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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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Targeting Suppressor of Variegation 3-9 Homologue 2 (SUV39H2) in Acute Lymphoblastic Leukemia (ALL)
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“As a proof-of-principle, we initially interrogated a region of the +85 enhancer containing three tandem ETS-binding motifs (E2, E3, E4, collectively 3×ETS), which when mutated abrogates transcriptional activity of the enhancer in MOLT-4 T-ALL cells (Figure 1B and (22)).”
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“Absence of RASGRP1 results in a complete loss of positive thymocyte selection and immune deficiency, while increased levels of RASGRP1 expression and Ras-MAPK signaling have been shown in T-ALL.”
InfluentialEZH2, HIF-1, and Their Inhibitors: An Overview on Pediatric Cancers
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“For example, early T cell precursor acute lymphoblastic leukemia (ETP-ALL) represents an aggressive subtype of ALL characterized by the presence of stem cells and transcriptional programs observed in myeloid cells (59).”
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“which is characterized by a very immature CD4− CD8− DN T-cell phenotype and the coexpression of stem cell and myeloid-associated markers [47], commonly harbor mutations in epigenetic regulators (EZH2, IDH1, IDH2, DNMT3A), transcription factors associated to hematopoietic and T-cell development (ETV6, GATA3, RUNX1), an…”
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A critical role of periostin in B-cell acute lymphoblastic leukemia
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“Monoallelic or subclonal deletions have also been observed in some cases in association with mutations.(12,28,29) Even if WT1 alterations clearly suggest a role as a tumor suppressor mediated at least in part by de-regulation of its transcriptional activity, its role in T-ALL is still poorly understood.”
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“…74 kb), medium density coverage (50 probes per gene) of 24 TSG and oncogenes known to be involved in human and mouse T cell leukaemia/lymphoma [22 – 24], and high density coverage (1 probe per 100 – 200 bp) of a further 15 primary candidate loci including Trp53 (MGI: 98834), Pten (MGI: 109583),…”
Molecular cytogenetic characterization of mammary neuroendocrine carcinoma
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“As for other cancers [89, 90], this could help to characterise leukaemia subgroups that might not show up in an overall approach, or detect common patterns/footprints possibly correlated to external risk factors [91–93].”
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“Abundant genetic alterations in T-ALL have been identified by whole-genome sequencing and DNA copy number analysis of candidate genes, including deletions and/or sequence mutations of the cyclin-dependent kinase inhibitor 2A/B, lymphoid enhancer binding factor 1, Notch homolog 1, translocation-associated (Drosophila)…”
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Self-citationSLC 2A5 overexpression in childhood philadelphia chromosome‐positive acute lymphoblastic leukaemia
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“Two of the unclassifiable samples (#099 and #252) were clinically designated as ETP-ALL, a subtype of T-ALL known to have a gene expression profile resembling AML.(35,39) One of the other unclassifiable samples (#063) had exceptionally poor cDNA quality, as evidenced by the proportion of reads representing full-length…”
BackgroundMethodInfluentialSelf-citationEndothelial cell–leukemia interactions remodel drug responses, uncovering T-ALL vulnerabilities
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“Mutations in epigenetic regulatory genes comprise a substantial portion of the mutational landscape of several hematologic malignancies, including T-ALL [32], AML [33], and B-cell lymphomas (reviewed in Lunning and Green [34]).”
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Self-citationGFI1 Cooperates with IKZF1/IKAROS to Activate Gene Expression in T-cell Acute Lymphoblastic Leukemia
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“Like acute myeloid leukemia, most ETP ALL harbor mutations that activate RAS and RAS pathway components.(63,65,66) JAK1 and JAK3 are also commonly mutated in ETP ALL.”
BackgroundLiver Effects of Clinical Drugs Differentiated in Human Liver Slices
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“Gene ranking is comprised of different gene expression parameters, such as fold change and its p-value, into one meta-characteristic, and the algorithm is described in detail elsewhere [88].”
BackgroundSelf-citationMutant IL-7Rα and mutant NRas are sufficient to induce murine T cell acute lymphoblastic leukemia
Cramer, S. D., Hixon, J. A., Andrews, C., Porter, R. J., Rodrigues, G. O. L., Wu, X., Back, T., Czarra, K., Michael, H., Cam, M., et al. (2018) · Leukemia · doi:10.1038/s41375-017-0001-0 · Cited by 17
“Concurrent NRAS and IL-7Rα pathway mutations also occurred in early T cell precursor leukemia and the T-ALL cell line DND41 [9, 10].”
