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The genetic basis of early T-cell precursor acute lymphoblastic leukaemia
Open accessAbstract
Early T-cell precursor acute lymphoblastic leukaemia (ETP ALL) is an aggressive malignancy of unknown genetic basis. We performed whole-genome sequencing of 12 ETP ALL cases and assessed the frequency of the identified somatic mutations in 94 T-cell acute lymphoblastic leukaemia cases. ETP ALL was characterized by activating mutations in genes regulating cytokine receptor and RAS signalling (67% of cases; NRAS, KRAS, FLT3, IL7R, JAK3, JAK1, SH2B3 and BRAF), inactivating lesions disrupting haematopoietic development (58%; GATA3, ETV6, RUNX1, IKZF1 and EP300) and histone-modifying genes (48%; EZH2, EED, SUZ12, SETD2 and EP300). We also identified new targets of recurrent mutation including DNM2, ECT2L and RELN. The mutational spectrum is similar to myeloid tumours, and moreover, the global transcriptional profile of ETP ALL was similar to that of normal and myeloid leukaemia haematopoietic stem cells. These findings suggest that addition of myeloid-directed therapies might improve the poor outcome of ETP ALL. This work shows that treatments used for acute myeloid leukaemia and targeted therapies could be used for early T-cell precursor acute lymphoblastic leukaemia. The early T-cell precursor (ETP) subtype of childhood acute lymphoblastic leukaemia (ALL) has a poor prognosis when treated with standard chemotherapy. Whole genome sequencing is used here to gain insights into the genetic basis of the condition. The results reveal a high frequency of activating mutations in genes regulating cytokine receptor and Ras signalling, lesions that disrupt haemopoiesis (many of which arise from chromosomal rearrangements that generate novel chimeric in-frame fusion genes), and inactivating mutations in histone modifying genes. This mutation pattern resembles that of myeloid malignancies, suggesting that myeloid-directed therapies such as high-dose cytarabine, or targeted therapies that inhibit cytokine receptor and JAK signalling, might be effective in ETP ALL.
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“High frequency of mutations in EZH2, EED, and SUZ12 are observed in patients with early T cell precursor ALL (ETP-ALL) [154, 155].”
From Proteolysis targeting chimeras (PROTACs) are emerging therapeutics for hematologic malignancies (2020) · cites this paper as [155]
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InfluentialHematopoietic Stem Cell Origin of BRAF V600E Mutations in Hairy Cell Leukemia
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BackgroundResultInfluentialSelf-citationTherapeutic antibody targeting of Notch1 in T-acute lymphoblastic leukemia xenografts
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Proteolysis targeting chimeras (PROTACs) are emerging therapeutics for hematologic malignancies
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“Abbreviations ABC-DLBCL: Activated B cell-like diffused large B cell lymphoma; AbPROTACs: Antibody-PROTAC conjugates; ADC: Antibody-drug conjugate; ALK: Anaplastic lymphoma kinase; AML: Acute myeloid leukemia; AR: Androgen receptor; BTK: Bruton’s tyrosine kinase; BAF: BRG-/BRMassociated factor; Bcl-2: B cell lymphoma…”
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BackgroundInfluentialTreatment of Childhood Acute Lymphoblastic Leukemia: Prognostic Factors and Clinical Advances
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Self-citationMutational spectrum of adult T-ALL
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“We were unable to confirm the high mutation rate in the PRC2 members described for pediatric patients, but we frequently found mutations in regulators of DNA methylation, possibly related to preexisting lesions in hematopoietic progenitors in the elderly[22,54].”
InfluentialETV6 in hematopoiesis and leukemia predisposition
Hock, H. R., & Shimamura, A. (2017) · Seminars in Hematology · doi:10.1053/j.seminhematol.2017.04.005 · Cited by 121
“One patient had pre-B ALL followed by MDS and AML.”
BackgroundInfluentialA new genomic framework to categorize pediatric acute myeloid leukemia
Umeda, M., Ma, J., Westover, T., Ni, Y., Song, G., Maciaszek, J. L., Rusch, M., Rahbarinia, D., Foy, S. G., Huang, B. J., et al. (2024) · Nature Genetics · doi:10.1038/s41588-023-01640-3 · Cited by 126
“These findings further suggest a continuum with other immature leukemias, such as early T cell precursor-ALL and mixed phenotype acute leukemias (T/My) with similar mutational features 72,73 .”
