Genomic and epigenomic landscapes of adult de novo acute myeloid leukemia

Timothy J. Ley; Christopher Miller; Li Ding; Benjamin J. Raphael; Andrew J. Mungall; Gordon Robertson; Katherine Hoadley; Timothy J. Triche; Peter W. Laird; Jack D. Baty; Lucinda L. Fulton; Robert Fulton; Sharon E. Heath; Joelle Kalicki-Veizer; Cyriac Kandoth; Jeffery M. Klco; Daniel C. Koboldt; Krishna Latha Kanchi; Shashikant Kulkarni; Tamara L. Lamprecht; David E. Larson; G. Lin; Charles Lu; Michael D. McLellan; Joshua F. McMichael; Jacqueline Payton; Heather Schmidt; David H. Spencer; Michael H. Tomasson; John W. Wallis; Lukas D. Wartman; Mark A. Watson; John Welch; Michael C. Wendl; Adrian Ally; Miruna Balasundaram; Inanc Birol; Yaron Butterfield; Readman Chiu; Andy Chu; Eric Chuah; Hye Jung Chun; Richard Corbett; Noreen Dhalla; Ranabir Guin; An He; Carrie Hirst; Martin Hirst; Robert A. Holt; Steven Jones; Aly Karsan; Darlene Lee; Haiyan I. Li; Marco A. Marra; Michael Mayo; Richard A. Moore; Karen Mungall; Jeremy Parker; Erin Pleasance; Patrick Plettner; Jacquie Schein; Dominik Stoll; Lucas Swanson; Angela Tam; Nina Thiessen; Richard Varhol; Natasja Wye; Yongjun Zhao; Stacey Gabriel; Gad Getz; Carrie Sougnez; Lihua Zou; Mark D.M. Leiserson; Fabio Vandin; Hsin Ta Wu; Frederick Applebaum; Stephen B. Baylin; Rehan Akbani; Bradley M. Broom; Ken Chen; Thomas C. Motter; Khanh Nguyen; John N. Weinstein; Nianziang Zhang; Martin L. Ferguson; Christopher Adams; Aaron Black; Jay Bowen; Julie Gastier-Foster; Thomas Grossman; Tara Lichtenberg; Lisa Wise; Tanja Davidsen; John A. Demchok; Kenna R. Mills Shaw; Margi Sheth; Heidi J. Sofia; Liming Yang; James R. Downing; Greg Eley; Shelley Alonso; Brenda Ayala; Julien Baboud; Mark Backus; Sean P. Barletta; Dominique L. Berton; Anna L. Chu; Stanley Girshik; Mark A. Jensen; Ari Kahn; Prachi Kothiyal; Matthew C. Nicholls; Todd D. Pihl; David A. Pot; Rohini Raman; Rashmi N. Sanbhadti; Eric E. Snyder; Deepak Srinivasan; Jessica Walton; Yunhu Wan; Zhining Wang; Jean Pierre J. Issa; Michelle Le Beau; Martin Carroll; Hagop Kantarjian; Steven Kornblau; Moiz S. Bootwalla; Phillip H. Lai; Hui Shen; David J. Van Den Berg; Daniel J. Weisenberger; Daniel C. Link; Matthew J. Walter; Bradley A. Ozenberger; Elaine R. Mardis; Peter Westervelt; Timothy A. Graubert; John F. DiPersio; Richard K. Wilson

