007, Leukemia.

Why is it critical to achieve a deep molecular response in chronic myeloid leukemia?

S. Branford, 2020, Haematologica.

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-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.

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.

Monitoring after successful therapy for chronic myeloid leukemia.

S. Branford, 2012, Hematology. American Society of Hematology. Education Program.

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 .

A novel, somatic, transforming mutation in the extracellular domain of Epidermal Growth Factor Receptor identified in myeloproliferative neoplasm

R. D'Andrea, A. Wee, I. Lewis, 2017, Scientific Reports.

Defining Higher-Risk Chronic Myeloid Leukemia: Risk Scores, Genomic Landscape, and Prognostication

S. Branford, C. Wadham, N. H. Shahrin, 2022, Current Hematologic Malignancy Reports.

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 .

Dasatinib (SPRYCEL®) in Patients (pts) with Chronic Myelogenous Leukemia in Accelerated Phase (AP-CML) That Is Imatinib-Resistant (im-r) or -Intolerant (im-i): Updated Results of the CA180–005 ’START-A’ Phase II Study.

J. Cortes, A. Gollerkeri, R. Silver, 2006 .

RNA-based targeted gene sequencing improves the diagnostic yield of mutant detection in chronic myeloid leukemia.

Paul P. S. Wang, D. Thomson, A. Schreiber, 2022, The Journal of molecular diagnostics : JMD.

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 .

BCR::ABL1 transcripts and clinical outcome ‐ interrogating the technique

S. Branford, 2022, British Journal of Haematology.

Commentary on Dominy et al., assessment of quantitative PCR for BCR::ABL1 Transcripts in CML: Are improved outcomes in patients with e14a2 transcripts an artefact of technology?

S. Branford, 2022, British journal of haematology.

S. Branford, T. Hughes, N. Shanmuganathan, 2021, Hematologic Malignancies.

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 and defining early response: Where to draw the line?

S. Branford, 2016, Best practice & research. Clinical haematology.

Development and evaluation of a secondary reference panel for BCR-ABL1 quantification on the International Scale

D. Colomer, R. Zadro, N. Cross, 2016, Leukemia.

Development and evaluation of a secondary reference panel for BCR-ABL1 quanti ﬁ cation on the International Scale

D. Colomer, R. Zadro, H. White, 2016 .

Development and evaluation of a secondary reference panel for BCR-ABL1 quantitation on the International Scale OPEN

R. Zadro, N. Cross, H. White, 2016 .

International Reporting Scale of BCR-ABL1 Fusion Transcript in Chronic Myeloid Leukemia: First Report from India

B. George, E. Chendamarai, P. Balasubramanian, 2012, Acta Haematologica.

Original Article

C. Watt, V. V. Van Deerlin, E. Labourier, 2013 .

Patients with chronic myeloid leukemia who maintain a complete molecular response after stopping imatinib treatment have evidence of persistent leukemia by DNA PCR

J. Melo, A. Schwarer, J. Seymour, 2010, Leukemia.

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.

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.

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.

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.

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 .

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 .

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.

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 .

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.

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.

Chronic Myelogenous Leukemia: Monitoring Response to Therapy

S. Branford, Jodi A. Prime, 2011, Current hematologic malignancy reports.

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 .

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.

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 .

Single Molecule Real Time (SMRT™) Sequencing Sensitively Detects the Evolution of Polyclonal and Compound BCR-ABL Mutations in Patients Who Relapse On Kinase Inhibitor Therapy

K. Travers, Susana Wang, Catherine C. Smith, 2012 .

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 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.

Molecular monitoring in chronic myeloid leukemia-how low can you go?

S. Branford, 2016, Hematology. American Society of Hematology. Education Program.

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.

Current developments in molecular monitoring in chronic myeloid leukemia

S. Branford, J. Marum, 2016, Therapeutic advances in hematology.

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

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

e8a2 BCR–ABL: more frequent than other atypical BCR–ABL variants?

P. Paschka, G. Martinelli, A. Hochhaus, 2005, Leukemia.

Grass carp (Ctenopharyngodon idella) translocations, including hitchhiker introductions, alter zooplankton communities in receiving ponds

S. Branford, I. Duggan, 2017 .

Defining Higher-Risk Chronic Myeloid Leukemia: Risk Scores, Genomic Landscape, and Prognostication

S. Branford, C. Wadham, N. H. Shahrin, 2022, Current Hematologic Malignancy Reports.

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.

International Consensus Classification of Myeloid Neoplasms and Acute Leukemia: Integrating Morphological, Clinical, and Genomic Data.

M. Loh, E. Estey, M. Cazzola, 2022, Blood.

Taming the gatekeeper: ponatinib dose holds the key.

S. Branford, 2021, Blood.

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.

Measurable residual disease in chronic myeloid leukemia

J. Apperley, S. Branford, 2022, Haematologica.

Epigenetic modifier gene mutations in chronic myeloid leukemia (CML) at diagnosis are associated with risk of relapse upon treatment discontinuation

S. Mustjoki, M. Kankainen, O. Brück, 2022, Blood Cancer Journal.

The allosteric inhibitor ABL001 enables dual targeting of BCR–ABL1

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

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.