ResultSelf-citationGenomic Characterization of Childhood Acute Lymphoblastic Leukemia
Mullighan, C. G. (2013) · Seminars in Hematology · doi:10.1053/j.seminhematol.2013.10.001 · Cited by 122
“The mutational spectrum of ETP ALL is similar to that observed in myeloid leukemias, and the transcriptional profile of ETP ALL is similar to that of normal and malignant human hematopoietic stem cells and myeloid progenitors, but not the normal human early T-cell precursor (10).”
BackgroundMethodResultInfluentialSelf-citationConter, V., Valsecchi, M. G., Buldini, B., Parasole, R., Locatelli, F., Colombini, A., Rizzari, C., Putti, M. C., Barisone, E., Nigro, L. L., et al. (2016) · The Lancet Haematology · doi:10.1016/s2352-3026(15)00254-9 · Cited by 120
Self-citationEmerging epigenetic-modulating therapies in lymphoma
Sermer, D. J., Pasqualucci, L., Wendel, H., Melnick, A. M., & Younes, A. (2019) · Nature Reviews Clinical Oncology · doi:10.1038/s41571-019-0190-8 · Cited by 125
A complex Polycomb issue: the two faces of EZH2 in cancerPreprint
Hock, H. R. (2012) · Genes & Development · doi:10.1101/gad.191163.112 · Cited by 124
“(2012) unequivocally demonstrate that disruption of EZH2 is sufficient to cause T-ALL in mice, and three concurrent studies implicate PRC2 in human T-ALL (Ntziachristos et al. 2012; Simon et al. 2012; Zhang et al. 2012).”
BackgroundInfluentialJAK-STAT signaling in human disease: From genetic syndromes to clinical inhibition
Luo, Y., Alexander, M. T., Gadina, M., O’Shea, J. J., Meylan, F., & Schwartz, D. M. (2021) · Journal of Allergy and Clinical Immunology · doi:10.1016/j.jaci.2021.08.004 · Cited by 121
The evolution of acute lymphoblastic leukemia research and therapy at MD Anderson over four decades
Jabbour, E. J., Short, N. J., Jain, N., Haddad, F., Welch, M. A., Ravandi, F., & Kantarjian, H. M. (2023) · Journal of Hematology & Oncology · doi:10.1186/s13045-023-01409-5 · Cited by 123
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Self-citationPiva, F., Santoni, M., Matrana, M. R., Satti, S., Giulietti, M., Occhipinti, G., Massari, F., Liang Cheng, C., Antonio Lopez-beltran, B., Scarpelli, M., et al. (2015) · Expert Review of Molecular Diagnostics · doi:10.1586/14737159.2015.1068122 · Cited by 116
“SETD2 has been found to act as tumor-suppressor gene in patients with breast cancer and leukemias [30,31].”
BackgroundTargeting the PI3K/mTOR Pathway in Pediatric Hematologic Malignancies
Tasian, S. K., Teachey, D. T., & Rheingold, S. R. (2014) · Frontiers in Oncology · doi:10.3389/fonc.2014.00108 · Cited by 114
“Correlation of mutation status with clinical outcomes data revealed that T-ALL patients with complete deletions of PTEN were far more likely to experience induction failure (>25% residual leukemia after 1 month of chemotherapy) than those with mutated PTEN (7).”
BackgroundInfluentialCai, H., Kumar, N., Bagheri, H. C., von Mering, C., Robinson, M. D., & Baudis, M. (2014) · BMC Genomics · doi:10.1186/1471-2164-15-82 · Cited by 111
Pérez-Andreu, V., Roberts, K. G., Xu, H. Y., Smith, C. J., Zhang, H., Yang, W., Harvey, R. C., Payne-Turner, D., Devidas, M., Cheng, I.-M., et al. (2014) · Blood · doi:10.1182/blood-2014-09-595744 · Cited by 113
“GATA3 encodes for a transcription factor critical for lymphoid cell lineage commitment and early T-cell differentiation,(48) and loss-offunction somatic mutations have been discovered in early T-cell precursor ALL.(49) Germline polymorphisms in GATA3, however, appear more important for B-cell malignancies.”
