Chronic Myeloid Leukemia--Prognostic Value of Mutations.

Chronic myeloid leukemia (CML) is a stem cell disorder characterized by unrestricted proliferation of the myeloid series that occurs due to the BCR-ABL fusion oncogene as a result of reciprocal translocation t(9;22) (q34;q11). This discovery has made this particular domain a target for future efforts to cure CML. Imatinib revolutionized the treatment options for CML and gave encouraging results both in case of safety as well as tolerability profile as compared to agents such as hydroxyurea or busulfan given before Imatinib. However, about 2-4% of patients show resistance and mutations have been found to be one of the reasons for its development. European Leukemianet gives recommendations for BCR-ABL mutational analysis along with other tyrosine kinase inhibitors (TKIs) that should be administered according to the mutations harbored in a patient. The following overview gives recommendations for monitoring patients on the basis of their mutational status.

• Publication year

  2015

• Venue

  Asian Pacific Journal of Cancer Prevention

• Publication date

  Unknown publication date

• Fields of study

  Medicine

• Identifiers
  DOI 10.7314/APJCP.2015.16.17.7415PMID 26625737
• External record

  Open on Semantic Scholar

• Source metadata

  Semantic Scholar, PubMed

• No claims are published for this paper.

• No concepts are published for this paper.

• Treatment Recommendations for Chronic Myeloid Leukemia

  2014influential reference
• Clinical significance of BCR-ABL fusion gene subtypes in chronic myelogenous and acute lymphoblastic leukemias.

  2014cited by this paper
• Low level of TERC gene amplification between chronic myeloid leukaemia patients resistant and respond to imatinib mesylate treatment.

  2014cited by this paper
• The gut in iron homeostasis: role of HIF-2 under normal and pathological conditions.

  2013cited by this paper
• The quantitative level of T315I mutated BCR-ABL predicts for major molecular response to second-line nilotinib or dasatinib treatment in patients with chronic myeloid leukemia

  2013cited by this paper
• European LeukemiaNet recommendations for the management of chronic myeloid leukemia: 2013.

  2013influential reference
• BCR-ABL1 compound mutations in tyrosine kinase inhibitor-resistant CML: frequency and clonal relationships.

  2013cited by this paper
• Imatinib mesylate resistance and mutations: An Indian experience

  2013cited by this paper
• Management of imatinib-resistant patients with chronic myeloid leukemia

  2013cited by this paper
• Sensitive Detection of Pre-Existing BCR-ABL Kinase Domain Mutations in CD34+ Cells of Newly Diagnosed Chronic-Phase Chronic Myeloid Leukemia Patients Is Associated with Imatinib Resistance: Implications in the Post-Imatinib Era

  2013cited by this paper
• Abl Kinase Domain Mutations in Imatinib-treated Egyptian Patients with Chronic Myeloid Leukemia

  2013cited by this paper
• Ponatinib Is a Pan-BCR-ABL Kinase Inhibitor: MD Simulations and SIE Study

  2013cited by this paper
• Polymorphic variation in glutathione-S-transferase genes and risk of chronic myeloid leukaemia in the Kashmiri population.

  2012cited by this paper
• Re-emergence of interferon-α in the treatment of chronic myeloid leukemia

  2012cited by this paper
• Three decades of transplantation for chronic myeloid leukemia: what have we learned?

  2011cited by this paper
• Additional Chromosome Abnormalities, BCR-ABL Tyrosine Kinase Domain Mutations and Clinical Outcome in Hungarian Tyrosine Kinase Inhibitor-Resistant Chronic Myelogenous Leukemia Patients

  2011cited by this paper
• Managing Philadelphia chromosome-positive acute lymphoblastic leukemia: role of tyrosine kinase inhibitors.

  2011cited by this paper
• Practical advice for determining the role of BCR‐ABL mutations in guiding tyrosine kinase inhibitor therapy in patients with chronic myeloid leukemia

  2011cited by this paper
• Success story of targeted therapy in chronic myeloid leukemia: a population-based study of patients diagnosed in Sweden from 1973 to 2008.

