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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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“…diseases such as severe combined immunodeficiency (SCID) (Puel et al. 1998; Kalman et al. 2004) and acute lymphoblastic leukemia (Korte et al. 2000; Zhang et al. 2012), while genetic variation in IL7R can predispose to such diseases as sarcoidosis (Heron et al. 2009), primary biliary cirrhosis…”
BackgroundDynamin 2–dependent endocytosis is required for normal megakaryocyte development in mice
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BackgroundThe genetic basis of early T–cell precursor acute lymphoblastic leukaemia
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β-Catenin activation synergizes with Pten loss and Myc overexpression in Notch-independent T-ALL
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“Additionally, IL7Rα mutations and JAK1 and JAK3 mutations are also reported in early T cell precursor (ETP) ALL, which historically has a poor prognosis [5].”
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“Somatic heterozygous mutations in the DNM2 gene were identified in children affected by early T-cell precursor acute lymphoblastic leukaemia (ETP-ALL), a form of ALL associated with a high risk of treatment failure [29].”
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“Whole genome sequencing of 12 cases of ETP ALL identified mutations in genes encoding components of the polycomb repressor complex 2 (PRC2), including deletions and sequence mutations of EZH2, SUZ12, and EED [33].”
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“Interestingly, recent exome sequencing studies have identified SETD2 mutations, although with a low percentage, in renal cell (24–27), lung (28, 29), and hematologic (30) cancers.”
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Targeting the PIM protein kinases for the treatment of a T-cell acute lymphoblastic leukemia subset
Padi, S. K. R., Luevano, L. A., An, N., Pandey, R., Singh, N., Song, J. H., Aster, J. C., Yu, X., Mehrotra, S., & Kraft, A. S. (2017) · Oncotarget · doi:10.18632/oncotarget.16320 · Cited by 42
“Previous genomic studies also suggested that JAK/STAT pathway hyper activation may be a hallmark of ETP-ALL [34].”
BackgroundMethodResultInfluentialOncogenic transcriptional program driven by TAL1 in T-cell acute lymphoblastic leukemia
Tan, T. K., Zhang, C., & Sanda, T. (2018) · International Journal of Hematology · doi:10.1007/s12185-018-2518-z · Cited by 42
Rashkovan, M., Alberó, R., Gianni, F., Perez-Duran, P., Miller, H. I., Mackey, A. L., Paietta, E. M., Tallman, M. S., Rowe, J. M., Litzow, M. R., et al. (2021) · Cancer Discovery · doi:10.1158/2159-8290.cd-21-0551 · Cited by 42
Gao, B., Liu, X., Li, Z., Zhao, L., & Pan, Y. (2021) · Frontiers in Oncology · doi:10.3389/fonc.2020.600514 · Cited by 41
“Additionally, inactivating mutations or deletion of EZH2 have been identified in several types of tumor, such as Kras-driven lung adenocarcinoma and T cell precursor acute lymphoblastic leukemia, suggesting the tumor-suppressive effect of EZH2 in certain contexts (51, 52).”
BackgroundTargeting oncogenic kinases: Insights on FDA approved tyrosine kinase inhibitors
Hussain, S., Mursal, M., Verma, G., Hasan, S. S., & Khan, M. F. (2024) · European Journal of Pharmacology · doi:10.1016/j.ejphar.2024.176484 · Cited by 41
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Endogenous dendritic cells from the tumor microenvironment support T-ALL growth via IGF1R activation
Triplett, T., Cardenas, K. T., Lancaster, J. N., Hu, Z., Selden, H. J., Jasso, G. J., Balasubramanyam, S., Chan, K., Li, L., Chen, X., et al. (2016) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1520245113 · Cited by 41
“7F) (25, 33), suggesting elevated PDGFRβ expression is Fig.”
BackgroundSelf-citationDing, Y., Zhang, B., Payne, J. L., Song, C., Ge, Z., Gowda, C. S., Iyer, S., Dhanyamraju, P. K., Dorsam, G. P., Reeves, M. E., et al. (2019) · Leukemia · doi:10.1038/s41375-019-0474-0 · Cited by 41
ARID5B Influences Antimetabolite Drug Sensitivity and Prognosis of Acute Lymphoblastic Leukemia
Xu, H. Y., Zhao, X., Bhojwani, D., Shuyu, E., Goodings, C., Zhang, H., Seibel, N. L., Yang, W., Li, C., Carroll, W. L., et al. (2019) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-19-0190 · Cited by 41
“These patients represent consecutively enrolled cases or were selected to represent the diversity of ALL subtypes (28, 29).”