doi:10.1056/NEJMoa1301689

Genomic and epigenomic landscapes of adult de novo acute myeloid leukemia

Timothy J. Ley, Christopher Miller, Li Ding, Benjamin J. Raphael, Andrew J. Mungall, Gordon Robertson, Katherine Hoadley, Timothy J. Triche, Peter W. Laird, Jack D. Baty, Lucinda L. Fulton, Robert Fulton, Sharon E. Heath, Joelle Kalicki-Veizer, Cyriac Kandoth, Jeffery M. Klco, Daniel C. Koboldt, Krishna Latha Kanchi, Shashikant Kulkarni, Tamara L. LamprechtDavid E. Larson, G. Lin, Charles Lu, Michael D. McLellan, Joshua F. McMichael, Jacqueline Payton, Heather Schmidt, David H. Spencer, Michael H. Tomasson, John W. Wallis, Lukas D. Wartman, Mark A. Watson, John Welch, Michael C. Wendl, Adrian Ally, Miruna Balasundaram, Inanc Birol, Yaron Butterfield, Readman Chiu, Andy Chu, Eric Chuah, Hye Jung Chun, Richard Corbett, Noreen Dhalla, Ranabir Guin, An He, Carrie Hirst, Martin Hirst, Robert A. Holt, Steven Jones, Aly Karsan, Darlene Lee, Haiyan I. Li, Marco A. Marra, Michael Mayo, Richard A. Moore, Karen Mungall, Jeremy Parker, Erin Pleasance, Patrick Plettner, Jacquie Schein, Dominik Stoll, Lucas Swanson, Angela Tam, Nina Thiessen, Richard Varhol, Natasja Wye, Yongjun Zhao, Stacey Gabriel, Gad Getz, Carrie Sougnez, Lihua Zou, Mark D.M. Leiserson, Fabio Vandin, Hsin Ta Wu, Frederick Applebaum, Stephen B. Baylin, Rehan Akbani, Bradley M. Broom, Ken Chen, Thomas C. Motter, Khanh Nguyen, John N. Weinstein, Nianziang Zhang, Martin L. Ferguson, Christopher Adams, Aaron Black, Jay Bowen, Julie Gastier-Foster, Thomas Grossman, Tara Lichtenberg, Lisa Wise, Tanja Davidsen, John A. Demchok, Kenna R. Mills Shaw, Margi Sheth, Heidi J. Sofia, Liming Yang, James R. Downing, Greg Eley, Shelley Alonso, Brenda Ayala, Julien Baboud, Mark Backus, Sean P. Barletta, Dominique L. Berton, Anna L. Chu, Stanley Girshik, Mark A. Jensen, Ari Kahn, Prachi Kothiyal, Matthew C. Nicholls, Todd D. Pihl, David A. Pot, Rohini Raman, Rashmi N. Sanbhadti, Eric E. Snyder, Deepak Srinivasan, Jessica Walton, Yunhu Wan, Zhining Wang, Jean Pierre J. Issa, Michelle Le Beau, Martin Carroll, Hagop Kantarjian, Steven Kornblau, Moiz S. Bootwalla, Phillip H. Lai, Hui Shen, David J. Van Den Berg, Daniel J. Weisenberger, Daniel C. Link, Matthew J. Walter, Bradley A. Ozenberger, Elaine R. Mardis, Peter Westervelt, Timothy A. Graubert, John F. DiPersio, Richard K. Wilson

Research output: Contribution to journal › Article › peer-review

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Abstract

BACKGROUND: Many mutations that contribute to the pathogenesis of acute myeloid leukemia (AML) are undefined. The relationships between patterns of mutations and epigenetic phenotypes are not yet clear. METHODS: We analyzed the genomes of 200 clinically annotated adult cases of de novo AML, using either whole-genome sequencing (50 cases) or whole-exome sequencing (150 cases), along with RNA and microRNA sequencing and DNA-methylation analysis. RESULTS: AML genomes have fewer mutations than most other adult cancers, with an average of only 13 mutations found in genes. Of these, an average of 5 are in genes that are recurrently mutated in AML. A total of 23 genes were significantly mutated, and another 237 were mutated in two or more samples. Nearly all samples had at least 1 nonsynonymous mutation in one of nine categories of genes that are almost certainly relevant for pathogenesis, including transcription-factor fusions (18% of cases), the gene encoding nucleophosmin (NPM1) (27%), tumor-suppressor genes (16%), DNA-methylation-related genes (44%), signaling genes (59%), chromatin-modifying genes (30%), myeloid transcription-factor genes (22%), cohesin-complex genes (13%), and spliceosome-complex genes (14%). Patterns of cooperation and mutual exclusivity suggested strong biologic relationships among several of the genes and categories. CONCLUSIONS: We identified at least one potential driver mutation in nearly all AML samples and found that a complex interplay of genetic events contributes to AML pathogenesis in individual patients. The databases from this study are widely available to serve as a foundation for further investigations of AML pathogenesis, classification, and risk stratification. (Funded by the National Institutes of Health.)