Andersson, A., Moorman, A. V., Harrison, C. J., & Mullighan, C. G. (2016) · Wiley eBooks · doi:10.1002/9781118527948.ch5 · Cited by 20
Self-citationMolecular Biology of Childhood Leukemia
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Self-citationThe pleiotropic roles of EZH2 in T-cell immunity and immunotherapy
Wang, Y., Bui, T., & Zhang, Y. (2022) · International Journal of Hematology · doi:10.1007/s12185-022-03466-x · Cited by 17
Lymphoid malignancies: Another face to the Janus kinases
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“Consistent with this possibility, the JAK2V617F mutation has not been detected in cases of chronic lymphocytic leukemia (CLL) or pediatric or adult ALL.36–38 Aberrant JAK2-mediated signaling can induce lymphoid transformation, however, as rare translocations between JAK2 and TEL, PCM1, SSBP2, STRN3, BCR or PAX5 occur…”
InfluentialBernt, K. M., Hunger, S. P., & Neff, T. (2016) · Frontiers in Pediatrics · doi:10.3389/fped.2016.00049 · Cited by 16
Self-citationClinical Trials in the Genomic Era
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Zooming in across the Skin: A Macro-to-Molecular Panorama
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Inside the biology of early T-cell precursor acute lymphoblastic leukemia: the perfect trick
Tarantini, F., Cumbo, C., Anelli, L., Zagaria, A., Specchia, G., Musto, P., & Albano, F. (2021) · Biomarker Research · doi:10.1186/s40364-021-00347-z · Cited by 16
“similar results, whereas no correlations with normal human ETPs were found [5].”
BackgroundResultInfluentialOrentas, R. J., Nordlund, J., He, J., Sindiri, S., Mackall, C. L., Fry, T. J., & Khan, J. I. (2014) · Frontiers in Oncology · doi:10.3389/fonc.2014.00134 · Cited by 15
“Jude – Washington University Pediatric Cancer Genome Project, early precursor T-cell ALL shares many similarities to double negative thymocytes that have the potential to differentiate into cells of either T-cell or myeloid lineage (8, 9).”
BackgroundHOX-mediated LMO2 expression in embryonic mesoderm is recapitulated in acute leukaemias
Calero‐Nieto, F. J., Joshi, A., Bonadies, N., Kinston, S., Chan, W.-I., Gudgin, E. J., Pridans, C., Landry, J.-R., Kikuchi, J., Huntly, B. J. P., et al. (2013) · Oncogene · doi:10.1038/onc.2013.175 · Cited by 16
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“ETP-ALLs have been reported with mutations in the JAKkinases (10).”
InfluentialSelf-citationMarques, L. V. C., Noronha, E. P., Andrade, F. G., dos Santos-Bueno, F. V., Mansur, M. B., Terra‐Granado, E., & Pombo‐de‐Oliveira, M. S. (2018) · Frontiers in Oncology · doi:10.3389/fonc.2018.00488 · Cited by 16
“Although clinically and genetically heterogeneous diseases, T-ALL and AML present overlaps in genetic alterations that lead to pathogenic pathways, such as mutations in genes of the RAS signaling pathway (8), and cellular expression of lineage development markers, such as CD7 expression in AML and CD13 or CD33 in T-AL…”
BackgroundDiagnosis and treatment of lymphomas in the era of epigenetics
Chebly, A., Chouery, É., Ropio, J., Kourié, H. R., Beylot-Barry, M., Merlio, J., Tomb, R. R., & Chevret, E. (2020) · Blood Reviews · doi:10.1016/j.blre.2020.100782 · Cited by 17
Coninck, S. D., Berx, G., Taghon, T., Vlierberghe, P. V., & Goossens, S. (2019) · Advances in Biological Regulation · doi:10.1016/j.jbior.2019.100639 · Cited by 15
Targeting the Ras pathway in pediatric hematologic malignancies
Pikman, Y., & Stieglitz, E. (2020) · Current Opinion in Pediatrics · doi:10.1097/mop.0000000000000981 · Cited by 15
“Although Ras pathway-mutant ALL has been associated with steroid resistance [42], glucocorticoids and the MEK inhibitor selumetinib, have been shown to be synergistic in preclinical models [43 && ] and led to the ongoing Seludex clinical trial (NCT03705507).”
BackgroundInfluentialMenne, T., Slade, D., Savage, J., Johnson, S., Irving, J. A. E., Kearns, P. R., Plummer, R., Shenton, G., Veal, G. J., Vormoor, B. J., et al. (2022) · BMJ Open · doi:10.1136/bmjopen-2021-059872 · Cited by 15
“Main exclusion criteria ► ALL without presence of RAS- pathway activating mutations.”