  2011cited by this paper
• Structural Mechanism of the Pan‐BCR‐ABL Inhibitor Ponatinib (AP24534): Lessons for Overcoming Kinase Inhibitor Resistance

  2011cited by this paper
• BCR-ABL kinase domain mutation analysis in chronic myeloid leukemia patients treated with tyrosine kinase inhibitors: recommendations from an expert panel on behalf of European LeukemiaNet.

  2011cited by this paper
• Monitoring response and resistance to treatment in chronic myeloid leukemia.

  2011cited by this paper
• Improved survival in chronic myeloid leukemia since the introduction of imatinib therapy: a single-institution historical experience.

  2011cited by this paper
• Optimizing therapy for patients with chronic myelogenous leukemia in chronic phase

  2010cited by this paper
• Choosing the best treatment strategy for chronic myeloid leukemia patients resistant to imatinib: weighing the efficacy and safety of individual drugs with BCR-ABL mutations and patient history

  2010cited by this paper
• Chronic myeloid leukemia: an update of concepts and management recommendations of European LeukemiaNet.

  2009influential reference
• Overview of chronic myeloid leukemia patients in Pakistan in the pre-imatanib era.

  2009cited by this paper
• A co-operative evaluation of different methods of detecting BCR-ABL kinase domain mutations in patients with chronic myeloid leukemia on second-line dasatinib or nilotinib therapy after failure of imatinib

  2009cited by this paper
• P-loop mutations and novel therapeutic approaches for imatinib failures in chronic myeloid leukemia

  2008influential reference
• Dynamics of BCR-ABL mutated clones prior to hematologic or cytogenetic resistance to imatinib

  2008cited by this paper
• molecule Beyond the increasing complexity of the immunomodulatory HLA-G

  2008influential reference
• 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.

  2008cited by this paper
• Resistance to dasatinib in Philadelphia-positive leukemia patients and the presence or the selection of mutations at residues 315 and 317 in the BCR-ABL kinase domain.

  2007cited by this paper
• Bcr-Abl kinase domain mutations, drug resistance, and the road to a cure for chronic myeloid leukemia.

  2007cited by this paper
• Chronic myeloid leukaemia.

  2007cited by this paper
• Targeted Chronic Myeloid Leukemia Therapy: Seeking a Cure

  2007cited by this paper
• Clinical outcome of 27 imatinib mesylate-resistant chronic myelogenous leukemia patients harboring a T315I BCR-ABL mutation

  2007cited by this paper
• Granulocyte transfusion: current status.

  2007cited by this paper
• Resistance to targeted therapy in chronic myelogenous leukemia.

  2007cited by this paper
• Part I: mechanisms of resistance to imatinib in chronic myeloid leukaemia.

  2007cited by this paper
• Defining and managing imatinib resistance.

  2006cited by this paper
• Detection of BCR-ABL mutations and resistance to imatinib mesylate.

  2006cited by this paper
• Molecular monitoring of BCR-ABL as a guide to clinical management in chronic myeloid leukaemia.

  2006cited by this paper
• Frequency and clinical significance of BCR-ABL mutations in patients with chronic myeloid leukemia treated with imatinib mesylate

  2006influential reference
• The presence of a BCR-ABL mutant allele in CML does not always explain clinical resistance to imatinib

  2006cited by this paper
• Mutation status and clinical outcome of 89 imatinib mesylate-resistant chronic myelogenous leukemia patients: a retrospective analysis from the French intergroup of CML (Fi(ϕ)-LMC GROUP)

  2006cited by this paper
• ABL Kinase Inhibitor Therapy for CML : Baseline Assessments and Response Monitoring

  2006influential reference
• Evolving concepts in the management of chronic myeloid leukemia: recommendations from an expert panel on behalf of the European LeukemiaNet.