Original language	English
Pages (from-to)	2059-2074
Number of pages	16
Journal	New England Journal of Medicine
Volume	368
Issue number	22
DOIs	https://doi.org/10.1056/NEJMoa1301689
State	Published - May 30 2013

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10.1056/NEJMoa1301689

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Ley, T. J., Miller, C., Ding, L., Raphael, B. J., Mungall, A. J., Robertson, G., Hoadley, K., Triche, T. J., Laird, P. W., Baty, J. D., Fulton, L. L., Fulton, R., Heath, S. E., Kalicki-Veizer, J., Kandoth, C., Klco, J. M., Koboldt, D. C., Kanchi, K. L., Kulkarni, S., ... Wilson, R. K. (2013). Genomic and epigenomic landscapes of adult de novo acute myeloid leukemia. New England Journal of Medicine, 368(22), 2059-2074. https://doi.org/10.1056/NEJMoa1301689

@article{b25141bcf80240ab951d52d8627f639c,

title = "Genomic and epigenomic landscapes of adult de novo acute myeloid leukemia",

abstract = "BACKGROUND: Many mutations that contribute to the pathogenesis of acute myeloid leukemia (AML) are undefined. The relationships between patterns of mutations and epigenetic phenotypes are not yet clear. METHODS: We analyzed the genomes of 200 clinically annotated adult cases of de novo AML, using either whole-genome sequencing (50 cases) or whole-exome sequencing (150 cases), along with RNA and microRNA sequencing and DNA-methylation analysis. RESULTS: AML genomes have fewer mutations than most other adult cancers, with an average of only 13 mutations found in genes. Of these, an average of 5 are in genes that are recurrently mutated in AML. A total of 23 genes were significantly mutated, and another 237 were mutated in two or more samples. Nearly all samples had at least 1 nonsynonymous mutation in one of nine categories of genes that are almost certainly relevant for pathogenesis, including transcription-factor fusions (18% of cases), the gene encoding nucleophosmin (NPM1) (27%), tumor-suppressor genes (16%), DNA-methylation-related genes (44%), signaling genes (59%), chromatin-modifying genes (30%), myeloid transcription-factor genes (22%), cohesin-complex genes (13%), and spliceosome-complex genes (14%). Patterns of cooperation and mutual exclusivity suggested strong biologic relationships among several of the genes and categories. CONCLUSIONS: We identified at least one potential driver mutation in nearly all AML samples and found that a complex interplay of genetic events contributes to AML pathogenesis in individual patients. The databases from this study are widely available to serve as a foundation for further investigations of AML pathogenesis, classification, and risk stratification. (Funded by the National Institutes of Health.)",

author = "Ley, {Timothy J.} and Christopher Miller and Li Ding and Raphael, {Benjamin J.} and Mungall, {Andrew J.} and Gordon Robertson and Katherine Hoadley and Triche, {Timothy J.} and Laird, {Peter W.} and Baty, {Jack D.} and Fulton, {Lucinda L.} and Robert Fulton and Heath, {Sharon E.} and Joelle Kalicki-Veizer and Cyriac Kandoth and Klco, {Jeffery M.} and Koboldt, {Daniel C.} and Kanchi, {Krishna Latha} and Shashikant Kulkarni and Lamprecht, {Tamara L.} and Larson, {David E.} and G. Lin and Charles Lu and McLellan, {Michael D.} and McMichael, {Joshua F.} and Jacqueline Payton and Heather Schmidt and Spencer, {David H.} and Tomasson, {Michael H.} and Wallis, {John W.} and Wartman, {Lukas D.} and Watson, {Mark A.} and John Welch and Wendl, {Michael C.} and Adrian Ally and Miruna Balasundaram and Inanc Birol and Yaron Butterfield and Readman Chiu and Andy Chu and Eric Chuah and Chun, {Hye Jung} and Richard Corbett and Noreen Dhalla and Ranabir Guin and An He and Carrie Hirst and Martin Hirst and Holt, {Robert A.} and Steven Jones and Aly Karsan and Darlene Lee and Li, {Haiyan I.} and Marra, {Marco A.} and Michael Mayo and Moore, {Richard A.} and Karen Mungall and Jeremy Parker and Erin Pleasance and Patrick Plettner and Jacquie Schein and Dominik Stoll and Lucas Swanson and Angela Tam and Nina Thiessen and Richard Varhol and Natasja Wye and Yongjun Zhao and Stacey Gabriel and Gad Getz and Carrie Sougnez and Lihua Zou and Leiserson, {Mark D.M.} and Fabio Vandin and Wu, {Hsin Ta} and Frederick Applebaum and Baylin, {Stephen B.} and Rehan Akbani and Broom, {Bradley M.} and Ken Chen and Motter, {Thomas C.} and Khanh Nguyen and Weinstein, {John N.} and Nianziang Zhang and Ferguson, {Martin L.} and Christopher Adams and Aaron Black and Jay Bowen and Julie Gastier-Foster and Thomas Grossman and Tara Lichtenberg and Lisa Wise and Tanja Davidsen and Demchok, {John A.} and {Mills Shaw}, {Kenna R.} and Margi Sheth and Sofia, {Heidi J.} and Liming Yang and Downing, {James R.} and Greg Eley and Shelley Alonso and Brenda Ayala and Julien Baboud and Mark Backus and Barletta, {Sean P.} and Berton, {Dominique L.} and Chu, {Anna L.} and Stanley Girshik and Jensen, {Mark A.} and Ari Kahn and Prachi Kothiyal and Nicholls, {Matthew C.} and Pihl, {Todd D.} and Pot, {David A.} and Rohini Raman and Sanbhadti, {Rashmi N.} and Snyder, {Eric E.} and Deepak Srinivasan and Jessica Walton and Yunhu Wan and Zhining Wang and Issa, {Jean Pierre J.} and Beau, {Michelle Le} and Martin Carroll and Hagop Kantarjian and Steven Kornblau and Bootwalla, {Moiz S.} and Lai, {Phillip H.} and Hui Shen and {Van Den Berg}, {David J.} and Weisenberger, {Daniel J.} and Link, {Daniel C.} and Walter, {Matthew J.} and Ozenberger, {Bradley A.} and Mardis, {Elaine R.} and Peter Westervelt and Graubert, {Timothy A.} and DiPersio, {John F.} and Wilson, {Richard K.}",