The Hidden Pathogenesis of CML: Is BCR-ABL1 the First Event?

S. Branford, N. Shanmuganathan, 2019, Current Hematologic Malignancy Reports.

A comparative analysis of algorithms for somatic SNV detection in cancer

R. Daniel Kortschak, David L. Adelson, Andreas W. Schreiber, 2013, Bioinform..

Dasatinib induces complete hematologic and cytogenetic responses in patients with imatinib-resistant or -intolerant chronic myeloid leukemia in blast crisis.

M. Baccarani, J. Cortes, A. Gollerkeri, 2007, Blood.

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.

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

J. Radich, M. Baccarani, J. Gabert, 2011 .

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.

De novo UBE2A mutations are recurrently acquired during chronic myeloid leukemia progression and interfere with myeloid differentiation pathways

Paul P. S. Wang, Nitesh D. Sharma, R. Rigolio, 2019, 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.

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.

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.

Harmonization of molecular monitoring of chronic myeloid leukemia therapy in Japan

J. Sakamoto, Toshikazu Yamaguchi, M. Shiseki, 2012, International Journal of Clinical Oncology.

Molecular methods in diagnosis and monitoring of haematological malignancies

S. Branford, D. Yeung, W. Parker, 2011, Pathology.

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.

Integrating genetic and epigenetic factors in chronic myeloid leukemia risk assessment: toward gene expression-based biomarkers

S. Branford, S. Ong, V. Krishnan, 2021, Haematologica.

Monitoring disease response to tyrosine kinase inhibitor therapy in CML.

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

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.

CRISPR-Cas9–mediated saturated mutagenesis screen predicts clinical drug resistance with improved accuracy

Michael R. Green, C. Schiffer, D. Bolon, 2017, Proceedings of the National Academy of Sciences.

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

Susan Branford, Ricardo Pasquini, Fabrizio Pane, 2010, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.

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.

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.

Dasatinib induces significant hematologic and cytogenetic responses in patients with imatinib-resistant or -intolerant chronic myeloid leukemia in accelerated phase.

R. Larson, M. Baccarani, J. Lipton, 2007, 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 .

Implications of BCR-ABL 1 kinase domain-mediated resistance in chronic myeloid leukemia

Martin C. Müller, J. Radich, M. Deininger, 2015 .

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.

Implications of BCR-ABL1 kinase domain-mediated resistance in chronic myeloid leukemia.

Martin C. Müller, J. Radich, G. Martinelli, 2014, Leukemia research.

What challenges remain in chronic myeloid leukemia research?

M. Deininger, J. Goldman, G. Saglio, 2013, Haematologica.

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.

Chronic myeloid leukaemia: The dangers of not knowing your BCR-ABL1 transcript.

S. Branford, H. Altamura, K. Taylor, 2019, Leukemia research.

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

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

Validation of a rapid one-step high sensitivity real-time quantitative PCR system for detecting major BCR-ABL1 mRNA on an International Scale

T. Naoe, I. Matsumura, Y. Kanakura, 2016, SpringerPlus.

A longitudinal evaluation of performance of automated BCR-ABL1 quantitation using cartridge-based detection system

A. Enjeti, A. Ashraf, P. Rowlings, 2015, Pathology.

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.

Establishment of a standardized multiplex assay with the analytical performance required for quantitative measurement of BCR–ABL1 on the international reporting scale

C. Watt, E. Labourier, V. Deerlin, 2011, Blood cancer journal.

Harmonization of molecular monitoring of CML therapy in Europe

N. Cross, G. Saglio, T. Schenk, 2009, Leukemia.

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.

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

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

Standardized practices for RNA diagnostics using clinically accessible specimens reclassifies 75% of putative splicing variants.

Robert J. Weatheritt, Stephanie L. White, N. Brown, 2021, Genetics in medicine : official journal of the American College of Medical Genetics.

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 .

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.

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.

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

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

RUNX1 mutations in blast-phase chronic myeloid leukemia associate with distinct phenotypes, transcriptional profiles, and drug responses

T. Aittokallio, S. Mustjoki, D. Thomson, 2020, Leukemia.

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.

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.

Reply to ‘What do we mean by sensitivity when we talk about detecting minimal residual disease?’ by Steinbach and Debatin

J. Melo, S. Branford, J V Melo, 2009, Leukemia.

Initial Rate of BCR::ABL1 Decline for Response Prediction in Chronic Myeloid Leukemia

S. Branford, 2022, Turkish journal of haematology : official journal of Turkish Society of Haematology.

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.

The mutational burden of therapy-related myeloid neoplasms is similar to primary myelodysplastic syndrome but has a distinctive distribution

Anna L. Brown, Paul P. S. Wang, J. Maciejewski, 2019, 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 .

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.

A novel BCR–ABL transcript (e8a2) with the insertion of an inverted sequence of ABL intron 1b in a patient with Philadelphia‐positive chronic myeloid leukaemia

Z. Rudzki, S. Branford, T. P. Hughes, 2000, British journal of haematology.

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 .

