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

Outcomes for patients with chronic myeloid leukemia (CML) have substantially improved due to advances in drug development and rational treatment intervention strategies. Despite these significant advances there are still unanswered questions on patient management regarding how to more reliably predi...

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Bibliographic Details
Published inLeukemia Vol. 33; no. 8; pp. 1835 - 1850
Main Authors Branford, Susan, Kim, Dennis Dong Hwan, Apperley, Jane F., Eide, Christopher A., Mustjoki, Satu, Ong, S. Tiong, Nteliopoulos, Georgios, Ernst, Thomas, Chuah, Charles, Gambacorti-Passerini, Carlo, Mauro, Michael J., Druker, Brian J., Kim, Dong-Wook, Mahon, Francois-Xavier, Cortes, Jorge, Radich, Jerry P., Hochhaus, Andreas, Hughes, Timothy P.
Format Journal Article
LanguageEnglish
Published London Nature Publishing Group UK 01.08.2019
Nature Publishing Group
Subjects
631/208
631/67
631/67/1990/283/1896
Cancer
Cancer Research
Chronic myeloid leukemia
Classification
Critical Care Medicine
Diagnosis
Diagnostic systems
Disease control
Disease resistance
Drug development
Enzyme inhibitors
Evaluation
Genes
Genes, Neoplasm
Genetic transformation
Genomic analysis
Hematology
Hematopoiesis
Humans
Intensive
Internal Medicine
Kinases
Leukemia
Leukemia, Myelogenous, Chronic, BCR-ABL Positive - drug therapy
Leukemia, Myelogenous, Chronic, BCR-ABL Positive - etiology
Leukemia, Myelogenous, Chronic, BCR-ABL Positive - genetics
Management
Medicine
Medicine & Public Health
Mutants
Mutation
Myeloid leukemia
Next-generation sequencing
Oncology
Patients
Protein Kinase Inhibitors - therapeutic use
Protein-tyrosine kinase
Protein-Tyrosine Kinases - antagonists & inhibitors
Repressor Proteins - genetics
Review Article
Risk Assessment
Sequences
Transcription
Tyrosine
Online AccessGet full text

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Abstract Outcomes for patients with chronic myeloid leukemia (CML) have substantially improved due to advances in drug development and rational treatment intervention strategies. Despite these significant advances there are still unanswered questions on patient management regarding how to more reliably predict treatment failure at the time of diagnosis and how to select frontline tyrosine kinase inhibitor (TKI) therapy for optimal outcome. The BCR-ABL1 transcript level at diagnosis has no established prognostic impact and cannot guide frontline TKI selection. BCR-ABL1 mutations are detected in ~50% of TKI resistant patients but are rarely responsible for primary resistance. Other resistance mechanisms are largely uncharacterized and there are no other routine molecular testing strategies to facilitate the evaluation and further stratification of TKI resistance. Advances in next-generation sequencing technology has aided the management of a growing number of other malignancies, enabling the incorporation of somatic mutation profiles in diagnosis, classification, and prognostication. A largely unexplored area in CML research is whether expanded genomic analysis at diagnosis, resistance, and disease transformation can enhance patient management decisions, as has occurred for other cancers. The aim of this article is to review publications that reported mutated cancer-associated genes in CML patients at various disease phases. We discuss the frequency and type of such variants at initial diagnosis and at the time of treatment failure and transformation. Current limitations in the evaluation of mutants and recommendations for future reporting are outlined. The collective evaluation of mutational studies over more than a decade suggests a limited set of cancer-associated genes are indeed recurrently mutated in CML and some at a relatively high frequency. Genomic studies have the potential to lay the foundation for improved diagnostic risk classification according to clinical and genomic risk, and to enable more precise early identification of TKI resistance.
