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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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BackgroundGenomic disruption of the histone methyltransferase SETD2 in chronic lymphocytic leukaemia
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“global transcriptional profile of ETP-ALL was similar to that of normal hematopoietic stem cells and myeloid leukemia [19].”
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“Recently whole-genome sequencing of early T-cell precursor ALL identified alterations in PRC2 genes, including SUZ12, EZH2 and EED [38].”
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“ETP-ALL is characterized by a distinct immunophenotype, with expression of myeloid/stem-cell markers, a high frequency of JAK–STAT-activating mutations (20), biochemical evidence of activated JAK–STAT signaling (21), and exquisite sensitivity to the JAK inhibitor ruxolitinib in preclinical models (22).”
BackgroundSelf-citationChromatin modifiers and the promise of epigenetic therapy in acute leukemia
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T-Cell Mechanobiology: Force Sensation, Potentiation, and Translation
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Wnt inhibition leads to improved chemosensitivity in paediatric acute lymphoblastic leukaemia
Dandekar, S. C., Romanos‐Sirakis, E., Pais, F. M., Bhatla, T., Jones, C. L., Bourgeois, W., Hunger, S. P., Raetz, E. A., Hermiston, M. L., DasGupta, R., et al. (2014) · British Journal of Haematology · doi:10.1111/bjh.13011 · Cited by 77
Self-citationDiagnostic Applications of High-Throughput DNA Sequencing
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“Novel recurrent mutations in genes DNM2, ECT2L, and RELN were also detected (94).”
BackgroundThe ribosomal RPL10 R98S mutation drives IRES-dependent BCL-2 translation in T-ALL
Kampen, K. R., Sulima, S. O., Verbelen, B., Girardi, T., Vereecke, S., Rinaldi, G., Verbeeck, J., de Beeck, J. O., Uyttebroeck, A., Meijerink, J. P. P., et al. (2018) · Leukemia · doi:10.1038/s41375-018-0176-z · Cited by 76
Self-citationChildhood acute lymphoblastic leukemia: Integrating genomics into therapy
Tasian, S. K., Loh, M. L., & Hunger, S. P. (2015) · Cancer · doi:10.1002/cncr.29573 · Cited by 84
Self-citationOlsson, L., & Johansson, B. (2015) · British Journal of Haematology · doi:10.1111/bjh.13342 · Cited by 76
Sequencing histone-modifying enzymes identifies UTX mutations in acute lymphoblastic leukemia
Mar, B. G., Bullinger, L., Basu, E. M., Schlis, K. D., Silverman, L. B., Döhner, K., & Armstrong, S. A. (2012) · Leukemia · doi:10.1038/leu.2012.56 · Cited by 76
Pharmacogenomics of acute lymphoblastic leukemia
Kager, L., & Evans, W. E. (2006) · Current Opinion in Hematology · doi:10.1097/01.moh.0000231424.46148.f9 · Cited by 75
Self-citationTranslating Genomics for Precision Cancer Medicine
Roychowdhury, S., & Chinnaiyan, A. M. (2014) · Annual Review of Genomics and Human Genetics · doi:10.1146/annurev-genom-090413-025552 · Cited by 75
Recent advances in genetic predisposition to pediatric acute lymphoblastic leukemia
Bloom, M., Maciaszek, J. L., Clark, M. E., Pui, C., & Nichols, K. E. (2019) · Expert Review of Hematology · doi:10.1080/17474086.2020.1685866 · Cited by 79
“5% (12/264) of pediatric and young adult T-ALL cases [75] and 30% (4/12) of early thymocyte precursor (ETP)-ALL cases [81].”
BackgroundSelf-citationKöhrer, S., Havránek, O., Seyfried, F., Hurtz, C., Coffey, G., Kim, E., ten Hacken, E., Jaeger, U., Vanura, K., O'Brien, S. M., et al. (2016) · Leukemia · doi:10.1038/leu.2016.9 · Cited by 78
Aberrant Signaling Pathways in T-Cell Acute Lymphoblastic Leukemia
Bongiovanni, D., Saccomani, V., & Piovan, E. (2017) · International Journal of Molecular Sciences · doi:10.3390/ijms18091904 · Cited by 78
“Gain-of-function mutations in JAK3 and JAK1 [42,128,129], as well as in STAT5 gene [130,131] have been detected in a variable fraction of T-ALL patients, along with a rare t(9;12)(p24;p13) translocation driving the expression of a constitutively active fusion protein ETV6-JAK2 [132,133].”