BackgroundSelf-citationChan, M. P., Plouffe, K. R., Liu, C., Palanisamy, N., Carskadon, S. L., Zhao, L., Nazarian, R. M., Durham, A. B., Johnson, T. M., Andea, A. A., et al. (2019) · Modern Pathology · doi:10.1038/s41379-019-0424-4 · Cited by 41
Roels, J., Thénoz, M., Szarzyńska‐Zawadzka, B., Landfors, M., Coninck, S. D., Demoen, L., Provez, L., Kuchmiy, A. A., Strubbe, S., Reunes, L., et al. (2020) · Blood Cancer Discovery · doi:10.1158/2643-3230.bcd-20-0059 · Cited by 40
“Of note, COSMe-II Cluster B− leukemias showed a trend for enrichment of genetic defects previously associated with early immature T-ALL and ETP-ALL (12,13), including 5q deletions, loss-of-function alterations targeting WT1, CTCF, PRC2 (EZH2, SUZ12 or EED), as well as leukemias displaying aberrant activation of HOXA g…”
BackgroundInfluentialEmerging molecular subtypes and therapeutic targets in B-cell precursor acute lymphoblastic leukemia
Li, J., Dai, Y., Wu, L., Zhang, M., Ouyang, W., Huang, J., & Chen, S. (2021) · Frontiers of Medicine · doi:10.1007/s11684-020-0821-6 · Cited by 44
Self-citationIn vivo single-cell CRISPR uncovers distinct TNF programmes in tumour evolution
Renz, P. F., Ghoshdastider, U., Baghai Sain, S., Valdivia-Francia, F., Khandekar, A., Ormiston, M., Bernasconi, M., Duré, C., Kretz, J. A., Lee, M., et al. (2024) · Nature · doi:10.1038/s41586-024-07663-y · Cited by 40
Characterization of a set of tumor suppressor microRNAs in T cell acute lymphoblastic leukemia
Sanghvi, V. R., Mavrakis, K. J., der Meulen, J. V., Boice, M., Wolfe, A. L., Carty, M., Mohan, P., Rondou, P., Socci, N. D., Benoît, Y., et al. (2014) · Science Signaling · doi:10.1126/scisignal.2005500 · Cited by 40
HSC commitment–associated epigenetic signature is prognostic in acute myeloid leukemia
Bartholdy, B., Christopeit, M., Will, B., Mo, Y., Barreyro, L., Yu, Y., Bhagat, T. D., Okoye-Okafor, U. C., Todorova, T. I., Greally, J. M., et al. (2014) · Journal of Clinical Investigation · doi:10.1172/jci71264 · Cited by 42
“Interestingly, this stem cell commitment–associated epigenetic signature was enriched in loci associated with several genes that are commonly implicated not only in human HSC function and commitment but also in leukemogenesis, such as CEBPA (27–29), E2F1 (30), KRAS (31, 32), and WEE1 (33) as well as a noncoding transc…”
Ksionda, O., Melton, A. A., Bache, J., Tenhagen, M., Bakker, J., Harvey, R. C., Winter, S. S., Rubio, I., & Roose, J. P. (2015) · Oncogene · doi:10.1038/onc.2015.431 · Cited by 39
Self-citationNonneuronal roles for the reelin signaling pathway
Khialeeva, E., & Carpenter, E. M. (2016) · Developmental Dynamics · doi:10.1002/dvdy.24462 · Cited by 40
“…implicated in liver fibrosis and rheumatoid arthritis, and alterations in reelin levels are observed in multiple cancers (Wang et al., 2002; Perrone et al., 2007; Seigel et al., 2007; Botella-L opez et al., 2008; Magnani et al., 2010; Stein et al., 2010; Zhang et al., 2012; Mansy et al., 2014).”