year = "2013",

month = may,

day = "30",

doi = "10.1056/NEJMoa1301689",

language = "English",

volume = "368",

pages = "2059--2074",

journal = "New England Journal of Medicine",

issn = "0028-4793",

number = "22",

}

Ley, TJ , Miller, C , Ding, L, Raphael, BJ, Mungall, AJ, Robertson, G, Hoadley, K, Triche, TJ, Laird, PW, Baty, JD, Fulton, LL , Fulton, R, Heath, SE, Kalicki-Veizer, J, Kandoth, C, Klco, JM, Koboldt, DC, Kanchi, KL, Kulkarni, S, Lamprecht, TL, Larson, DE, Lin, G, Lu, C, McLellan, MD, McMichael, JF, Payton, J, Schmidt, H, Spencer, DH, Tomasson, MH, Wallis, JW, Wartman, LD, Watson, MA, Welch, J, Wendl, MC, Ally, A, Balasundaram, M, Birol, I, Butterfield, Y, Chiu, R, Chu, A, Chuah, E, Chun, HJ, Corbett, R, Dhalla, N, Guin, R, He, A, Hirst, C, Hirst, M, Holt, RA, Jones, S, Karsan, A, Lee, D, Li, HI, Marra, MA, Mayo, M, Moore, RA, Mungall, K, Parker, J, Pleasance, E, Plettner, P, Schein, J, Stoll, D, Swanson, L, Tam, A, Thiessen, N, Varhol, R, Wye, N, Zhao, Y, Gabriel, S, Getz, G, Sougnez, C, Zou, L, Leiserson, MDM, Vandin, F, Wu, HT, Applebaum, F, Baylin, SB, Akbani, R, Broom, BM, Chen, K, Motter, TC, Nguyen, K, Weinstein, JN, Zhang, N, Ferguson, ML, Adams, C, Black, A, Bowen, J, Gastier-Foster, J, Grossman, T, Lichtenberg, T, Wise, L, Davidsen, T, Demchok, JA, Mills Shaw, KR, Sheth, M, Sofia, HJ, Yang, L, Downing, JR, Eley, G, Alonso, S, Ayala, B, Baboud, J, Backus, M, Barletta, SP, Berton, DL, Chu, AL, Girshik, S, Jensen, MA, Kahn, A, Kothiyal, P, Nicholls, MC, Pihl, TD, Pot, DA, Raman, R, Sanbhadti, RN, Snyder, EE, Srinivasan, D, Walton, J, Wan, Y, Wang, Z, Issa, JPJ, Beau, ML, Carroll, M, Kantarjian, H, Kornblau, S, Bootwalla, MS, Lai, PH, Shen, H, Van Den Berg, DJ, Weisenberger, DJ, Link, DC , Walter, MJ, Ozenberger, BA, Mardis, ER, Westervelt, P, Graubert, TA, DiPersio, JF & Wilson, RK 2013, 'Genomic and epigenomic landscapes of adult de novo acute myeloid leukemia', New England Journal of Medicine, vol. 368, no. 22, pp. 2059-2074. https://doi.org/10.1056/NEJMoa1301689

TY - JOUR

T1 - Genomic and epigenomic landscapes of adult de novo acute myeloid leukemia

AU - Ley, Timothy J.