BackgroundInfluentialCDKN2B downregulation and other genetic characteristics in T-acute lymphoblastic leukemia
Jang, W., Park, J., Kwon, A., Choi, H., Kim, J., Lee, D., Han, E., Jekarl, D. W., Chae, H., Han, K., et al. (2019) · Experimental & Molecular Medicine · doi:10.1038/s12276-018-0195-x · Cited by 74
Malignant Peripheral Nerve Sheath Tumors: From Epigenome to Bedside
Korfhage, J. L., & Lombard, D. B. (2019) · Molecular Cancer Research · doi:10.1158/1541-7786.mcr-19-0147 · Cited by 78
LNK/SH2B3 regulates IL-7 receptor signaling in normal and malignant B-progenitors
Cheng, Y., Chikwava, K. R., Wu, C., Zhang, H., Bhagat, A., Pei, D., Choi, J. K., & Tong, W. (2016) · Journal of Clinical Investigation · doi:10.1172/jci81468 · Cited by 74
“Recently, somatic deletion/mutations in LNK (also known as SH2B3) were found in various B-ALLs and T-ALLs in children (2, 6, 29, 30).”
BackgroundSelf-citationGenomic aberrations frequently alter chromatin regulatory genes in chordoma
Wang, L., Zehir, A., Nafa, K., Zhou, N., Berger, M. F., Casanova, J., Sadowska, J., Lü, C., Allis, C. D., Gounder, M. M., et al. (2016) · Genes Chromosomes and Cancer · doi:10.1002/gcc.22362 · Cited by 75
Requirement for Lyl1 in a model of Lmo2-driven early T-cell precursor ALL
McCormack, M. P., Shields, B. J., Jackson, J. T., Nasa, C., Shi, W., Slater, N. J., Tremblay, C. S., Rabbitts, T. H., & Curtis, D. J. (2013) · Blood · doi:10.1182/blood-2012-09-458570 · Cited by 74
“LYL1 is expressed in ETP-ALL and required for growth of ETP-ALL cell lines Finally, we sought to examine the functional relevance of the Lmo2- Lyl1 interaction in human T-ALL.”
BackgroundMethodResultInfluentialGenome-Wide Characterization of Pancreatic Adenocarcinoma Patients Using Next Generation Sequencing
Liang, W. S., Craig, D. W., Carpten, J. D., Borad, M. J., Demeure, M. J., Weiss, G. J., Izatt, T., Sinari, S. A., Christoforides, A., Aldrich, J., et al. (2012) · PLoS ONE · doi:10.1371/journal.pone.0043192 · Cited by 73
“IL7R also has not been previously reported in PAC, but has been found to demonstrate activating mutations in lymphoblastic leukemias [62,63,64].”
BackgroundEpigenetics in T‐cell acute lymphoblastic leukemia
Peirs, S., der Meulen, J. V., de Walle, I. V., Taghon, T., Speleman, F., Poppe, B. G., & Vlierberghe, P. V. (2014) · Immunological Reviews · doi:10.1111/imr.12237 · Cited by 76
“In addition, the concept of DNMT3A mutant preleukemic HSCs, which emerge in aging adults, might also explain why DNMT3A mutations are not identified in pediatric ETP-ALL (15) but are mainly present in early immature adult T-ALLs (31, 32).”
BackgroundInfluentialPalmitoylacyltransferase Zdhhc9 inactivation mitigates leukemogenic potential of oncogenic Nras
Liu, P., Jiao, B., Zhang, R., Zhao, H., Zhang, C., Wu, M. H., Li, D., Zhao, X., Qiu, Q., Li, J., et al. (2015) · Leukemia · doi:10.1038/leu.2015.293 · Cited by 72
Hyperactivation of JAK1 tyrosine kinase induces stepwise, progressive pruritic dermatitis
Yasuda, T., Fukada, T., Nishida, K., Nakayama, M., Matsuda, M., Miura, I., Dainichi, T., Fukuda, S., Kabashima, K., Nakaoka, S., et al. (2016) · Journal of Clinical Investigation · doi:10.1172/jci82887 · Cited by 72
“This may reflect multiple incidental alterations in the genome in early T-ALL genesis (46), and JAK1R878H may not be a driver mutation.”
BackgroundMixed-Phenotype Acute Leukemia: Diagnostic Criteria and Pitfalls
Charles, N. J., & Boyer, D. F. (2017) · Archives of Pathology & Laboratory Medicine · doi:10.5858/arpa.2017-0218-ra · Cited by 72
The Biology of B-Progenitor Acute Lymphoblastic LeukemiaPreprint
Roberts, K. G., & Mullighan, C. G. (2019) · Cold Spring Harbor Perspectives in Medicine · doi:10.1101/cshperspect.a034835 · Cited by 76
Self-citationLópez, C., Bergmann, A. K., Paul, U., Penas, E. M. M., Nagel, I., Betts, M. J., Johansson, P., Ritgen, M., Baumann, T., Aymerich, M., et al. (2016) · British Journal of Haematology · doi:10.1111/bjh.13952 · Cited by 71
“(Elliott et al, 2011; Bains et al, 2012; Koo et al, 2012; Zhang et al, 2012; Bouchekioua et al, 2014).”
Patient-derived orthotopic xenografts of pediatric brain tumors: a St. Jude resource
Smith, K. S., Xu, K., Mercer, K., Boop, F. A., Klimo, P., DeCupyere, M., Grenet, J. A., Robinson, S., Dunphy, P. S., Baker, S. J., et al. (2020) · Acta Neuropathologica · doi:10.1007/s00401-020-02171-5 · Cited by 69
“Quality control, somatic mutation calling and classification were then conducted, as previously described [49, 50].”