AbstractList Outcomes for patients with chronic myeloid leukemia (CML) have substantially improved due to advances in drug development and rational treatment intervention strategies. Despite these significant advances there are still unanswered questions on patient management regarding how to more reliably predict treatment failure at the time of diagnosis and how to select frontline tyrosine kinase inhibitor (TKI) therapy for optimal outcome. The BCR-ABL1 transcript level at diagnosis has no established prognostic impact and cannot guide frontline TKI selection. BCR-ABL1 mutations are detected in ~50% of TKI resistant patients but are rarely responsible for primary resistance. Other resistance mechanisms are largely uncharacterized and there are no other routine molecular testing strategies to facilitate the evaluation and further stratification of TKI resistance. Advances in next-generation sequencing technology has aided the management of a growing number of other malignancies, enabling the incorporation of somatic mutation profiles in diagnosis, classification, and prognostication. A largely unexplored area in CML research is whether expanded genomic analysis at diagnosis, resistance, and disease transformation can enhance patient management decisions, as has occurred for other cancers. The aim of this article is to review publications that reported mutated cancer-associated genes in CML patients at various disease phases. We discuss the frequency and type of such variants at initial diagnosis and at the time of treatment failure and transformation. Current limitations in the evaluation of mutants and recommendations for future reporting are outlined. The collective evaluation of mutational studies over more than a decade suggests a limited set of cancer-associated genes are indeed recurrently mutated in CML and some at a relatively high frequency. Genomic studies have the potential to lay the foundation for improved diagnostic risk classification according to clinical and genomic risk, and to enable more precise early identification of TKI resistance.
Outcomes for patients with chronic myeloid leukemia (CML) have substantially improved due to advances in drug development and rational treatment intervention strategies. Despite these significant advances there are still unanswered questions on patient management regarding how to more reliably predict treatment failure at the time of diagnosis and how to select frontline tyrosine kinase inhibitor (TKI) therapy for optimal outcome. The BCR-ABL1 transcript level at diagnosis has no established prognostic impact and cannot guide frontline TKI selection. BCR-ABL1 mutations are detected in ~50% of TKI resistant patients but are rarely responsible for primary resistance. Other resistance mechanisms are largely uncharacterized and there are no other routine molecular testing strategies to facilitate the evaluation and further stratification of TKI resistance. Advances in next-generation sequencing technology has aided the management of a growing number of other malignancies, enabling the incorporation of somatic mutation profiles in diagnosis, classification, and prognostication. A largely unexplored area in CML research is whether expanded genomic analysis at diagnosis, resistance, and disease transformation can enhance patient management decisions, as has occurred for other cancers. The aim of this article is to review publications that reported mutated cancer-associated genes in CML patients at various disease phases. We discuss the frequency and type of such variants at initial diagnosis and at the time of treatment failure and transformation. Current limitations in the evaluation of mutants and recommendations for future reporting are outlined. The collective evaluation of mutational studies over more than a decade suggests a limited set of cancer-associated genes are indeed recurrently mutated in CML and some at a relatively high frequency. Genomic studies have the potential to lay the foundation for improved diagnostic risk classification according to clinical and genomic risk, and to enable more precise early identification of TKI resistance.
Outcomes for patients with chronic myeloid leukemia (CML) have substantially improved due to advances in drug development and rational treatment intervention strategies. Despite these significant advances there are still unanswered questions on patient management regarding how to more reliably predict treatment failure at the time of diagnosis and how to select frontline tyrosine kinase inhibitor (TKI) therapy for optimal outcome. The BCR-ABL1 transcript level at diagnosis has no established prognostic impact and cannot guide frontline TKI selection. BCR-ABL1 mutations are detected in approximately 50% of TKI resistant patients but are rarely responsible for primary resistance. Other resistance mechanisms are largely uncharacterized and there are no other routine molecular testing strategies to facilitate the evaluation and further stratification of TKI resistance. Advances in next-generation sequencing technology has aided the management of a growing number of other malignancies, enabling the incorporation of somatic mutation profiles in diagnosis, classification and prognostication. A largely unexplored area in CML research is whether expanded genomic analysis at diagnosis, resistance and disease transformation can enhance patient management decisions, as has occurred for other cancers. The aim of this article is to review publications that reported mutated cancer-associated genes in CML patients at various disease phases. We discuss the frequency and type of such variants at initial diagnosis and at the time of treatment failure and transformation. Current limitations in the evaluation of mutants and recommendations for future reporting are outlined. The collective evaluation of mutational studies over more than a decade suggests a limited set of cancer-associated genes are indeed recurrently mutated in CML and some at a relatively high frequency. Genomic studies have the potential to lay the foundation for improved diagnostic risk classification according to clinical and genomic risk, and to enable more precise early identification of TKI resistance.
