A. Reid

发表

Large deletions at the t(9;22) breakpoint are common and may identify a poor-prognosis subgroup of patients with chronic myeloid leukemia.

M. Leversha, A. Green, J. Chang, 2000, Blood.

Clinical drug resistance linked to interconvertible phenotypic and functional states of tumor-propagating cells in multiple myeloma.

M. Dimopoulos, K. Naresh, C. Barnes, 2012, Blood.

Lineage-Specific Genes Are Prominent DNA Damage Hotspots during Leukemic Transformation of B Cell Precursors

L. Castellano, J. Stebbing, P. May, 2017, Cell reports.

Imatinib improves but may not fully reverse the poor prognosis of patients with CML with derivative chromosome 9 deletions.

A. Green, R. Clark, G. Vassiliou, 2003, Blood.

Derivative chromosome 9 deletions in chronic myeloid leukemia: poor prognosis is not associated with loss of ABL-BCR expression, elevated BCR-ABL levels, or karyotypic instability.

L. Campbell, A. Green, A. Bench, 2002, Blood.

Efficacy of tyrosine kinase inhibitors (TKIs) as third-line therapy in patients with chronic myeloid leukemia in chronic phase who have failed 2 prior lines of TKI therapy.

K. Rezvani, D. Marin, J. Goldman, 2010, Blood.

Antagonistic activities of the immunomodulator and PP2A-activating drug FTY720 (Fingolimod, Gilenya) in Jak2-driven hematologic malignancies.

M. Caligiuri, O. Abdel-Wahab, R. Levine, 2013, Blood.

The level of BCR-ABL1 kinase activity before treatment does not identify chronic myeloid leukemia patients who fail to achieve a complete cytogenetic response on imatinib

J. Melo, D. Marin, J. Goldman, 2009, Haematologica.

European LeukemiaNet criteria for failure or suboptimal response reliably identify patients with CML in early chronic phase treated with imatinib whose eventual outcome is poor.

K. Rezvani, D. Marin, J. Goldman, 2008, Blood.

2 prior lines of TKI therapy failed patients with chronic myeloid leukemia in chronic phase who have Efficacy of tyrosine kinase inhibitors (TKIs) as third-line therapy in

K. Rezvani, J. Goldman, L. Foroni, 2013 .

Early prediction of success or failure of treatment with second-generation tyrosine kinase inhibitors in patients with chronic myeloid leukemia

D. Marin, T. Holyoake, J. Goldman, 2010, Haematologica.

Finding of kinase domain mutations in patients with chronic phase chronic myeloid leukemia responding to imatinib may identify those at high risk of disease progression.

D. Marin, J. Goldman, D. Milojković, 2008, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.

Molecular Monitoring of Chronic Myeloid Leukemia.

A. Reid, K. Mokretar, K. Dominy, 2019, Methods in molecular biology.

Variant Isoforms of BCR-ABL1 in Chronic Myelogenous Leukemia Reflect Alternative Splicing of ABL1 in Normal Tissue – Letter

D. Milojković, A. Reid, J. Khorashad, 2010, Molecular Cancer Therapeutics.

Preclinical and clinical efficacy of XPO1/CRM1 inhibition by the karyopherin inhibitor KPT-330 in Ph+ leukemias.

M. Caligiuri, R. Garzon, J. Goldman, 2013, Blood.

Significant weight gain in patients with chronic myeloid leukemia after imatinib therapy.

D. Marin, J. Goldman, L. Foroni, 2012, Blood.

Interphase FISH using a BCL3 probe to diagnose the t(14;19)(q32;q13)-positive small B-cell leukemia

K. Naresh, A. Reid, S. Wagner, 2008, Leukemia & lymphoma.

RAPID CONVERSION OF CHRONIC MYELOID LEUKEMIA TO CHRONIC MYELOMONOCYTIC LEUKEMIA IN A PATIENT ON IMATINIB THERAPY

Gabor T. Marth, G. Marth, M. Deininger, 2016, Leukemia.

In vivo kinetics of kinase domain mutations in CML patients treated with dasatinib after failing imatinib.

D. Marin, J. Goldman, P. Mehta, 2008, Blood.

Does the P 2 X 1 del variant lacking 17 amino acids in its extracellular domain represent a relevant functional ion channel in platelets ?

L. Campbell, A. Green, D. Niederwieser, 2002 .

BCR-ABL1 compound mutations in tyrosine kinase inhibitor-resistant CML: frequency and clonal relationships.

