DNMT3A and IDH mutations in acute myeloid leukemia and other myeloid malignancies: associations with prognosis and potential treatment strategies.
Identifieur interne : 001C25 ( PubMed/Corpus ); précédent : 001C24; suivant : 001C26DNMT3A and IDH mutations in acute myeloid leukemia and other myeloid malignancies: associations with prognosis and potential treatment strategies.
Auteurs : A P Im ; A R Sehgal ; M P Carroll ; B D Smith ; A. Tefferi ; D E Johnson ; M. BoyiadzisSource :
- Leukemia [ 1476-5551 ] ; 2014.
English descriptors
- KwdEn :
- DNA (Cytosine-5-)-Methyltransferase (genetics), Humans, Isocitrate Dehydrogenase (genetics), Leukemia, Myeloid, Acute (drug therapy), Leukemia, Myeloid, Acute (genetics), Mutation, Myelodysplastic Syndromes (genetics), Myeloproliferative Disorders (genetics), Nuclear Proteins (genetics), Prognosis, fms-Like Tyrosine Kinase 3 (genetics).
- MESH :
- chemical , genetics : DNA (Cytosine-5-)-Methyltransferase, Isocitrate Dehydrogenase, Nuclear Proteins, fms-Like Tyrosine Kinase 3.
- drug therapy : Leukemia, Myeloid, Acute.
- genetics : Leukemia, Myeloid, Acute, Myelodysplastic Syndromes, Myeloproliferative Disorders.
- Humans, Mutation, Prognosis.
Abstract
The development of effective treatment strategies for most forms of acute myeloid leukemia (AML) has languished for the past several decades. There are a number of reasons for this, but key among them is the considerable heterogeneity of this disease and the paucity of molecular markers that can be used to predict clinical outcomes and responsiveness to different therapies. The recent large-scale sequencing of AML genomes is now providing opportunities for patient stratification and personalized approaches to treatment that are based on individual mutational profiles. It is particularly notable that studies by The Cancer Genome Atlas and others have determined that 44% of patients with AML exhibit mutations in genes that regulate methylation of genomic DNA. In particular, frequent mutation has been observed in the genes encoding DNA methyltransferase 3A (DNMT3A), isocitrate dehydrogenase 1 (IDH1) and isocitrate dehydrogenase 2 (IDH2), as well as Tet oncogene family member 2. This review will summarize the incidence of these mutations, their impact on biochemical functions including epigenetic modification of genomic DNA and their potential usefulness as prognostic indicators. Importantly, the presence of DNMT3A, IDH1 or IDH2 mutations may confer sensitivity to novel therapeutic approaches, including the use of demethylating agents. Therefore, the clinical experience with decitabine and azacitidine in the treatment of patients harboring these mutations will be reviewed. Overall, we propose that understanding the role of these mutations in AML biology will lead to more rational therapeutic approaches targeting molecularly defined subtypes of the disease.
DOI: 10.1038/leu.2014.124
PubMed: 24699305
Links to Exploration step
pubmed:24699305Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">DNMT3A and IDH mutations in acute myeloid leukemia and other myeloid malignancies: associations with prognosis and potential treatment strategies.</title><author><name sortKey="Im, A P" sort="Im, A P" uniqKey="Im A" first="A P" last="Im">A P Im</name><affiliation><nlm:affiliation>Division of Hematology/Oncology, University of Pittsburgh Cancer Institute, Pittsburgh, PA, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Sehgal, A R" sort="Sehgal, A R" uniqKey="Sehgal A" first="A R" last="Sehgal">A R Sehgal</name><affiliation><nlm:affiliation>Division of Hematology/Oncology, University of Pittsburgh Cancer Institute, Pittsburgh, PA, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Carroll, M P" sort="Carroll, M P" uniqKey="Carroll M" first="M P" last="Carroll">M P Carroll</name><affiliation><nlm:affiliation>Division of Hematology and Oncology, University of Pennsylvania, Philadelphia, PA, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Smith, B D" sort="Smith, B D" uniqKey="Smith B" first="B D" last="Smith">B D Smith</name><affiliation><nlm:affiliation>The Sidney Kimmel Comprehensive Cancer Center, Department of Oncology at the Johns Hopkins University, Baltimore, MD, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Tefferi, A" sort="Tefferi, A" uniqKey="Tefferi A" first="A" last="Tefferi">A. Tefferi</name><affiliation><nlm:affiliation>Division of Hematology, Department of Medicine, Mayo Clinic, Rochester, MN, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Johnson, D E" sort="Johnson, D E" uniqKey="Johnson D" first="D E" last="Johnson">D E Johnson</name><affiliation><nlm:affiliation>Division of Hematology/Oncology, University of Pittsburgh Cancer Institute, Pittsburgh, PA, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Boyiadzis, M" sort="Boyiadzis, M" uniqKey="Boyiadzis M" first="M" last="Boyiadzis">M. Boyiadzis</name><affiliation><nlm:affiliation>Division of Hematology/Oncology, University of Pittsburgh Cancer Institute, Pittsburgh, PA, USA.</nlm:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2014">2014</date><idno type="RBID">pubmed:24699305</idno><idno type="pmid">24699305</idno><idno type="doi">10.1038/leu.2014.124</idno><idno type="wicri:Area/PubMed/Corpus">001C25</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">001C25</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">DNMT3A and IDH mutations in acute myeloid leukemia and other myeloid malignancies: associations with prognosis and potential treatment strategies.