Outcomes for patients with chronic myeloid leukemia (CML) have substantially improved due to advances in drug development and rational treatment intervention strategies. Despite these significant advances there are still unanswered questions on patient management regarding how to more reliably predict treatment failure at the time of diagnosis and how to select frontline tyrosine kinase inhibitor (TKI) therapy for optimal outcome. The BCR-ABL1 transcript level at diagnosis has no established prognostic impact and cannot guide frontline TKI selection. BCR-ABL1 mutations are detected in ~50% of TKI resistant patients but are rarely responsible for primary resistance. Other resistance mechanisms are largely uncharacterized and there are no other routine molecular testing strategies to facilitate the evaluation and further stratification of TKI resistance. Advances in next-generation sequencing technology has aided the management of a growing number of other malignancies, enabling the incorporation of somatic mutation profiles in diagnosis, classification, and prognostication. A largely unexplored area in CML research is whether expanded genomic analysis at diagnosis, resistance, and disease transformation can enhance patient management decisions, as has occurred for other cancers. The aim of this article is to review publications that reported mutated cancer-associated genes in CML patients at various disease phases. We discuss the frequency and type of such variants at initial diagnosis and at the time of treatment failure and transformation. Current limitations in the evaluation of mutants and recommendations for future reporting are outlined. The collective evaluation of mutational studies over more than a decade suggests a limited set of cancer-associated genes are indeed recurrently mutated in CML and some at a relatively high frequency. Genomic studies have the potential to lay the foundation for improved diagnostic risk classification according to clinical and genomic risk, and to enable more precise early identification of TKI resistance.Outcomes for patients with chronic myeloid leukemia (CML) have substantially improved due to advances in drug development and rational treatment intervention strategies. Despite these significant advances there are still unanswered questions on patient management regarding how to more reliably predict treatment failure at the time of diagnosis and how to select frontline tyrosine kinase inhibitor (TKI) therapy for optimal outcome. The BCR-ABL1 transcript level at diagnosis has no established prognostic impact and cannot guide frontline TKI selection. BCR-ABL1 mutations are detected in ~50% of TKI resistant patients but are rarely responsible for primary resistance. Other resistance mechanisms are largely uncharacterized and there are no other routine molecular testing strategies to facilitate the evaluation and further stratification of TKI resistance. Advances in next-generation sequencing technology has aided the management of a growing number of other malignancies, enabling the incorporation of somatic mutation profiles in diagnosis, classification, and prognostication. A largely unexplored area in CML research is whether expanded genomic analysis at diagnosis, resistance, and disease transformation can enhance patient management decisions, as has occurred for other cancers. The aim of this article is to review publications that reported mutated cancer-associated genes in CML patients at various disease phases. We discuss the frequency and type of such variants at initial diagnosis and at the time of treatment failure and transformation. Current limitations in the evaluation of mutants and recommendations for future reporting are outlined. The collective evaluation of mutational studies over more than a decade suggests a limited set of cancer-associated genes are indeed recurrently mutated in CML and some at a relatively high frequency. Genomic studies have the potential to lay the foundation for improved diagnostic risk classification according to clinical and genomic risk, and to enable more precise early identification of TKI resistance.