P. Szankasi, D. Marin, B. Druker, 2013, Blood.

T cell lymphoblastic leukaemia/lymphoma associated with a microenvironment of thymic asteroid B cells in the bone marrow

K. Naresh, P. May, A. Reid, 2010, Histopathology.

Duplex quantitative PCR for molecular monitoring of BCR‐ABL1‐associated hematological malignancies

D. Marin, J. Goldman, L. Foroni, 2011, American journal of hematology.

Cardiac iron overload assessed by T2* magnetic resonance imaging and cardiac function in regularly transfused myelodysplastic syndrome patients

D. Marin, J. Goldman, D. Milojković, 2014 .

Does a rise in the BCR‐ABL1 transcript level identify chronic phase CML patients responding to imatinib who have a high risk of cytogenetic relapse?

K. Rezvani, D. Marin, J. Goldman, 2009, British journal of haematology.

Poor outcome after reintroduction of imatinib in patients with chronic myeloid leukemia who interrupt therapy on account of pregnancy without having achieved an optimal response.

K. Rezvani, D. Marin, J. Goldman, 2010, Blood.

Multiple sub-microscopic genomic lesions are a universal feature of chronic myeloid leukaemia at diagnosis

H. Fiegler, J. Goldman, L. Foroni, 2008, Leukemia.

A potential role for PRDM12 in the pathogenesis of chronic myeloid leukaemia with derivative chromosome 9 deletion

A. Reid, E. Nacheva, 2004, Leukemia.

Survival implications of molecular heterogeneity in variant Philadelphia‐positive chronic myeloid leukaemia

A. Green, B. Huntly, A. Reid, 2003, British journal of haematology.

Excellent outcome after repeated changes of tyrosine kinase inhibitor therapy for chronic myeloid leukaemia in complete cytogenetic response due to minor side effects

K. Rezvani, D. Marin, J. Goldman, 2014, British journal of haematology.

BCR‐ABL1 kinase domain mutations: Methodology and clinical evaluation

D. Marin, J. Goldman, L. Foroni, 2012, American journal of hematology.

karyopherin inhibitor KPT-330 in Ph Preclinical and clinical efficacy of XPO 1 / CRM 1 inhibition by the

M. Caligiuri, R. Garzon, J. Goldman, 2013 .

Philadelphia-negative clonal hematopoiesis is a significant feature of dasatinib therapy for chronic myeloid leukemia.

D. Marin, J. Goldman, D. Milojković, 2007, Blood.

EVI-1 oncogene expression predicts survival in chronic-phase CML patients resistant to imatinib treated with second-generation tyrosine kinase inhibitors.

R. Clark, D. Marin, J. Goldman, 2010, Blood.

Brief report EVI-1 oncogene expression predicts survival in chronic-phase CML patients resistant to imatinib treated with second-generation tyrosine kinase inhibitors

D. Marin, J. Goldman, L. Foroni, 2010 .

Brief report Poor adherence is the main reason for loss of CCyR and imatinib failure for chronic myeloid leukemia patients on long-term therapy

K. Rezvani, D. Marin, J. Goldman, 2011 .

Double Philadelphia masquerading as chromosome 20q deletion – a new recurrent abnormality in chronic myeloid leukaemia blast crisis

L. Campbell, A. Green, S. Swanton, 2003, British journal of haematology.

A t(12;17)(p13;q12) identifies a distinct TEL rearrangement-negative subtype of precursor-B acute lymphoblastic leukemia.

D. Betts, A. Reid, F. Niggli, 2006, Cancer genetics and cytogenetics.

Short communication A t(12;17)(p13;q12) identifies a distinct TEL rearrangement-negative subtype of precursor-B acute lymphoblastic leukemia

D. Betts, A. Reid, F. Niggli, 2006 .

Phenotype of blasts in chronic myeloid leukemia in blastic phase-Analysis of bone marrow trephine biopsies and correlation with cytogenetics.

K. Naresh, D. Marin, A. Reid, 2009, Leukemia research.

A new rapid and sensitive assay for detecting the T315I BCR-ABL kinase domain mutation in chronic myeloid leukaemia

J. Goldman, L. Foroni, N. Thelwell, 2008, Journal of Clinical Pathology.

The Natural History of RTQ-PCR Levels After the Achievement of Complete Molecular Remission (CMR): Implications for ‘Stopping' Studies

D. Marin, J. Goldman, L. Foroni, 2011 .

Efficacy of combining dasatinib and FLAG-IDA for patients with chronic myeloid leukemia in blastic transformation

D. Marin, L. Foroni, A. Reid, 2012, Haematologica.

Efficacy of combining dasatinib and intensive chemotherapy for patients with chronic myeloid leukemia in blastic transformation

D. Marin, L. Foroni, A. Reid, 2011 .

FISH mapping of Philadelphia negative BCR/ABL1 positive CML

D. Marin, A. Reid, J. Apperley, 2008, Molecular Cytogenetics.

The Genetic Basis of Haematological Cancers: Tosi/The Genetic Basis of Haematological Cancers

A. Reid, S. Tosi, 2016 .

8 – Molecular and Cytogenetic Analysis

L. Foroni, G. Gerrard, A. Reid, 2017 .

Persistence of Drug-Resistant Leukemic Stem Cells and Impaired NK Cell Immunity in CML Patients Depend on MIR300 Antiproliferative and PP2A-Activating Functions.