</title><author><name sortKey="Im, A P" sort="Im, A P" uniqKey="Im A" first="A P" last="Im">A P Im</name><affiliation><nlm:affiliation>Division of Hematology/Oncology, University of Pittsburgh Cancer Institute, Pittsburgh, PA, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Sehgal, A R" sort="Sehgal, A R" uniqKey="Sehgal A" first="A R" last="Sehgal">A R Sehgal</name><affiliation><nlm:affiliation>Division of Hematology/Oncology, University of Pittsburgh Cancer Institute, Pittsburgh, PA, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Carroll, M P" sort="Carroll, M P" uniqKey="Carroll M" first="M P" last="Carroll">M P Carroll</name><affiliation><nlm:affiliation>Division of Hematology and Oncology, University of Pennsylvania, Philadelphia, PA, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Smith, B D" sort="Smith, B D" uniqKey="Smith B" first="B D" last="Smith">B D Smith</name><affiliation><nlm:affiliation>The Sidney Kimmel Comprehensive Cancer Center, Department of Oncology at the Johns Hopkins University, Baltimore, MD, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Tefferi, A" sort="Tefferi, A" uniqKey="Tefferi A" first="A" last="Tefferi">A. Tefferi</name><affiliation><nlm:affiliation>Division of Hematology, Department of Medicine, Mayo Clinic, Rochester, MN, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Johnson, D E" sort="Johnson, D E" uniqKey="Johnson D" first="D E" last="Johnson">D E Johnson</name><affiliation><nlm:affiliation>Division of Hematology/Oncology, University of Pittsburgh Cancer Institute, Pittsburgh, PA, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Boyiadzis, M" sort="Boyiadzis, M" uniqKey="Boyiadzis M" first="M" last="Boyiadzis">M. Boyiadzis</name><affiliation><nlm:affiliation>Division of Hematology/Oncology, University of Pittsburgh Cancer Institute, Pittsburgh, PA, USA.</nlm:affiliation></affiliation></author></analytic><series><title level="j">Leukemia</title><idno type="eISSN">1476-5551</idno><imprint><date when="2014" type="published">2014</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>DNA (Cytosine-5-)-Methyltransferase (genetics)</term><term>Humans</term><term>Isocitrate Dehydrogenase (genetics)</term><term>Leukemia, Myeloid, Acute (drug therapy)</term><term>Leukemia, Myeloid, Acute (genetics)</term><term>Mutation</term><term>Myelodysplastic Syndromes (genetics)</term><term>Myeloproliferative Disorders (genetics)</term><term>Nuclear Proteins (genetics)</term><term>Prognosis</term><term>fms-Like Tyrosine Kinase 3 (genetics)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>DNA (Cytosine-5-)-Methyltransferase</term><term>Isocitrate Dehydrogenase</term><term>Nuclear Proteins</term><term>fms-Like Tyrosine Kinase 3</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Leukemia, Myeloid, Acute</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Leukemia, Myeloid, Acute</term><term>Myelodysplastic Syndromes</term><term>Myeloproliferative Disorders</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Humans</term><term>Mutation</term><term>Prognosis</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The development of effective treatment strategies for most forms of acute myeloid leukemia (AML) has languished for the past several decades. There are a number of reasons for this, but key among them is the considerable heterogeneity of this disease and the paucity of molecular markers that can be used to predict clinical outcomes and responsiveness to different therapies. The recent large-scale sequencing of AML genomes is now providing opportunities for patient stratification and personalized approaches to treatment that are based on individual mutational profiles. It is particularly notable that studies by The Cancer Genome Atlas and others have determined that 44% of patients with AML exhibit mutations in genes that regulate methylation of genomic DNA. In particular, frequent mutation has been observed in the genes encoding DNA methyltransferase 3A (DNMT3A), isocitrate dehydrogenase 1 (IDH1) and isocitrate dehydrogenase 2 (IDH2), as well as Tet oncogene family member 2. This review will summarize the incidence of these mutations, their impact on biochemical functions including epigenetic modification of genomic DNA and their potential usefulness as prognostic indicators. Importantly, the presence of DNMT3A, IDH1 or IDH2 mutations may confer sensitivity to novel therapeutic approaches, including the use of demethylating agents. Therefore, the clinical experience with decitabine and azacitidine in the treatment of patients harboring these mutations will be reviewed. Overall, we propose that understanding the role of these mutations in AML biology will lead to more rational therapeutic approaches targeting molecularly defined subtypes of the disease.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">24699305</PMID><DateCreated><Year>2014</Year><Month>09</Month><Day>03</Day></DateCreated><DateCompleted><Year>2014</Year><Month>10</Month><Day>31</Day></DateCompleted><DateRevised><Year>2017</Year><Month>02</Month><Day>20</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1476-5551</ISSN><JournalIssue CitedMedium="Internet"><Volume>28</Volume><Issue>9</Issue><PubDate><Year>2014</Year><Month>Sep</Month></PubDate></JournalIssue><Title>Leukemia</Title><ISOAbbreviation>Leukemia</ISOAbbreviation></Journal><ArticleTitle>DNMT3A and IDH mutations in acute myeloid leukemia and other myeloid malignancies: associations with prognosis and potential treatment strategies.