AU - Miller, Christopher

AU - Ding, Li

AU - Raphael, Benjamin J.

AU - Mungall, Andrew J.

AU - Robertson, Gordon

AU - Hoadley, Katherine

AU - Triche, Timothy J.

AU - Laird, Peter W.

AU - Baty, Jack D.

AU - Fulton, Lucinda L.

AU - Fulton, Robert

AU - Heath, Sharon E.

AU - Kalicki-Veizer, Joelle

AU - Kandoth, Cyriac

AU - Klco, Jeffery M.

AU - Koboldt, Daniel C.

AU - Kanchi, Krishna Latha

AU - Kulkarni, Shashikant

AU - Lamprecht, Tamara L.

AU - Larson, David E.

AU - Lin, G.

AU - Lu, Charles

AU - McLellan, Michael D.

AU - McMichael, Joshua F.

AU - Payton, Jacqueline

AU - Schmidt, Heather

AU - Spencer, David H.

AU - Tomasson, Michael H.

AU - Wallis, John W.

AU - Wartman, Lukas D.

AU - Watson, Mark A.

AU - Welch, John

AU - Wendl, Michael C.

AU - Ally, Adrian

AU - Balasundaram, Miruna

AU - Birol, Inanc

AU - Butterfield, Yaron

AU - Chiu, Readman

AU - Chu, Andy

AU - Chuah, Eric

AU - Chun, Hye Jung

AU - Corbett, Richard

AU - Dhalla, Noreen

AU - Guin, Ranabir

AU - He, An

AU - Hirst, Carrie

AU - Hirst, Martin

AU - Holt, Robert A.

AU - Jones, Steven

AU - Karsan, Aly

AU - Lee, Darlene

AU - Li, Haiyan I.

AU - Marra, Marco A.

AU - Mayo, Michael

AU - Moore, Richard A.

AU - Mungall, Karen

AU - Parker, Jeremy

AU - Pleasance, Erin

AU - Plettner, Patrick

AU - Schein, Jacquie

AU - Stoll, Dominik

AU - Swanson, Lucas

AU - Tam, Angela

AU - Thiessen, Nina

AU - Varhol, Richard

AU - Wye, Natasja

AU - Zhao, Yongjun

AU - Gabriel, Stacey

AU - Getz, Gad

AU - Sougnez, Carrie

AU - Zou, Lihua

AU - Leiserson, Mark D.M.

AU - Vandin, Fabio

AU - Wu, Hsin Ta

AU - Applebaum, Frederick

AU - Baylin, Stephen B.

AU - Akbani, Rehan

AU - Broom, Bradley M.

AU - Chen, Ken

AU - Motter, Thomas C.

AU - Nguyen, Khanh

AU - Weinstein, John N.

AU - Zhang, Nianziang

AU - Ferguson, Martin L.

AU - Adams, Christopher

AU - Black, Aaron

AU - Bowen, Jay

AU - Gastier-Foster, Julie

AU - Grossman, Thomas

AU - Lichtenberg, Tara

AU - Wise, Lisa

AU - Davidsen, Tanja

AU - Demchok, John A.

AU - Mills Shaw, Kenna R.

AU - Sheth, Margi

AU - Sofia, Heidi J.

AU - Yang, Liming

AU - Downing, James R.

AU - Eley, Greg

AU - Alonso, Shelley

AU - Ayala, Brenda

AU - Baboud, Julien

AU - Backus, Mark

AU - Barletta, Sean P.

AU - Berton, Dominique L.

AU - Chu, Anna L.

AU - Girshik, Stanley

AU - Jensen, Mark A.

AU - Kahn, Ari

AU - Kothiyal, Prachi

AU - Nicholls, Matthew C.

AU - Pihl, Todd D.

AU - Pot, David A.

AU - Raman, Rohini

AU - Sanbhadti, Rashmi N.

AU - Snyder, Eric E.

AU - Srinivasan, Deepak

AU - Walton, Jessica

AU - Wan, Yunhu

AU - Wang, Zhining

AU - Issa, Jean Pierre J.