  2006influential reference
• Kinase Domain Mutants of Bcr-Abl Exhibit Altered Transformation Potency, Kinase Activity, and Substrate Utilization, Irrespective of Sensitivity to Imatinib

  2006cited by this paper
• Contribution of ABL Kinase Domain Mutations to Imatinib Resistance in Different Subsets of Philadelphia-Positive Patients: By the GIMEMA Working Party on Chronic Myeloid Leukemia

  2006influential reference
• Asthma Is Associated with Mortality in Children with Sickle Cell Anemia.

  2005cited by this paper
• Response and resistance in 300 patients with BCR‐ABL–positive leukemias treated with imatinib in a single center

  2005influential reference
• Double-gradient-denaturing-gradient gel electrophoresis for mutation screening of the BCR-ABL tyrosine kinase domain in chronic myeloid leukemia patients.

  2005cited by this paper
• Early Detection of Imminent Hematologic Relapse Due to BCR-ABL Kinase Domain Mutations in CML Patients on Imatinib Therapy by D-HPLC.

  2005cited by this paper
• Resistance to imatinib: mechanisms and management.

  2005cited by this paper
• A cell-based screen for resistance of Bcr-Abl-positive leukemia identifies the mutation pattern for PD166326, an alternative Abl kinase inhibitor.

  2005cited by this paper
• High-sensitivity detection of BCR-ABL kinase domain mutations in imatinib-naive patients: correlation with clonal cytogenetic evolution but not response to therapy.

  2005influential reference
• Detection of ABL kinase domain mutations with denaturing high-performance liquid chromatography

  2004cited by this paper
• Use of denaturing HPLC for detection of mutations in the BCR-ABL kinase domain in patients resistant to Imatinib.

  2004cited by this paper
• Preexistence and evolution of imatinib mesylate-resistant clones in chronic myelogenous leukemia detected by a PNA-based PCR clamping technique

  2003cited by this paper
• A myristoyl/phosphotyrosine switch regulates c-Abl.

  2003cited by this paper
• Structural basis for the autoinhibition of c-Abl tyrosine kinase.

  2003cited by this paper
• Several Bcr-Abl kinase domain mutants associated with imatinib mesylate resistance remain sensitive to imatinib.

  2003cited by this paper
• A mutation conferring resistance to imatinib at the time of diagnosis of chronic myelogenous leukemia.

  2003cited by this paper
• 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.

  2003influential reference
• Multiple BCR-ABL kinase domain mutations confer polyclonal resistance to the tyrosine kinase inhibitor imatinib (STI571) in chronic phase and blast crisis chronic myeloid leukemia.

  2002cited by this paper
• Molecular and chromosomal mechanisms of resistance to imatinib (STI571) therapy

  2002cited by this paper
• Several types of mutations of the Abl gene can be found in chronic myeloid leukemia patients resistant to STI571, and they can pre-exist to the onset of treatment.

  2002cited by this paper
• Analysis of the Structural Basis of Specificity of Inhibition of the Abl Kinase by STI571*

  2002cited by this paper
• Hematologic and cytogenetic responses to imatinib mesylate in chronic myelogenous leukemia.

  2002cited by this paper
• 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.

  2002cited by this paper
• Clinical Resistance to STI-571 Cancer Therapy Caused by BCR-ABL Gene Mutation or Amplification

  2001influential reference
• Structural mechanism for STI-571 inhibition of abelson tyrosine kinase.

  2000influential reference
• Determination of single-nucleotide polymorphisms by real-time pyrophosphate DNA sequencing.

  2000cited by this paper
• The P-loop--a common motif in ATP- and GTP-binding proteins.

  1990cited by this paper
• Primary human myeloid leukemia cells: comparative responsiveness to proliferative stimulation by GM-CSF or G-CSF and membrane expression of CSF receptors.