Author Kim, Dong-Wook
Kim, Dennis Dong Hwan
Eide, Christopher A.
Mustjoki, Satu
Ong, S. Tiong
Ernst, Thomas
Mauro, Michael J.
Cortes, Jorge
Apperley, Jane F.
Radich, Jerry P.
Hochhaus, Andreas
Branford, Susan
Druker, Brian J.
Chuah, Charles
Gambacorti-Passerini, Carlo
Mahon, Francois-Xavier
Hughes, Timothy P.
Nteliopoulos, Georgios
AuthorAffiliation 18 Department of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA
3 School of Medicine, University of Adelaide, Adelaide, South Australia
10 Cancer and Stem Cell Biology Signature Research Program, Duke–NUS Medical School, Singapore, Singapore
12 Abteilung Hämatologie und Internistische Onkologie, Klinik für Innere Medizin II, Universitätsklinikum Jena, Jena, Germany
6 Division of Hematology and Medical Oncology, Oregon Health & Science University Knight Cancer Institute, Portland, Oregon, USA
19 Fred Hutchinson Cancer Research Center, Seattle, Washington, USA
20 South Australian Health & Medical Research Institute, Adelaide, South Australia
11 Department of Haematology, Singapore General Hospital, Singapore, Singapore
17 Bergonié Cancer Institute, Inserm Unit 916, University of Bordeaux, Bordeaux, France
13 University of Milano Bicocca, San Gerardo Hospital, Monza, Italy
14 Myeloproliferative Neoplasms Program, Leukemia Service, Memorial Sloan Kettering Cancer Ce
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– name: 4 Department of Medical Oncology and Hematology, Princess Margaret Cancer Centre, University Health Network, University of Toronto, Toronto, Canada
– name: 13 University of Milano Bicocca, San Gerardo Hospital, Monza, Italy
– name: 18 Department of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA
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– name: 3 School of Medicine, University of Adelaide, Adelaide, South Australia
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BackLink https://www.ncbi.nlm.nih.gov/pubmed/31209280$$D View this record in MEDLINE/PubMed
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Snippet Outcomes for patients with chronic myeloid leukemia (CML) have substantially improved due to advances in drug development and rational treatment intervention...
SourceID pubmedcentral
proquest
pubmed
crossref
springer
SourceType Open Access Repository
Aggregation Database
Index Database
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Publisher
StartPage 1835
SubjectTerms 631/208
631/67
631/67/1990/283/1896
Cancer
Cancer Research
Chronic myeloid leukemia
Classification
Critical Care Medicine
Diagnosis
Diagnostic systems
Disease control
Disease resistance
Drug development
Enzyme inhibitors
Evaluation
Genes
Genes, Neoplasm
Genetic transformation
Genomic analysis
Hematology
Hematopoiesis
Humans
Intensive
Internal Medicine
Kinases
Leukemia
Leukemia, Myelogenous, Chronic, BCR-ABL Positive - drug therapy
Leukemia, Myelogenous, Chronic, BCR-ABL Positive - etiology
Leukemia, Myelogenous, Chronic, BCR-ABL Positive - genetics
Management
Medicine
Medicine & Public Health
Mutants
Mutation
Myeloid leukemia
Next-generation sequencing
Oncology
Patients
Protein Kinase Inhibitors - therapeutic use
Protein-tyrosine kinase
Protein-Tyrosine Kinases - antagonists & inhibitors
Repressor Proteins - genetics
Review Article
Risk Assessment
Sequences
Transcription
Tyrosine
Title Laying the foundation for genomically-based risk assessment in chronic myeloid leukemia
URI https://link.springer.com/article/10.1038/s41375-019-0512-y
https://www.ncbi.nlm.nih.gov/pubmed/31209280
https://www.proquest.com/docview/2269410788
https://www.proquest.com/docview/2242829839
https://pubmed.ncbi.nlm.nih.gov/PMC6893870
Volume 33
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