A new genomic framework to categorize pediatric acute myeloid leukemia
Recent studies on pediatric acute myeloid leukemia (pAML) have revealed pediatric-specific driver alterations, many of which are underrepresented in the current classification schemas. To comprehensively define the genomic landscape of pAML, we systematically categorized 887 pAML into 23 mutually di...
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| Veröffentlicht in: | Nature genetics 2024-02, Vol.56 (2), p.281-293 |
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| creator | Umeda, Masayuki Ma, Jing Westover, Tamara Ni, Yonghui Song, Guangchun Maciaszek, Jamie L. Rusch, Michael Rahbarinia, Delaram Foy, Scott Huang, Benjamin J. Walsh, Michael P. Kumar, Priyadarshini Liu, Yanling Yang, Wenjian Fan, Yiping Wu, Gang Baker, Sharyn D. Ma, Xiaotu Wang, Lu Alonzo, Todd A. Rubnitz, Jeffrey E. Pounds, Stanley Klco, Jeffery M. |
| description | Recent studies on pediatric acute myeloid leukemia (pAML) have revealed pediatric-specific driver alterations, many of which are underrepresented in the current classification schemas. To comprehensively define the genomic landscape of pAML, we systematically categorized 887 pAML into 23 mutually distinct molecular categories, including new major entities such as
UBTF
or
BCL11B
, covering 91.4% of the cohort. These molecular categories were associated with unique expression profiles and mutational patterns. For instance, molecular categories characterized by specific
HOXA
or
HOXB
expression signatures showed distinct mutation patterns of
RAS
pathway genes,
FLT3
or
WT1
, suggesting shared biological mechanisms. We show that molecular categories were strongly associated with clinical outcomes using two independent cohorts, leading to the establishment of a new prognostic framework for pAML based on these updated molecular categories and minimal residual disease. Together, this comprehensive diagnostic and prognostic framework forms the basis for future classification of pAML and treatment strategies.
Genomic profiling of 887 pediatric AML samples highlights 23 groups with distinct molecular and clinical features. |
| doi_str_mv | 10.1038/s41588-023-01640-3 |
| format | Article |
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UBTF
or
BCL11B
, covering 91.4% of the cohort. These molecular categories were associated with unique expression profiles and mutational patterns. For instance, molecular categories characterized by specific
HOXA
or
HOXB
expression signatures showed distinct mutation patterns of
RAS
pathway genes,
FLT3
or
WT1
, suggesting shared biological mechanisms. We show that molecular categories were strongly associated with clinical outcomes using two independent cohorts, leading to the establishment of a new prognostic framework for pAML based on these updated molecular categories and minimal residual disease. Together, this comprehensive diagnostic and prognostic framework forms the basis for future classification of pAML and treatment strategies.
Genomic profiling of 887 pediatric AML samples highlights 23 groups with distinct molecular and clinical features.</description><identifier>ISSN: 1061-4036</identifier><identifier>ISSN: 1546-1718</identifier><identifier>EISSN: 1546-1718</identifier><identifier>DOI: 10.1038/s41588-023-01640-3</identifier><identifier>PMID: 38212634</identifier><language>eng</language><publisher>New York: Nature Publishing Group US</publisher><subject>631/208/212 ; 631/67/1990/283/1897 ; 692/699/1541/1990/283/1897 ; Acute myeloid leukemia ; Agriculture ; Animal Genetics and Genomics ; Biomedical and Life Sciences ; Biomedicine ; Cancer Research ; Categories ; Child ; Chromosomes ; Classification ; Clinical outcomes ; Gene Function ; Genes ; Genomes ; Genomics ; Human Genetics ; Humans ; Leukemia ; Leukemia, Myeloid, Acute - genetics ; Minimal residual disease ; Mutation ; Pediatrics ; Prognosis ; Repressor Proteins - genetics ; Transcription Factors - genetics ; Tumor Suppressor Proteins - genetics ; Young adults</subject><ispartof>Nature genetics, 2024-02, Vol.56 (2), p.281-293</ispartof><rights>The Author(s) 2024</rights><rights>2024. The Author(s).