R. Garzon, B. Calabretta, M. Deininger, 2020, Blood cancer discovery.

a powerful and independent prognostic indicator in chronic myeloid leukemia

L. Campbell, A. Green, J. Szer, 2001 .

Adherence is the critical factor for achieving molecular responses in patients with chronic myeloid leukemia who achieve complete cytogenetic responses on imatinib.

D. Marin, J. Goldman, L. Foroni, 2010, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.

Specific patterns of chromosomal gains and losses associate with t(3;14), t(8;14), and t(14;18) in diffuse large B-cell lymphoma.

A. Reid, S. Wagner, Richard Szydlo, 2009, Cancer genetics and cytogenetics.

Technical aspects and clinical applications of measuring BCR‐ABL1 transcripts number in chronic myeloid leukemia

Letizia Foroni, John Goldman, D. Marin, 2009, American journal of hematology.

Responses to second-line tyrosine kinase inhibitors are durable: an intention-to-treat analysis in chronic myeloid leukemia patients.

L. Staudt, A. Rosenwald, T. Greiner, 2012, Blood.

Carfilzomib Enhances the Suppressive Effect of Ruxolitinib in Myelofibrosis

K. Naresh, M. Deininger, K. Ponnusamy, 2021, Cancers.

Poor adherence is the main reason for loss of CCyR and imatinib failure for chronic myeloid leukemia patients on long-term therapy.

K. Rezvani, D. Marin, J. Goldman, 2010, Blood.

Regulation of multiple myeloma survival and progression by CD1d.

K. Naresh, E. Terpos, I. Kotsianidis, 2008, Blood.

LMTK3 Represses Tumor Suppressor-like Genes through Chromatin Remodeling in Breast Cancer.

V. T. Nguyen, L. Magnani, L. Buluwela, 2015, Cell reports.

Hotspots during Leukemic Transformation of B Cell Precursors Graphical

L. Castellano, J. Stebbing, P. May, 2017 .

The genetics of chronic myelogenous leukaemia

D. Perrotti, M. Alikian, P. May, 2016 .

Imatinib for newly diagnosed patients with chronic myeloid leukemia: incidence of sustained responses in an intention-to-treat analysis.

Jaspal Kaeda, D. Marin, J. Goldman, 2008, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.

Proteasome 26S subunit, non-ATPases 1 (PSMD1) and 3 (PSMD3), play an oncogenic role in chronic myeloid leukemia by stabilizing nuclear factor-kappa B

B. Druker, L. Jave-Suárez, A. Reid, 2021, Oncogene.

PP2A-activating drugs selectively eradicate TKI-resistant chronic myeloid leukemic stem cells.

M. Caligiuri, J. Byrd, C. Croce, 2013, The Journal of clinical investigation.

RT-qPCR and RT-Digital PCR: A Comparison of Different Platforms for the Evaluation of Residual Disease in Chronic Myeloid Leukemia.

Jim F Huggett, Alexandra S Whale, Simon Cowen, 2016, Clinical chemistry.

intention-to-treat analysis in chronic myeloid leukemia patients Responses to second-line tyrosine kinase inhibitors are durable: an

K. Rezvani, D. Marin, J. Goldman, 2013 .

Assessment of BCR-ABL1 transcript levels at 3 months is the only requirement for predicting outcome for patients with chronic myeloid leukemia treated with tyrosine kinase inhibitors.

Katayoun Rezvani, Letizia Foroni, K. Rezvani, 2012, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.

Molecular cytogenetics of polycythaemia vera: lack of occult rearrangements detectable by 20q LSP screening, CGH, and M-FISH

A. Green, A. Bench, E. Nacheva, 2003, Leukemia.

Identification of genetic targets in acute myeloid leukaemia for designing targeted therapy

A. Reid, C. Mason, J. Apperley, 2020, British journal of haematology.

A simple FISH assay for the detection of 3q26 rearrangements in myeloid malignancy

D. Betts, E. Nacheva, A. Reid, 2008, Leukemia.

MYC and BCL2 evaluation in routine diagnostics of aggressive B‐cell lymphomas – presentation of a work‐flow and the experience with 248 cases

K. Naresh, R. Flora, Raida Ahmad, 2017, British journal of haematology.

PTCH1 expression at diagnosis predicts imatinib failure in chronic myeloid leukaemia patients in chronic phase

R. Clark, D. Marin, L. Foroni, 2015, American journal of hematology.

Combining BCR-ABL1 transcript levels at 3 and 6 months in chronic myeloid leukemia: implications for early intervention strategies.