  1987cited by this paper
• Penn Carey Law: Legal Scholarship Repository Penn Carey Law: Legal Scholarship Repository

  year unknowncited by this paper
• Clinical Trials and Observations

  year unknowncited by this paper

• Mesenchymal stromal cells in myeloid malignancies: Immunotherapeutic opportunities

  2024cites this paper
• Myeloid-derived suppressor cells: Implication in myeloid malignancies and immunotherapy.

  2024cites this paper
• Upregulation of SNHG7 and FAIM2 Expression Levels in Chronic Myelogenous Leukemia Patients Compared with Normal Subjects

  2023cites this paper
• Disease Response Assessment Modalities in Chronic Myeloid Leukemia: Past, Present, and Future

  2023cites this paper
• Anti-Cancer Effects of Oxygen-Atom-Modified Derivatives of Wasabi Components on Human Leukemia Cells

  2023cites this paper
• Critical Requirement of SOS1 for Development of BCR/ABL-Driven Chronic Myelogenous Leukemia

  2022cites this paper
• Chronic myeloid leukemia-from the Philadelphia chromosome to specific target drugs: A literature review

  2021cites this paper
• Genetic Biomarkers in Chronic Myeloid Leukemia: What Have We Learned So Far?

  2021cites this paper
• ND-09 inhibits chronic myeloid leukemia K562 cell growth by regulating BCR-ABL signaling

  2021cites this paper
• Myeloid-Derived Suppressor Cells and Mesenchymal Stem/Stromal Cells in Myeloid Malignancies

  2021cites this paper
• Checkpoint kinase-1 inhibition and etoposide exhibit a strong synergistic anticancer effect on chronic myeloid leukemia cell line K562 by impairing homologous recombination DNA damage repair

  2020cites this paper
• Circular RNAs in Embryogenesis and Cell Differentiation With a Focus on Cancer Development

  2020cites this paper
• Mutations in the BCR-ABL1 kinase domain in patients with chronic myeloid leukaemia treated with TKIs or at diagnosis

  2020influential citation
• Practical Laboratory Tools for Monitoring of BCR-ABL1 Transcripts and Tyrosine Kinase (TK) Domain Mutations in Chronic Myeloid Leukemia Patients Undergoing TK Inhibitor Therapy: A Single-Center Experience in Thailand

  2020cites this paper
• CircRNAs: biogenesis, functions, and role in drug-resistant Tumours

  2020cites this paper
• Bias and Racism Teaching Rounds at an Academic Medical Center

  2020cites this paper
• A diverse global fungal library for drug discovery

  2020cites this paper
• Characteristics of BCR/ABL1 kinase domain mutations in the patients with chronic myeloid leukemia who are primary resistant to the imatinib therapy

  2019cites this paper
• Sweet dreams: How mini-invasive surgery tackles obstructive sleep apnea

  2019cites this paper
• Prognostic factors for overall survival in patients with chronic myeloid leukemia treated with imatinib at the National Cancer Institute – Mexico, from 2000 to 2016

  2019cites this paper
• Leucemias

  2019cites this paper
• Association between C1236T Genetic Variant of ABCB1 Gene and Molecular Response to Imatinib in Indonesian Chronic Myeloid Patients

  2019cites this paper
• Druggable Biochemical Pathways and Potential Therapeutic Alternatives to Target Leukemic Stem Cells and Eliminate the Residual Disease in Chronic Myeloid Leukemia

  2019cites this paper
• Role of circular RNA in hematological malignancies

  2019cites this paper
• Long Noncoding RNA (lncRNA) Small Nucleolar RNA Host Gene 5 (SNHG5) Regulates Proliferation, Differentiation, and Apoptosis of K562 Cells in Chronic Myeliod Leukemia

  2019cites this paper
• Occupational Radiation Exposure and Leukemia Mortality among Nuclear Workers in Japan: J-EPISODE, 1991-2010

  2018cites this paper
• Prevalence of BCR-ABL T315I Mutation in Malaysian Patients with Imatinib-Resistant Chronic Myeloid Leukemia

  2018cites this paper