BackgroundInfluentialSelf-citationPetit, A., Trinquand, A., Chevret, S., Ballerini, P. F., Cayuela, J., Grardel, N., Touzart, A., Brethon, B., Lapillonne, H., Schmitt, C., et al. (2017) · Blood · doi:10.1182/blood-2017-04-778829 · Cited by 112
Super-enhancers: critical roles and therapeutic targets in hematologic malignancies
Jia, Y., Chng, W. J., & Zhou, J. (2019) · Journal of Hematology & Oncology · doi:10.1186/s13045-019-0757-y · Cited by 120
The genomic landscape of acute lymphoblastic leukemia in children and young adults
Mullighan, C. G. (2014) · Hematology · doi:10.1182/asheducation-2014.1.174 · Cited by 111
“Over the last decade, there have been extensive efforts to use genome-wide profiling of genomic alterations in ALL to: (1) identify additional subtypes of ALL in cases lacking known aneuploidy or chromosomal rearrangements on cytogenetic analysis; (2) characterize the constellations of genetic alterations that define…”
BackgroundSelf-citationBlackburn, J. S., Liu, S., Wilder, J. L., Dobrinski, K. P., Lobbardi, R., Moore, F. E., Martinez, S. A., Chen, E. Y., Lee, C., & Langenau, D. M. (2014) · Cancer Cell · doi:10.1016/j.ccr.2014.01.032 · Cited by 111
“Additionally, RAS is known to activate the PI3K/Akt signaling cascade and is activated in a subset of human T-ALL (Kawamura et al., 1999; Trinquand et al., 2013; Zhang et al., 2012).”
BackgroundMaslah, N., Cassinat, B., Verger, E., Kiladjian, J., & Velazquez, L. (2017) · Leukemia · doi:10.1038/leu.2017.139 · Cited by 111
Novel biological insights in T-cell acute lymphoblastic leukemia
Durinck, K., Goossens, S., Peirs, S., Wallaert, A., Loocke, W. V., Matthijssens, F., Pieters, T., Milani, G., Lammens, T., Rondou, P., et al. (2015) · Experimental Hematology · doi:10.1016/j.exphem.2015.05.017 · Cited by 111
“These studies showed that the genetic landscape of immature T-ALL is highly heterogeneous, with aberrant expression of the MEF2C gene [23,24]; genetic alterations in hematopoietic transcription factors such as RUNX1, GATA3, BCL11B, PU.1, and ETV6 [24]; activating mutations in critical mediators of cytokine receptor an…”
BackgroundInfluentialPredicting relapse risk in childhood acute lymphoblastic leukaemia
Teachey, D. T., & Hunger, S. P. (2013) · British Journal of Haematology · doi:10.1111/bjh.12442 · Cited by 117
Self-citationEarly lesions of follicular lymphoma: a genetic perspective
Mamessier, É., Song, J. Y., Eberle, F. C., Pack, S., Drevet, C., Chetaille, B., Abdullaev, Z., Adélaı̈de, J., Birnbaum, D., Chaffanet, M., et al. (2013) · Haematologica · doi:10.3324/haematol.2013.094474 · Cited by 112
“Sixty-seven of them (~6%) were known oncogenes, 6 of which (BCL2, RUNX1, NACA (26), CARD11 (27), ELN (28) & IKZF1 (29)) previously identified as major players in leukemia/lymphoma oncogenesis (Supplemental Table S3).”
BackgroundAntonysamy, S., Condon, B., Druzina, Z., Bonanno, J. B., Gheyi, T., Zhang, F., MacEwan, I. J., Zhang, A., Ashok, S., Rodgers, L. A., et al. (2013) · PLoS ONE · doi:10.1371/journal.pone.0084147 · Cited by 116
Neumann, M., Coskun, E., Fransecky, L. R., Mochmann, L. H., Bartram, I., Sartangi, N. F., Heesch, S., Gökbuget, N., Schwartz, S., Brandts, C., et al. (2013) · PLoS ONE · doi:10.1371/journal.pone.0053190 · Cited by 108
“FLT3 mutations, although in a lower frequency (14%), occurred exclusively in ETP-ALL [6].”
BackgroundInfluentialBurkhardt, B., & Hermiston, M. L. (2019) · British Journal of Haematology · doi:10.1111/bjh.15793 · Cited by 104
“It occurs in 10–15% of patients with T-ALL and is defined by expression of CD7 and low level CD5 (and occasionally cytoplasmic CD3) and absence of CD1a, CD4 and CD8 expression (Coustan-Smith et al, 2009a; Zhang et al, 2012; You et al, 2015).”