</rights><rights>Copyright Nature Publishing Group Feb 2024</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c475t-aa0455366477fe6cc13e05e9dc037e6a5e70eb9385afbd71e4c059118addbf4b3</citedby><cites>FETCH-LOGICAL-c475t-aa0455366477fe6cc13e05e9dc037e6a5e70eb9385afbd71e4c059118addbf4b3</cites><orcidid>0000-0001-9885-3527 ; 0000-0002-1000-6698 ; 0000-0001-6996-0833 ; 0000-0002-9167-2114 ; 0000-0002-1678-5864 ; 0000-0002-0073-0666 ; 0000-0002-5363-1848 ; 0000-0002-7305-5649 ; 0000-0002-6233-2145 ; 0000-0003-2961-6960</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1038/s41588-023-01640-3$$EPDF$$P50$$Gspringer$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1038/s41588-023-01640-3$$EHTML$$P50$$Gspringer$$Hfree_for_read</linktohtml><link.rule.ids>230,314,776,780,881,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/38212634$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Umeda, Masayuki</creatorcontrib><creatorcontrib>Ma, Jing</creatorcontrib><creatorcontrib>Westover, Tamara</creatorcontrib><creatorcontrib>Ni, Yonghui</creatorcontrib><creatorcontrib>Song, Guangchun</creatorcontrib><creatorcontrib>Maciaszek, Jamie L.</creatorcontrib><creatorcontrib>Rusch, Michael</creatorcontrib><creatorcontrib>Rahbarinia, Delaram</creatorcontrib><creatorcontrib>Foy, Scott</creatorcontrib><creatorcontrib>Huang, Benjamin J.</creatorcontrib><creatorcontrib>Walsh, Michael P.</creatorcontrib><creatorcontrib>Kumar, Priyadarshini</creatorcontrib><creatorcontrib>Liu, Yanling</creatorcontrib><creatorcontrib>Yang, Wenjian</creatorcontrib><creatorcontrib>Fan, Yiping</creatorcontrib><creatorcontrib>Wu, Gang</creatorcontrib><creatorcontrib>Baker, Sharyn D.</creatorcontrib><creatorcontrib>Ma, Xiaotu</creatorcontrib><creatorcontrib>Wang, Lu</creatorcontrib><creatorcontrib>Alonzo, Todd A.</creatorcontrib><creatorcontrib>Rubnitz, Jeffrey E.</creatorcontrib><creatorcontrib>Pounds, Stanley</creatorcontrib><creatorcontrib>Klco, Jeffery M.</creatorcontrib><title>A new genomic framework to categorize pediatric acute myeloid leukemia</title><title>Nature genetics</title><addtitle>Nat Genet</addtitle><addtitle>Nat Genet</addtitle><description>Recent studies on pediatric acute myeloid leukemia (pAML) have revealed pediatric-specific driver alterations, many of which are underrepresented in the current classification schemas. To comprehensively define the genomic landscape of pAML, we systematically categorized 887 pAML into 23 mutually distinct molecular categories, including new major entities such as
UBTF
or
BCL11B
, covering 91.4% of the cohort. These molecular categories were associated with unique expression profiles and mutational patterns. For instance, molecular categories characterized by specific
HOXA
or
HOXB
expression signatures showed distinct mutation patterns of
RAS
pathway genes,
FLT3
or
WT1
, suggesting shared biological mechanisms. We show that molecular categories were strongly associated with clinical outcomes using two independent cohorts, leading to the establishment of a new prognostic framework for pAML based on these updated molecular categories and minimal residual disease. Together, this comprehensive diagnostic and prognostic framework forms the basis for future classification of pAML and treatment strategies.
Genomic profiling of 887 pediatric AML samples highlights 23 groups with distinct molecular and clinical features.</description><subject>631/208/212</subject><subject>631/67/1990/283/1897</subject><subject>692/699/1541/1990/283/1897</subject><subject>Acute myeloid leukemia</subject><subject>Agriculture</subject><subject>Animal Genetics and Genomics</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Cancer Research</subject><subject>Categories</subject><subject>Child</subject><subject>Chromosomes</subject><subject>Classification</subject><subject>Clinical outcomes</subject><subject>Gene Function</subject><subject>Genes</subject><subject>Genomes</subject><subject>Genomics</subject><subject>Human Genetics</subject><subject>Humans</subject><subject>Leukemia</subject><subject>Leukemia, Myeloid, Acute - genetics</subject><subject>Minimal residual disease</subject><subject>Mutation</subject><subject>Pediatrics</subject><subject>Prognosis</subject><subject>Repressor Proteins - 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genetics</topic><topic>Minimal residual disease</topic><topic>Mutation</topic><topic>Pediatrics</topic><topic>Prognosis</topic><topic>Repressor Proteins - genetics</topic><topic>Transcription Factors - genetics</topic><topic>Tumor Suppressor Proteins - genetics</topic><topic>Young adults</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Umeda, Masayuki</creatorcontrib><creatorcontrib>Ma, Jing</creatorcontrib><creatorcontrib>Westover, Tamara</creatorcontrib><creatorcontrib>Ni, Yonghui</creatorcontrib><creatorcontrib>Song, Guangchun</creatorcontrib><creatorcontrib>Maciaszek, Jamie L.