K. Rezvani, R. Clark, D. Marin, 2013, Blood.

Diagnosis of Burkitt lymphoma using an algorithmic approach – applicable in both resource‐poor and resource‐rich countries

K. Naresh, I. Magrath, L. Leoncini, 2011, British journal of haematology.

The 14q32.31 DLK1-DIO3 MIR300 tumor suppressor promotes leukemogenesis by inducing cancer stem cell quiescence and inhibiting NK cell anti-cancer immunity

R. Garzon, B. Calabretta, M. Deininger, 2019, bioRxiv.

Long Term Adherence to Imatinib Therapy Is the Critical Factor for Achieving Molecular Responses in Chronic Myeloid Leukemia Patients.

D. Marin, J. Goldman, L. Foroni, 2009 .

Prediction of Cytogenetic Response to Second Generation TKI Therapy in CML Chronic Phase Patients Who Have Failed Imatinib Therapy and Early Identification of Factors That Influence Survival

D. Marin, J. Goldman, L. Foroni, 2008 .

hOCT1 transcript levels and single nucleotide polymorphisms as predictive factors for response to imatinib in chronic myeloid leukemia

D. Marin, J. Goldman, L. Foroni, 2010, Leukemia.

myeloid leukemia: implications for early intervention strategies Combining BCR-ABL1 transcript levels at 3 and 6 months in chronic

K. Rezvani, D. Marin, J. Goldman, 2013 .

Can the Combination of the Measurement of BCR-ABL1 Transcript Levels At 3 and 6 Months Improve the Prognostic Value of the 3 Month Measurement?

D. Marin, J. Goldman, L. Foroni, 2012 .

Deletions adjacent to BCR and ABL1 breakpoints occur in a substantial minority of chronic myeloid leukemia patients with masked Philadelphia rearrangements.

D. Marin, A. Reid, J. Apperley, 2008, Cancer genetics and cytogenetics.

BCL3 rearrangement, amplification and expression in diffuse large B‐cell lymphoma

K. Naresh, A. Reid, F. Amen, 2011, European journal of haematology.

Deletions of the derivative chromosome 9 do not account for the poor prognosis associated with Philadelphia-positive acute lymphoblastic leukemia.

L. Campbell, A. Green, D. Niederwieser, 2002, Blood.

chronic myeloid leukemia translocation and provide a powerful and independent prognostic indicator in Deletions of the derivative chromosome 9 occur at the time of the Philadelphia

L. Campbell, A. Green, A. Bench, 2008 .

Next-Generation Sequencing-Assisted DNA-Based Digital PCR for a Personalized Approach to the Detection and Quantification of Residual Disease in Chronic Myeloid Leukemia Patients.

D. Kasperavičiūtė, J. Huggett, Michael Mueller, 2016, The Journal of molecular diagnostics : JMD.

for chronic myeloid leukemia patients on long-term therapy Poor adherence is the main reason for loss of CCyR and imatinib failure

K. Rezvani, D. Marin, L. Foroni, 2013 .

Responses to second-line tyrosine kinase inhibitors are durable : an intention-to-treat analysis in chronic myeloid leukemia patients

K. Rezvani, D. Marin, J. Goldman, 2012 .

Responses to second-line tyrosine kinase inhibitors are durable: an intention-to-treat analysis in chronic myeloid leukemia patients.

K. Rezvani, D. Marin, J. Goldman, 2012, Blood.

EVI-1 oncogene expression predicts survival in chronic-phase CML patients resistant to imatinib treated with second-generation tyrosine kinase inhibitors.

R. Clark, D. Marin, J. Goldman, 2010, Blood.

Assessment of BCR-ABL1 Transcript Levels At 3 Months Is the Only Requirement for Predicting Outcome for Patients with Chronic Myeloid Leukemia Treated with Imatinib

R. Clark, D. Marin, J. Goldman, 2011 .

Clinical drug resistance linked to interconvertible phenotypic and functional states of tumor-propagating cells in multiple myeloma.

Chris P. Barnes, M. Dimopoulos, K. Naresh, 2012, Blood.

ALK‐positive anaplastic large cell lymphoma presenting with hemophagocytic lymphohistiocytosis

B. Bain, A. Reid, M. Shah, 2015, American journal of hematology/oncology.

Development of artificial bone marrow fibre scaffolds to study resistance to anti‐leukaemia agents

M. Edirisinghe, A. Reid, J. Khorashad, 2018, British journal of haematology.

Poor outcome after reintroduction of imatinib in patients with chronic myeloid leukemia who interrupt therapy on account of pregnancy without having achieved an optimal response.

K. Rezvani, D. Marin, J. Goldman, 2010, Blood.