BackgroundSelf-citationGökbuget, N., Boissel, N., Chiaretti, S., Dombret, H., Doubek, M., Fielding, A. K., Foà, R., Giebel, S., Hoelzer, D. F., Hunault, M., et al. (2024) · Blood · doi:10.1182/blood.2023020794 · Cited by 116
“ETP-ALL 10 is genetically heterogeneous, with mutations of multiple pathways including hematopoietic and lymphoid development, Ras, cytokine receptor, and kinase signaling, and loss-of-function mutations targeting epigenetic regulators 17,18 .”
BackgroundRecurrent JAK1 and JAK3 somatic mutations in T-cell prolymphocytic leukemia
Bellanger, D., Jacquemin, V., Chopin, M., Pierron, G., Bernard, O., Ghysdael, J., & Stern, M. (2013) · Leukemia · doi:10.1038/leu.2013.271 · Cited by 105
An epigenetic gateway to brain tumor cell identity
Mack, S. C., Hubert, C. G., Miller, T. E., Taylor, M. D., & Rich, J. N. (2015) · Nature Neuroscience · doi:10.1038/nn.4190 · Cited by 106
HOXA9 Cooperates with Activated JAK/STAT Signaling to Drive Leukemia Development
de Bock, C. E., Demeyer, S., Degryse, S., Verbeke, D., Sweron, B., Gielen, O., Vandepoel, R., Vicente, C., Bempt, M. V., Dagklis, A., et al. (2018) · Cancer Discovery · doi:10.1158/2159-8290.cd-17-0583 · Cited by 103
“RESULTS JAK3 Mutations Are Significantly Associated with HOXA+ T-ALL Cases Based on results of large-scale sequencing studies in T-ALL (4, 5, 8, 9, 20), it is becoming clear that some mutations frequently co-occur, whereas others are mutually exclusive.”
BackgroundSelf-citationCancer genome-sequencing study design
Mwenifumbo, J. C., & Marra, M. A. (2013) · Nature Reviews Genetics · doi:10.1038/nrg3445 · Cited by 104
Early T-cell precursor acute lymphoblastic leukaemia
Haydu, J. E., & Ferrando, A. A. (2013) · Current Opinion in Hematology · doi:10.1097/moh.0b013e3283623c61 · Cited by 101
Biologic and Therapeutic Implications of Genomic Alterations in Acute Lymphoblastic Leukemia
Iacobucci, I., Kimura, S., & Mullighan, C. G. (2021) · Journal of Clinical Medicine · doi:10.3390/jcm10173792 · Cited by 106
Self-citationThatikonda, V., Islam, S. M. A., Autry, R. J., Jones, B. C., Gröbner, S. N., Warsow, G., Hutter, B., Hüebschmann, D., Fröhling, S., Kool, M., et al. (2023) · Nature Cancer · doi:10.1038/s43018-022-00509-4 · Cited by 100
Cross-Species Genomics Identifies TAF12, NFYC, and RAD54L as Choroid Plexus Carcinoma Oncogenes
Tong, Y., Merino, D. M., Nimmervoll, B. V., Gupta, K., Wang, Y., Finkelstein, D., Dalton, J., Ellison, D. W., Ma, X., Zhang, J., et al. (2015) · Cancer Cell · doi:10.1016/j.ccell.2015.04.005 · Cited by 98
Self-citationBentley, V. L., Veinotte, C. J., Corkery, D., Pinder, J. B., LeBlanc, M. A., Bedard, K., Weng, A. P., Berman, J. N., & Dellaire, G. (2014) · Haematologica · doi:10.3324/haematol.2014.110742 · Cited by 99
Tasian, S. K., & Hunger, S. P. (2016) · British Journal of Haematology · doi:10.1111/bjh.14474 · Cited by 101
“As in other ALL subtypes, frequent activating mutations in RAS pathway and cytokine receptor signalling genes, IL7R pathway genes and haematopoietic development and histone modification genes have been reported in ETP-ALL (Zenatti et al, 2011; Zhang et al, 2012).”