BackgroundInfluentialNunes, S. C., Vita, S. D., Anighoro, A., Autelitano, F., Beaumont, E., Klingbeil, P., McGuinness, M. K., Duvert, B., Harris, C. E., Yang, L., et al. (2022) · Blood Cancer Journal · doi:10.1038/s41408-022-00663-z · Cited by 16
“Specifically, RAS mutations are highly prevalent in relapsed high-risk ALL after combination chemotherapy, and the activation of RAS signaling has been shown to act as the driver of both de novo and relapsed, chemotherapy-resistant disease [10, 11].”
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Self-citationDynamins in human diseases: differential requirement of dynamin activity in distinct tissues
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Multifaceted roles of IKZF1 gene, perspectives from bench to bedside
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FLT3 pathway is a potential therapeutic target for PRC2-mutated T-cell acute lymphoblastic leukemia
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Self-citationThe effect of co-occurring lesions on leukaemogenesis and drug response in T-ALL and ETP-ALL
Shirazi, P. T., Eadie, L. N., Heatley, S. L., Hughes, T. P., Yeung, D. T. O., & White, D. L. (2019) · British Journal of Cancer · doi:10.1038/s41416-019-0647-7 · Cited by 15
“ETP-ALL patients harbouring mutations in PRC2 core components have poor outcomes, particularly in EZH2-mutated cases, with an estimated 60% of these patients relapsing within 5 years.(58) Novel targeted treatment approaches are required based on an individual’s mutational profile in order to improve survival outcomes…”
BackgroundInfluentialSelf-citationLi, L., Mitra, A., Cui, K., Zhao, B., Choi, S., Lee, J. Y., Stamos, D. B., El‐Khoury, D., Warzecha, C. C., Pfeifer, K. E., et al. (2020) · Blood · doi:10.1182/blood.2019000794 · Cited by 16
Epigenetic regulation of protein translation in KMT2A-rearranged AML
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“ETP-ALL (characterized by a very immature CD4− CD8− DN phenotype and the expression of both stem cell and myeloid-associated markers [183], commonly display mutations in transcription factors associated to hematopoietic and T-cell development (GATA3, ETV6, RUNX1), to epigenetic regulators (DNMT3A, IDH1, IDH2, EZH2,),…”
BackgroundKato, M., Seki, M., Yoshida, K., Sato, Y., Oyama, R., Arakawa, Y., Kishimoto, H., Taki, T., Akiyama, M., Shiraishi, Y., et al. (2015) · British Journal of Haematology · doi:10.1111/bjh.13841 · Cited by 15
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Leveraging Cancer Genome Information in Hematologic Malignancies
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Non-coding RNA ANRIL and the number of plexiform neurofibromas in patients with NF1microdeletions
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“The SUZ12 protein is an essential component of the polycomb repressive complex 2 (PRC2) and somatic mutations as well as deletions of SUZ12 have recently been identified in various haematological malignancies indicating an important role for chromatin modifiers (such as the polycomb repressive complexes) in tumorigene…”
LMO2 Oncoprotein Stability in T-Cell Leukemia Requires Direct LDB1 Binding
Layer, J. H., Alford, C. E., McDonald, W. H., & Davé, U. P. (2015) · Molecular and Cellular Biology · doi:10.1128/mcb.00901-15 · Cited by 14
“RLIM, an E3 ubiquitin ligase which can be deleted in ETP-ALL cells (30), can accelerate the turnover of both LMO2 and LDB1; however, LMO2 turnover in this context is contingent upon LDB1 binding (32, 34).”
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The role of noncoding mutations in blood cancers
Rahman, S., & Mansour, M. R. (2019) · Disease Models & Mechanisms · doi:10.1242/dmm.041988 · Cited by 16
“…diseases, such as T cell ALL (T-ALL) and AML, have identified coding variants, chromosomal translocations, chimeric fusions (Box 1) and mutations, which have then been coupled with clinical outcome data for improved prognostication (Liu et al., 2017; Papaemmanuil et al., 2016; Zhang et al., 2012).”
Sakhdari, A., Thakral, B., Loghavi, S., Kanagal‐Shamanna, R., Yin, C. C., Zuo, Z., Routbort, M. J., Luthra, R., Medeiros, L. J., Wang, S. A., et al. (2019) · Cancer Medicine · doi:10.1002/cam4.2757 · Cited by 15
“Well-known translocations involving T-cell receptor gene loci, t(10;11)(p13;q14), or t(11;19)(q23;p13) were not present.”
BackgroundInterleukin‐7 in the transition of bone marrow progenitors to the thymus
Plumb, A. W., Sheikh, A., Carlow, D. A., Patton, D. T., Ziltener, H. J., & Abraham, N. (2017) · Immunology and Cell Biology · doi:10.1038/icb.2017.68 · Cited by 15
La leucemia linfoblástica aguda y modelos animales alternativos para su estudio en Colombia
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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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