</ArticleTitle><Pagination><MedlinePgn>1774-83</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1038/leu.2014.124</ELocationID><Abstract><AbstractText>The development of effective treatment strategies for most forms of acute myeloid leukemia (AML) has languished for the past several decades. There are a number of reasons for this, but key among them is the considerable heterogeneity of this disease and the paucity of molecular markers that can be used to predict clinical outcomes and responsiveness to different therapies. The recent large-scale sequencing of AML genomes is now providing opportunities for patient stratification and personalized approaches to treatment that are based on individual mutational profiles. It is particularly notable that studies by The Cancer Genome Atlas and others have determined that 44% of patients with AML exhibit mutations in genes that regulate methylation of genomic DNA. In particular, frequent mutation has been observed in the genes encoding DNA methyltransferase 3A (DNMT3A), isocitrate dehydrogenase 1 (IDH1) and isocitrate dehydrogenase 2 (IDH2), as well as Tet oncogene family member 2. This review will summarize the incidence of these mutations, their impact on biochemical functions including epigenetic modification of genomic DNA and their potential usefulness as prognostic indicators. Importantly, the presence of DNMT3A, IDH1 or IDH2 mutations may confer sensitivity to novel therapeutic approaches, including the use of demethylating agents. Therefore, the clinical experience with decitabine and azacitidine in the treatment of patients harboring these mutations will be reviewed. Overall, we propose that understanding the role of these mutations in AML biology will lead to more rational therapeutic approaches targeting molecularly defined subtypes of the disease.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Im</LastName><ForeName>A P</ForeName><Initials>AP</Initials><AffiliationInfo><Affiliation>Division of Hematology/Oncology, University of Pittsburgh Cancer Institute, Pittsburgh, PA, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Sehgal</LastName><ForeName>A R</ForeName><Initials>AR</Initials><AffiliationInfo><Affiliation>Division of Hematology/Oncology, University of Pittsburgh Cancer Institute, Pittsburgh, PA, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Carroll</LastName><ForeName>M P</ForeName><Initials>MP</Initials><AffiliationInfo><Affiliation>Division of Hematology and Oncology, University of Pennsylvania, Philadelphia, PA, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Smith</LastName><ForeName>B D</ForeName><Initials>BD</Initials><AffiliationInfo><Affiliation>The Sidney Kimmel Comprehensive Cancer Center, Department of Oncology at the Johns Hopkins University, Baltimore, MD, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Tefferi</LastName><ForeName>A</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Division of Hematology, Department of Medicine, Mayo Clinic, Rochester, MN, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Johnson</LastName><ForeName>D E</ForeName><Initials>DE</Initials><AffiliationInfo><Affiliation>Division of Hematology/Oncology, University of Pittsburgh Cancer Institute, Pittsburgh, PA, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Boyiadzis</LastName><ForeName>M</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Division of Hematology/Oncology, University of Pittsburgh Cancer Institute, Pittsburgh, PA, USA.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>P30 CA006973</GrantID><Acronym>CA</Acronym><Agency>NCI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 CA149566</GrantID><Acronym>CA</Acronym><Agency>NCI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>T32 CA009679</GrantID><Acronym>CA</Acronym><Agency>NCI NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2014</Year><Month>04</Month><Day>04</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Leukemia</MedlineTA><NlmUniqueID>8704895</NlmUniqueID><ISSNLinking>0887-6924</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D009687">Nuclear Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>117896-08-9</RegistryNumber><NameOfSubstance UI="C029739">nucleophosmin</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 1.1.1.41</RegistryNumber><NameOfSubstance UI="D007521">Isocitrate Dehydrogenase</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 1.1.1.41</RegistryNumber><NameOfSubstance UI="C538784">isocitrate dehydrogenase 2, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 1.1.1.42.</RegistryNumber><NameOfSubstance UI="C543588">IDH1 protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 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IdType="pubmed">24699305</ArticleId><ArticleId IdType="pii">leu2014124</ArticleId><ArticleId IdType="doi">10.1038/leu.2014.124</ArticleId><ArticleId IdType="pmc">PMC4234093</ArticleId><ArticleId IdType="mid">NIHMS632983</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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