BackgroundSelf-citationOrchestration of H3K27 methylation: mechanisms and therapeutic implication
Pan, M., Hsu, M., Chen, L., & Hung, W. (2017) · Cellular and Molecular Life Sciences · doi:10.1007/s00018-017-2596-8 · Cited by 111
Treanor, L. M., Zhou, S., Janke, L. J., Churchman, M. L., Ma, Z., Lu, T., Chen, S.-C., Mullighan, C. G., & Sorrentino, B. P. (2014) · The Journal of Experimental Medicine · doi:10.1084/jem.20122727 · Cited by 98
“To determine whether these IL7R mutations are oncogenic drivers in ETP-ALL, DN thymocytes from Arf/ mice were transduced with MSCV vectors that expressed murine homologues of either of two IL7R mutations identified in human ETP-ALL, IL7R-241-242TC and IL7R-GCinsL243 (Zhang et al., 2012).”
BackgroundInfluentialSelf-citationThe neoepitope landscape in pediatric cancers
Chang, T., Carter, R. A., Li, Y., Li, Y., Wang, H., Edmonson, M. N., Chen, X. '., Arnold, P. Y., Geiger, T. L., Wu, G., et al. (2017) · Genome Medicine · doi:10.1186/s13073-017-0468-3 · Cited by 99
“The sequencing, alignment against human reference genome using BWA [31, 32], and the identification and validation of somatic alterations including missense mutations and gene fusions were described previously [33, 34].”
MethodSelf-citationNew Approaches to the Management of Adult Acute Lymphoblastic Leukemia
Bassan, R., Bourquin, J., DeAngelo, D. J., & Chiaretti, S. (2018) · Journal of Clinical Oncology · doi:10.1200/jco.2017.77.3648 · Cited by 100
EZH2 abnormalities in lymphoid malignancies: underlying mechanisms and therapeutic implications
Li, B., & Chng, W. J. (2019) · Journal of Hematology & Oncology · doi:10.1186/s13045-019-0814-6 · Cited by 101
Extracellular assembly and activation principles of oncogenic class III receptor tyrosine kinases
Verstraete, K., & Savvides, S. N. (2012) · Nature reviews. Cancer · doi:10.1038/nrc3371 · Cited by 102
Canté-Barrett, K., Spijkers-Hagelstein, J. A. P., Buijs-Gladdines, J. G. C. A. M., Uitdehaag, J. C. M., Smits, W. K., van der Zwet, J., Buijsman, R. C., Zaman, G. J. R., Pieters, R., & Meijerink, J. P. P. (2016) · Leukemia · doi:10.1038/leu.2016.83 · Cited by 94
Metadata
- Authors
- Zhang, J., Ding, L., Holmfeldt, L., Wu, G., Heatley, S. L., Payne-Turner, D., Easton, J., Chen, X., Wang, J., Rusch, M., Lu, C., Chen, S.-C., Wei, L., Collins-Underwood, J. R., Ma, J., Roberts, K. G., Pounds, S. B., Ulyanov, A., Becksfort, J., Gupta, P., Huether, R., Kriwacki, R. W., Parker, M., McGoldrick, D. J., Zhao, D., Alford, D., Espy, S., Bobba, K. C., Song, G., Pei, D., Cheng, C., Roberts, S., Barbato, M. I., Campana, D., Coustan-Smith, E., Shurtleff, S. A., Raimondi, S. C., Kleppe, M., Cools, J., Shimano, K. A., Hermiston, M. L., Doulatov, S., Eppert, K., Laurenti, E., Notta, F., Dick, J. E., Basso, G., Hunger, S. P., Loh, M. L., Devidas, M., Wood, B., Winter, S., Dunsmore, K. P., Fulton, R. S., Fulton, L. L., Hong, X., Harris, C. C., Dooling, D. J., Ochoa, K., Johnson, K. J., Obenauer, J. C., Evans, W. E., Pui, C.-H., Naeve, C. W., Ley, T. J., Mardis, E. R., Wilson, R. K., Downing, J. R., & Mullighan, C. G.
- Affiliations
- St. Jude Children's Research Hospital (US)
- Washington University in St. Louis (US)
- KU Leuven (BE)
- University of California, San Francisco (US)
- University Health Network (CA)
- University of Padua (IT)
- Children's Hospital Colorado (US)
- University of Florida Health (US)
- Seattle Children's Hospital (US)
- University of New Mexico (US)
- Corresponding author
- Downing, James R.