MethodSelf-citationBandapalli, O. R., Zimmermann, M., Kox, C., Stanulla, M., Schrappe, M., Ludwig, W.-D., Koehler, R., Muckenthaler, M. U., & Kulozik, A. E. (2013) · Haematologica · doi:10.3324/haematol.2012.073585 · Cited by 71
Wendorff, A. A., Quinn, S. A., Rashkovan, M., Madubata, C. J., Ambesi‐Impiombato, A., Litzow, M. R., Tallman, M. S., Paietta, E. M., Paganin, M., Basso, G., et al. (2018) · Cancer Discovery · doi:10.1158/2159-8290.cd-18-1005 · Cited by 72
“Notably, suppression of Phf6 in mouse B-cell lymphoma cells has been described to increase lineage plasticity, in this case resulting in decreased expression of B-cell lineage genes and upregulation of T-cell markers (26), and PHF6 mutations are prevalent in ETP ALLs and myeloid/T MPALs, which are characterized by mix…”
BackgroundSelf-citationRoles of SETD2 in Leukemia—Transcription, DNA-Damage, and Beyond
Skucha, A., Ebner, J., & Grebien, F. (2019) · International Journal of Molecular Sciences · doi:10.3390/ijms20051029 · Cited by 74
“Focal deletions of SETD2 were identified in 10% of patients suffering from early T-cell precursor acute lymphoblastic leukemia (ETP-ALL) [19].”
BackgroundStrategies to Overcome Resistance Mechanisms in T-Cell Acute Lymphoblastic Leukemia
Follini, E., Marchesini, M., & Roti, G. (2019) · International Journal of Molecular Sciences · doi:10.3390/ijms20123021 · Cited by 73
MuPIT interactive: webserver for mapping variant positions to annotated, interactive 3D structures
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Meacham, C. E., Lawton, L. N., Soto‐Feliciano, Y. M., Pritchard, J. R., Joughin, B. A., Ehrenberger, T., Fenouille, N., Zuber, J. A., Williams, R. T., Young, R. A., et al. (2015) · Genes & Development · doi:10.1101/gad.254151.114 · Cited by 67
“Recently, inactivating PHF6 mutations have been identified in ;25%–30% of human T-cell ALLs (Van Vlierberghe et al. 2010; Zhang et al. 2012) and in 2%–3% of acute myeloid leukemias (AMLs) (Supplemental Table 5; Van Vlierberghe et al.”
BackgroundMethodInfluentialThe acquisition of molecular drivers in pediatric therapy-related myeloid neoplasms
Schwartz, J. R., Ma, J., Kamens, J. L., Westover, T., Walsh, M. P., Brady, S. W., Michael, J. R., Chen, X., Montefiori, L. E., Song, G., et al. (2021) · Nature Communications · doi:10.1038/s41467-021-21255-8 · Cited by 69
Self-citationAdult Acute Lymphoblastic Leukemia: 2025 Update on Diagnosis, Therapy, and Monitoring
Kantarjian, H. M., & Jabbour, E. J. (2025) · American Journal of Hematology · doi:10.1002/ajh.27708 · Cited by 81
“[79, 80].”
Posttranslational modifications of RUNX1 as potential anticancer targets
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Xu, J., Haigis, K. M., Firestone, A. J., McNerney, M. E., Li, Q., Davis, E., Chen, S.-C., Nakitandwe, J., Downing, J. R., Jacks, T., et al. (2013) · Cancer Discovery · doi:10.1158/2159-8290.cd-13-0096 · Cited by 68
Self-citationKhan, M., Siddiqi, R. L., & Naqvi, K. (2018) · Annals of Hematology · doi:10.1007/s00277-018-3297-6 · Cited by 69
The Genetics and Mechanisms of T-Cell Acute Lymphoblastic LeukemiaPreprint
Gianni, F., Belver, L., & Ferrando, A. A. (2019) · Cold Spring Harbor Perspectives in Medicine · doi:10.1101/cshperspect.a035246 · Cited by 69
“(Ntziachristos et al. 2012; Zhang et al. 2012), and the KDM6A histone demethylase (Ntziachristos et al.”
BackgroundInfluentialOshima, K., Zhao, J., Pérez‐Durán, P., Brown, J. A., Patiño-Galindo, J. Á., Chu, T. H., Quinn, S. A., Gunning, T. S., Belver, L., Ambesi‐Impiombato, A., et al. (2020) · Nature Cancer · doi:10.1038/s43018-020-00124-1 · Cited by 67
Self-citationJAK/STAT in leukemia: a clinical update
Liang, D., Wang, Q.-L., Zhang, W., Tang, H., Song, C., Yan, Z., Liang, Y., & Wang, H. (2024) · Molecular Cancer · doi:10.1186/s12943-023-01929-1 · Cited by 82
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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