BackgroundWilliams, L. A., Yang, J. J. J., Hirsch, B. A., Marcotte, E. L., & Spector, L. G. (2019) · Cancer Epidemiology Biomarkers & Prevention · doi:10.1158/1055-9965.epi-18-0801 · Cited by 38
Sharma, N. D., Nickl, C. K., Kang, H., Ornatowski, W., Brown, R. B., Ness, S. A., Loh, M. L., Mullighan, C. G., Winter, S. S., Hunger, S. P., et al. (2019) · Cancer Science · doi:10.1111/cas.14021 · Cited by 40
Self-citationXu, J. Z., Chen, C., Sussman, J., Yoshimura, S., Vincent, T. L., Pölönen, P., Hu, J., Bandyopadhyay, S., Elghawy, O., Yu, W., et al. (2024) · Nature Cancer · doi:10.1038/s43018-024-00863-5 · Cited by 40
“A primary hypothesis for ETP-ALL treatment resistance has been that ETP-ALL retains myeloid populations that confer resistance to ALL-directed therapy 20,21 .”
Self-citationDistinctive genotypes in infants with T‐cell acute lymphoblastic leukaemia
Mansur, M. B., van Delft, F. W., Colman, S., Furness, C. L., Gibson, J., Emerenciano, M., Kempski, H. M., Clappier, E., Cavé, H., Soulier, J., et al. (2015) · British Journal of Haematology · doi:10.1111/bjh.13613 · Cited by 39
Degryse, S., Bornschein, S., de Bock, C. E., Leroy, E., Bempt, M. V., Demeyer, S., Jacobs, K., Geerdens, E., Gielen, O., Soulier, J., et al. (2017) · Blood · doi:10.1182/blood-2017-07-797597 · Cited by 39
Self-citationBiology of Childhood Acute Lymphoblastic Leukemia
Nigro, L. L. (2013) · Journal of Pediatric Hematology/Oncology · doi:10.1097/mph.0b013e31828f8746 · Cited by 38
Wang, C., Oshima, M., Sato, D., Matsui, H., Kubota, S., Aoyama, K., Nakajima‐Takagi, Y., Koide, S., Matsubayashi, J., Mochizuki‐Kashio, M., et al. (2018) · Journal of Clinical Investigation · doi:10.1172/jci94645 · Cited by 40
León, T. E., Rapoz-D’Silva, T., Bertoli, C., Rahman, S., Magnussen, M., Philip, B., Farah, N., Richardson, S. E., Ahrabi, S., Guerra‐Assunção, J. A., et al. (2020) · Cancer Discovery · doi:10.1158/2159-8290.cd-19-0789 · Cited by 39
“5) A) GSEA analysis of EZH2-KO1 and EZH2-WT cells for genes upregulated in human ETP- ALL relative to non-ETP T-ALL cases (Zhang et al, 2012).”
BackgroundResultGiacomo, D. D., Starza, R. L., Gorello, P., Pellanera, F., Atak, Z. K., Keersmaecker, K. D., Pierini, V., Harrison, C. J., Arniani, S., Moretti, M., et al. (2021) · Blood · doi:10.1182/blood.2020010510 · Cited by 39
Self-citationPHF6 Mutations in Hematologic Malignancies
Kurzer, J. H., & Weinberg, O. K. (2021) · Frontiers in Oncology · doi:10.3389/fonc.2021.704471 · Cited by 41
“B-Lymphoblastic Leukemia Despite their prevalence in T-ALL, PHF6 mutations have only rarely been identified in B-lymphoblastic leukemia (4, 41, 67).”
BackgroundRole of the adaptor protein LNK in normal and malignant hematopoiesis
Gery, S., & Koeffler, H. P. (2012) · Oncogene · doi:10.1038/onc.2012.435 · Cited by 42
Nelarabine: when and how to use in the treatment of T-cell acute lymphoblastic leukemia
Shimony, S. O., DeAngelo, D. J., & Luskin, M. R. (2023) · Blood Advances · doi:10.1182/bloodadvances.2023010303 · Cited by 38
“1 19-21 It can affect individuals of any age, does not present with bulky mediastinal disease or hyperleukocytosis, and is de fi ned immunophenotypically as being CD8 − , CD1a − , and CD5 dim / CD5 − .”