- Mullighan, Charles G.
- ORCID
- Zhang, Jinghui
- Ding, Li
- Holmfeldt, Linda
- Wu, Gang
- Payne-Turner, Debbie
- Easton, John
- Chen, Xiang
- Wang, Jianmin
- Rusch, Michael
- Lu, Charles
- Chen, Shann-Ching
- Wei, Lei
- Ma, Jing
- Roberts, Kathryn G.
- Pounds, Stanley B.
- Ulyanov, Anatoly
- Becksfort, Jared
- Gupta, Pankaj
- Huether, Robert
- Kriwacki, Richard W.
- Parker, Matthew
- Zhao, David
- Espy, Stephen
- Song, Guangchun
- Cheng, Cheng
- Barbato, Michael I.
- Campana, Dario
- Raimondi, Susana C.
- Cools, Jan
- Shimano, Kristin A.
- Hermiston, Michelle L.
- Doulatov, Sergei
- Eppert, Kolja
- Laurenti, Elisa
- Notta, Faiyaz
- Dick, John E.
- Basso, Giuseppe
- Hunger, Stephen P.
- Loh, Mignon L.
- Devidas, Meenakshi
- Wood, Brent
- Winter, Stuart
- Fulton, Robert S.
- Fulton, Lucinda L.
- Johnson, Kimberly J.
- Obenauer, John C.
- Evans, William E.
- Pui, Ching-Hon
- Ley, Timothy J.
- Mardis, Elaine R.
- Wilson, Richard K.
- Downing, James R.
- Mullighan, Charles G.
- Venue
- Nature
- Published
- 2012-01
- Volume
- 481
- Issue
- 7380
- Pages
- 157-163
- ISSN
- 0028-0836 (ISSN-L)
- 1476-4687
- PMC
- PMC3267575
- OpenAlex
- W2060605982
- Cited by
- 1,596
- References
- 45
- Citations by year
- 2026: 28 · 2025: 61 · 2024: 85 · 2023: 72 · 2022: 98 · 2021: 131 · 2020: 106 · 2019: 123 · 2018: 100 · 2017: 119 · 2016: 138 · 2015: 122 · 2014: 156 · 2013: 162 · 2012: 90
- FWCI
- 164.44
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Nature (publishedVersion, cc-by-nc-sa)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Padua Research Archive (University of Padova) (submittedVersion, cc-by-nc-sa)
- RePEc: Research Papers in Economics (submittedVersion)
- Adelaide Research & Scholarship (AR&S) (University of Adelaide) (submittedVersion)
- Funders
- Alex's Lemonade Stand Foundation for Childhood Cancer
- Washington University in St. Louis
- American Lebanese Syrian Associated Charities (CA021765)
- Alvin J. Siteman Cancer Center
- Children’s Oncology Group
- National Institutes of Health (CA 021765, CA98543)
- National Human Genome Research Institute (U54HG003079, HG003079, NHGRI U54 HG003079)
- National Cancer Institute (CA114766, CA‐98413, U10CA098413, U24CA114766, CA021765, U10CA098543, CA-98543, R25CA023944, T32CA128583, P30CA021765)
- National Institute of General Medical Sciences (U01GM92666, U01GM092666)
- Topics
- Health Sciences › Medicine › Hematology › Acute Lymphoblastic Leukemia research
- Health Sciences › Medicine › Hematology › Acute Myeloid Leukemia Research
- Health Sciences › Medicine › Pathology and Forensic Medicine › Lymphoma Diagnosis and Treatment
- Keywords
- somatic mutations, Ras signaling, cytokine receptor signalling, chromosomal rearrangements, mutation spectrum, high-dose cytarabine, gene expression profiling, hematopoietic stem cells, pediatric leukemia
- MeSH terms
- Reelin Protein, Child, Hematopoiesis, Histones, Humans, Molecular Sequence Data, Mutation, Genes, ras, Stem Cells, T-Lymphocytes, Translocation, Genetic, Signal Transduction, Leukemia, Myeloid, Acute, Genome, Human, Sequence Analysis, DNA, Age of Onset, Genetic Predisposition to Disease, Receptors, Interleukin-7, Genomics, Janus Kinases, Precursor T-Cell Lymphoblastic Leukemia-Lymphoma, DNA Copy Number Variations
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