</creatorcontrib><creatorcontrib>Rusch, Michael</creatorcontrib><creatorcontrib>Rahbarinia, Delaram</creatorcontrib><creatorcontrib>Foy, Scott</creatorcontrib><creatorcontrib>Huang, Benjamin J.</creatorcontrib><creatorcontrib>Walsh, Michael P.</creatorcontrib><creatorcontrib>Kumar, Priyadarshini</creatorcontrib><creatorcontrib>Liu, Yanling</creatorcontrib><creatorcontrib>Yang, Wenjian</creatorcontrib><creatorcontrib>Fan, Yiping</creatorcontrib><creatorcontrib>Wu, Gang</creatorcontrib><creatorcontrib>Baker, Sharyn D.</creatorcontrib><creatorcontrib>Ma, Xiaotu</creatorcontrib><creatorcontrib>Wang, Lu</creatorcontrib><creatorcontrib>Alonzo, Todd A.</creatorcontrib><creatorcontrib>Rubnitz, Jeffrey E.</creatorcontrib><creatorcontrib>Pounds, Stanley</creatorcontrib><creatorcontrib>Klco, Jeffery M.</creatorcontrib><collection>Springer Nature OA Free Journals</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Entomology Abstracts (Full archive)</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Nature genetics</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Umeda, Masayuki</au><au>Ma, Jing</au><au>Westover, Tamara</au><au>Ni, Yonghui</au><au>Song, Guangchun</au><au>Maciaszek, Jamie L.</au><au>Rusch, Michael</au><au>Rahbarinia, Delaram</au><au>Foy, Scott</au><au>Huang, Benjamin J.</au><au>Walsh, Michael P.</au><au>Kumar, Priyadarshini</au><au>Liu, Yanling</au><au>Yang, Wenjian</au><au>Fan, Yiping</au><au>Wu, Gang</au><au>Baker, Sharyn D.</au><au>Ma, Xiaotu</au><au>Wang, Lu</au><au>Alonzo, Todd A.</au><au>Rubnitz, Jeffrey E.</au><au>Pounds, Stanley</au><au>Klco, Jeffery M.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>A new genomic framework to categorize pediatric acute myeloid leukemia</atitle><jtitle>Nature genetics</jtitle><stitle>Nat Genet</stitle><addtitle>Nat Genet</addtitle><date>2024-02-01</date><risdate>2024</risdate><volume>56</volume><issue>2</issue><spage>281</spage><epage>293</epage><pages>281-293</pages><issn>1061-4036</issn><issn>1546-1718</issn><eissn>1546-1718</eissn><abstract>Recent studies on pediatric acute myeloid leukemia (pAML) have revealed pediatric-specific driver alterations, many of which are underrepresented in the current classification schemas. To comprehensively define the genomic landscape of pAML, we systematically categorized 887 pAML into 23 mutually distinct molecular categories, including new major entities such as
UBTF
or
BCL11B
, covering 91.4% of the cohort. These molecular categories were associated with unique expression profiles and mutational patterns. For instance, molecular categories characterized by specific
HOXA
or
HOXB
expression signatures showed distinct mutation patterns of
RAS
pathway genes,
FLT3
or
WT1
, suggesting shared biological mechanisms. We show that molecular categories were strongly associated with clinical outcomes using two independent cohorts, leading to the establishment of a new prognostic framework for pAML based on these updated molecular categories and minimal residual disease. Together, this comprehensive diagnostic and prognostic framework forms the basis for future classification of pAML and treatment strategies.
Genomic profiling of 887 pediatric AML samples highlights 23 groups with distinct molecular and clinical features.</abstract><cop>New York</cop><pub>Nature Publishing Group US</pub><pmid>38212634</pmid><doi>10.1038/s41588-023-01640-3</doi><tpages>13</tpages><orcidid>https://orcid.org/0000-0001-9885-3527</orcidid><orcidid>https://orcid.org/0000-0002-1000-6698</orcidid><orcidid>https://orcid.org/0000-0001-6996-0833</orcidid><orcidid>https://orcid.org/0000-0002-9167-2114</orcidid><orcidid>https://orcid.org/0000-0002-1678-5864</orcidid><orcidid>https://orcid.org/0000-0002-0073-0666</orcidid><orcidid>https://orcid.org/0000-0002-5363-1848</orcidid><orcidid>https://orcid.org/0000-0002-7305-5649</orcidid><orcidid>https://orcid.org/0000-0002-6233-2145</orcidid><orcidid>https://orcid.org/0000-0003-2961-6960</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | 631/208/212 631/67/1990/283/1897 692/699/1541/1990/283/1897 Acute myeloid leukemia Agriculture Animal Genetics and Genomics Biomedical and Life Sciences Biomedicine Cancer Research Categories Child Chromosomes Classification Clinical outcomes Gene Function Genes Genomes Genomics Human Genetics Humans Leukemia Leukemia, Myeloid, Acute - genetics Minimal residual disease Mutation Pediatrics Prognosis Repressor Proteins - genetics Transcription Factors - genetics Tumor Suppressor Proteins - genetics Young adults |
| title | A new genomic framework to categorize pediatric acute myeloid leukemia |
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