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 .

NGS in CML - New standard diagnostic procedure?

Susan Branford, Naranie Shanmuganathan, S. Branford, 2019, HemaSphere.

Continued therapeutic response monitoring in optimal responders with CML.

S. Branford, 2012, Clinical advances in hematology & oncology : H&O.

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 .

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 .

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 .

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

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

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 .

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.

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 .

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 .

The effect of tyrosine kinase inhibitor interruption and interferon use on pregnancy outcomes and long-term disease control in chronic myeloid leukemia

C. Tam, M. Lasica, J. Butler, 2019, Leukemia & lymphoma.

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 .

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 .

Multiplex technologies for the assessment of minimal residual disease and low‐level mutation detection in leukaemia: mass spectrometry versus next‐generation sequencing

S. Branford, N. Shanmuganathan, 2021, British journal of haematology.

Association of TIM-3 checkpoint receptor expression on T cells with treatment-free remission in chronic myeloid leukemia

C. Kok, S. Branford, D. Yeung, 2023, Blood advances.

Grass carp and incidental invaders from aquaculture: a study of impacts on zooplankton communities and invader origins

S. Branford, 2016 .

Genomic Profiling for Clinical Decision Making in Myeloid Neoplasms and Acute Leukemia.

Anna L. Brown, Annette S. Kim, M. Loh, 2022, Blood.

BAM-matcher: a tool for rapid NGS sample matching

Andreas W. Schreiber, Susan Branford, Wendy T. Parker, 2016, Bioinform..

Molecular response in newly diagnosed chronic-phase chronic myeloid leukemia: prediction modeling and pathway analysis

J. Radich, R. Larson, J. Guinney, 2023, Haematologica.

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 .

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 .

A novel, somatic, transforming mutation in the extracellular domain of Epidermal Growth Factor Receptor identified in myeloproliferative neoplasm

A. Wee, I. Lewis, H. Scott, 2017, Scientific Reports.

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 .

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

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

Monitoring chronic myeloid leukaemia therapy by real‐time quantitative PCR in blood is a reliable alternative to bone marrow cytogenetics

Branford, Z. Rudzki, S. Branford, 1999, British journal of haematology.

The e13a2 BCR-ABL1 Transcript Is Associated with Higher Rates of Molecular Recurrence after Treatment-Free Remission Attempts: Retrospective Analysis of the Adelaide Cohort

S. Branford, D. Yeung, A. Yong, 2018, Blood.

Minimal residual disease: the advantages of digital over analog polymerase chain reaction.

S. Branford, D. Ross, 2011 .

First Results from a Collaborative Initiative To Develop an International Scale for the Measurement of BCR-ABL by RQ-PCR Based on Deriving Laboratory-Specific Conversion Factors.

J. Radich, L. Shih, E. Ma, 2006 .

Mitochondrial DNA indicates different North American east coast origins for New Zealand and German invasions of Skistodiaptomus pallidus (Copepoda: Calanoida)

I. Hogg, S. Branford, I. Duggan, 2017 .

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 STI 571 ( IRIS ) *

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

Impact of additional genetic abnormalities at diagnosis of chronic myeloid leukemia for first-line imatinib-treated patients receiving proactive treatment intervention

Paul P. S. Wang, D. Thomson, H. Scott, 2023, Haematologica.

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.

Minimal residual disease: the advantages of digital over analog polymerase chain reaction

S. Branford, D. Ross, 2011, Leukemia & lymphoma.

Early Molecular Response and Female Sex Strongly Predict Achievement of Stable Undetectable BCR-ABL1, a Criterion for Imatinib Discontinuation in Patients with CML

S. Branford, D. Yeung, Chani R Field, 2012 .

Increasing Frequency and Marked Stability of Complete Molecular Response Is Observed in Imatinib-Treated CML Patients with Long-Term Follow Up.

J. Seymour, S. Branford, A. Grigg, 2006 .

Correlation of Clinical Response to Nilotinib with BCR-ABL Mutation Status in Advanced Phase Chronic Myelogenous Leukemia (CML-AP) Patients with Imatinib-Resistance or Intolerance.

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

Immune modulation in chronic myeloid leukaemia patients treated with nilotinib and interferon‐alpha

C. Kok, S. Branford, Amy Hughes, 2023, British journal of haematology.

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

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

J. Radich, B. Druker, S. O’Brien, 2010, Blood.

Monitoring and defining early response: Where to draw the line?

S. Branford, 2016, Baillière's Best Practice & Research: Clinical Haematology.

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

H. Scott, S. Branford, M. Ho, 2012, Blood.

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

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

European LeukemiaNet laboratory recommendations for the diagnosis and management of chronic myeloid leukemia.

J. Radich, S. Soverini, A. Fabarius, 2023, Leukemia.

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

Martin C. Müller, D. Colomer, J. Gabert, 2010, Blood.

Practical advice for determining the role of BCR‐ABL mutations in guiding tyrosine kinase inhibitor therapy in patients with chronic myeloid leukemia

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

Practical considerations for monitoring patients with chronic myeloid leukemia.

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