BackgroundChimeric antigen receptor T-cell therapy for T-cell acute lymphoblastic leukemia
Oh, B. L. Z., Vinanica, N., Wong, D., & Campana, D. (2024) · Haematologica · doi:10.3324/haematol.2023.283848 · Cited by 43
Self-citationKantarjian, H. M., Pui, C., & Jabbour, E. J. (2025) · The Lancet · doi:10.1016/s0140-6736(25)00864-5 · Cited by 49
Self-citationWild-type KRAS inhibits oncogenic KRAS-induced T-ALL in mice
Staffas, A., Karlsson, C., Persson, M., Palmqvist, L., & Bergö, M. O. (2014) · Leukemia · doi:10.1038/leu.2014.315 · Cited by 36
Schwann cells, but not Oligodendrocytes, Depend Strictly on Dynamin 2 Function
Gerber, D., Ghidinelli, M., Tinelli, E., Somandin, C., Gerber, J., Pereira, J. A., Ommer, A., Figlia, G., Miehe, M., Nägeli, L. G., et al. (2019) · eLife · doi:10.7554/elife.42404 · Cited by 39
Pikman, Y., Tasian, S. K., Sulis, M. L., Stevenson, K. E., Blonquist, T. M., Winger, B. A., Cooper, T. M., Pauly, M. G., Maloney, K. W., Burke, M. J., et al. (2021) · Cancer Discovery · doi:10.1158/2159-8290.cd-20-0564 · Cited by 38
“© 2021 American Association for Cancercancerdiscovery.aacrjournals.org Downloaded from Pikman et al.RESEARCH ARTiCLE OF5 | CANCER DISCOVERY june 2021 AACRJournals.org have been described in B-ALL (24, 25) and T-ALL (6, 26), it is not known whether FLT3 inhibitors have efficacy in patients with these leukemias.”
BackgroundInfluentialSelf-citationNRASG12V oncogene facilitates self-renewal in a murine model of acute myelogenous leukemia.
Sachs, Z., LaRue, R., Nguyen, H. T. Q., Sachs, K., Noble, K. E., Hassan, N. A. M., Diaz-Flores, E., Rathe, S., Sarver, A., Bendall, S., et al. (2014) · Blood · doi:10.1182/blood-2013-08-521708 · Cited by 30
Zhang, Y., Yan, X., Sashida, G., Zhao, X., Rao, Y., Goyama, S., Whitman, S. P., Zorko, N. A., Bernot, K. M., Conway, R. M., et al. (2012) · Blood · doi:10.1182/blood-2012-02-412379 · Cited by 39
DNA Methylation and Chromatin Remodeling: The Blueprint of Cancer Epigenetics
Bhattacharjee, D., Shenoy, S., & Bairy, L. K. (2016) · Scientifica · doi:10.1155/2016/6072357 · Cited by 37
EZH2 mutations and promoter hypermethylation in childhood acute lymphoblastic leukemia
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Gowda, C. S., Song, C., Kapadia, M. A., Payne, J. L., Hu, T., Ding, Y., & Dovat, S. (2016) · Advances in Biological Regulation · doi:10.1016/j.jbior.2016.09.003 · Cited by 37
Spurious transcription and its impact on cell function
Wade, J. T., & Grainger, D. C. (2017) · Transcription · doi:10.1080/21541264.2017.1381794 · Cited by 38
Hixon, J. A., Andrews, C., Kashi, L., Kohnhorst, C. L., Senkevitch, E., Czarra, K., Barata, J. T., Li, W., Schneider, J. P., Walsh, S. T. R., et al. (2019) · Leukemia · doi:10.1038/s41375-019-0531-8 · Cited by 37
Genetic abnormalities associated with acute lymphoblastic leukemia
Yokota, T., & Kanakura, Y. (2016) · Cancer Science · doi:10.1111/cas.12927 · Cited by 37
Adolescent and young adult non‐Hodgkin lymphoma
Hochberg, J. C., El‐Mallawany, N. K., & Abla, O. (2016) · British Journal of Haematology · doi:10.1111/bjh.14074 · Cited by 37
“…in children showed a cohort of early T-cell phenotype suggesting a trend toward decreased EFS and OS in these patients (Coustan-Smith et al, 2009; Zhang et al, 2012), however, there is conflicting data in the literature about this and it remains to be seen what the exact prognostic significance…”
Background
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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