AU - Beau, Michelle Le

AU - Carroll, Martin

AU - Kantarjian, Hagop

AU - Kornblau, Steven

AU - Bootwalla, Moiz S.

AU - Lai, Phillip H.

AU - Shen, Hui

AU - Van Den Berg, David J.

AU - Weisenberger, Daniel J.

AU - Link, Daniel C.

AU - Walter, Matthew J.

AU - Ozenberger, Bradley A.

AU - Mardis, Elaine R.

AU - Westervelt, Peter

AU - Graubert, Timothy A.

AU - DiPersio, John F.

AU - Wilson, Richard K.

PY - 2013/5/30

Y1 - 2013/5/30

N2 - BACKGROUND: Many mutations that contribute to the pathogenesis of acute myeloid leukemia (AML) are undefined. The relationships between patterns of mutations and epigenetic phenotypes are not yet clear. METHODS: We analyzed the genomes of 200 clinically annotated adult cases of de novo AML, using either whole-genome sequencing (50 cases) or whole-exome sequencing (150 cases), along with RNA and microRNA sequencing and DNA-methylation analysis. RESULTS: AML genomes have fewer mutations than most other adult cancers, with an average of only 13 mutations found in genes. Of these, an average of 5 are in genes that are recurrently mutated in AML. A total of 23 genes were significantly mutated, and another 237 were mutated in two or more samples. Nearly all samples had at least 1 nonsynonymous mutation in one of nine categories of genes that are almost certainly relevant for pathogenesis, including transcription-factor fusions (18% of cases), the gene encoding nucleophosmin (NPM1) (27%), tumor-suppressor genes (16%), DNA-methylation-related genes (44%), signaling genes (59%), chromatin-modifying genes (30%), myeloid transcription-factor genes (22%), cohesin-complex genes (13%), and spliceosome-complex genes (14%). Patterns of cooperation and mutual exclusivity suggested strong biologic relationships among several of the genes and categories. CONCLUSIONS: We identified at least one potential driver mutation in nearly all AML samples and found that a complex interplay of genetic events contributes to AML pathogenesis in individual patients. The databases from this study are widely available to serve as a foundation for further investigations of AML pathogenesis, classification, and risk stratification. (Funded by the National Institutes of Health.)

AB - BACKGROUND: Many mutations that contribute to the pathogenesis of acute myeloid leukemia (AML) are undefined. The relationships between patterns of mutations and epigenetic phenotypes are not yet clear. METHODS: We analyzed the genomes of 200 clinically annotated adult cases of de novo AML, using either whole-genome sequencing (50 cases) or whole-exome sequencing (150 cases), along with RNA and microRNA sequencing and DNA-methylation analysis. RESULTS: AML genomes have fewer mutations than most other adult cancers, with an average of only 13 mutations found in genes. Of these, an average of 5 are in genes that are recurrently mutated in AML. A total of 23 genes were significantly mutated, and another 237 were mutated in two or more samples. Nearly all samples had at least 1 nonsynonymous mutation in one of nine categories of genes that are almost certainly relevant for pathogenesis, including transcription-factor fusions (18% of cases), the gene encoding nucleophosmin (NPM1) (27%), tumor-suppressor genes (16%), DNA-methylation-related genes (44%), signaling genes (59%), chromatin-modifying genes (30%), myeloid transcription-factor genes (22%), cohesin-complex genes (13%), and spliceosome-complex genes (14%). Patterns of cooperation and mutual exclusivity suggested strong biologic relationships among several of the genes and categories. CONCLUSIONS: We identified at least one potential driver mutation in nearly all AML samples and found that a complex interplay of genetic events contributes to AML pathogenesis in individual patients. The databases from this study are widely available to serve as a foundation for further investigations of AML pathogenesis, classification, and risk stratification. (Funded by the National Institutes of Health.)

UR - http://www.scopus.com/inward/record.url?scp=84878372012&partnerID=8YFLogxK

U2 - 10.1056/NEJMoa1301689

DO - 10.1056/NEJMoa1301689

M3 - Article

C2 - 23634996

AN - SCOPUS:84878372012

SN - 0028-4793

VL - 368

SP - 2059

EP - 2074

JO - New England Journal of Medicine

JF - New England Journal of Medicine

IS - 22

ER -

Genomic and epigenomic landscapes of adult de novo acute myeloid leukemia

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