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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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Self-citationMEF2C opposes Notch in lymphoid lineage decision and drives leukemia in the thymus
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Influential14-3-3 regulates the LNK/JAK2 pathway in mouse hematopoietic stem and progenitor cells.
Jiang, J., Balcerek, J., Rozenova, K. A., Cheng, Y., Bersenev, A., Wu, C., Song, Y., & Tong, W. (2012) · Journal of Clinical Investigation · doi:10.1172/jci59719 · Cited by 26
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Self-citationConcomitant germ‐line RUNX 1 and acquired ASXL 1 mutations in a T‐cell acute lymphoblastic leukemia
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“Remarkably, about half of the ETP-ALL patients seem to have an activated Notch signaling pathway based on measured activity scores, despite their overall lower incidence of NOTCH-activating mutations [105].”
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“Reelin (RELN) has been shown to mutate in early T-cell precursors, inherited disorders, and T-ALL.(13) The inhibition of RELN can block activation of the phosphoinositide 3-kinase (PI3K)/AKT/mammalian target of rapamycin (mTOR) signaling pathway, and induce cell apoptosis and autophagy in prostate cancer.”
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Genescà, E., & Starza, R. L. (2022) · Cancers · doi:10.3390/cancers14081873 · Cited by 26
“In fact, either an internal tandem duplication (FLT3-ITD) or point mutations in the tyrosine kinase domain (FLT3-TKD) [39,40] have been detected in 35% of adult and less than 10% of pediatric ETP-ALL cases [30,41].”
BackgroundMutant IL7R collaborates with MYC to induce T-cell acute lymphoblastic leukemia
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“Several groups recently reported the presence of somatically acquired activating IL7R mutations occurring in approximately 10% of T-ALL cases (Shochat et al, 2011; Zenatti et al, 2011; Zhang et al, 2012).”
InfluentialLNK (SH2B3): paradoxical effects in ovarian cancer
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“Activating IL7R mutations are also recurrently found in T-ALL patients.(28) Interestingly, overexpression of gain-of-function mutant variants of IL7R in p19(Arf) mouse hematopoietic progenitors resulted in a similar T-ALL formation with an immature Lyl1 expression profile, and high levels of Lmo2.”
BackgroundSelf-citationThe complexity of epigenetic diseases
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“However, both gain-of-function [79] and loss-of-function [80–83] mutations have been observed in lymphoma and leukaemia, respectively (reviewed in refs 84 and 85).”
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“Yet additional activating NOTCH1 mutations were found in more than 50% of T-ALL patients [29].”
BackgroundInfluentialNovel epigenetic therapies in hematological malignancies: Current status and beyond
Gallipoli, P., & Huntly, B. J. P. (2017) · Seminars in Cancer Biology · doi:10.1016/j.semcancer.2017.07.005 · Cited by 25
“In T-cell ALL, up to 25% of cases have been reported to carry loss-of-function mutations in PRC2 members (mostly EZH2)[13] and in early T-cell precursor (ETP) ALL, EZH2 loss-of-function mutations are present in almost 50% of patients [78].”
BackgroundNoronha, E. P., Marques, L. V. C., Andrade, F. G., Sardou-Cezar, I., dos Santos-Bueno, F. V., Zampier, C. D. P., Terra‐Granado, E., & Pombo‐de‐Oliveira, M. S. (2019) · Cancer Management and Research · doi:10.2147/cmar.s196574 · Cited by 25
“The genomic profiles of ETP-ALL and T/M-MPAL have demonstrated that both diseases might have gene aberrations with potential to target therapy.(6,7) It is important to highlight that B/ M-MPAL, when associated with BCR-ABL1 and KMT2A/ AFF1 genetic abnormalities, determines the treatment strategy.”
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Targeting the JAK/STAT Pathway in T Cell Lymphoproliferative Disorders
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“We recently reported that mutations of genes encoding PRC2 subunits (EZH2, EED or SUZ12) induce apoptosis resistance in T-ALL [20], and both JAK3 and PRC2 mutations have been reported at high frequency in ETP T-ALL [31, 34, 35].”
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“Several studies have explored the genetic traits of ALL samples and have identified various mutational and transcriptional signatures unique to ETP-ALL (Zhang et al., 2012; Neumann et al., 2013; Zuurbier et al., 2014; Kumar et al., 2019; Wang and Zhang, 2020).”
BackgroundOncohistones and disrupted development in pediatric-type diffuse high-grade glioma
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“Of note, PRC2 loss of function, through inactivating mutation in essential components such as EZH2, EED, or SUZ12, is found in other cancers like early T-progenitor ALL, and leads to a more complete loss of H3K27me3 than H3 K27M-mediated PRC2 dysfunction [43].”
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“More recently, mutations in PRC2 members and other chromatin modifiers have also been demonstrated in T-cell acute lymphoblastic leukemia [Zhang et al. 2012].”
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“Here, we identified a number of novel putative ZEB2 interaction partners, including recurrently mutated proteins in T-ALL, such as the essential hematopoietic transcription factor RUNX1,35 the RNA processing protein HNRNPH1,36 and NUMA1, a protein involved in regulation of mitotic spindle organization and asymmetric/s…”
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“Discussion Elevated IL-7 levels and activating IL-7Ra Cys-substitutions are associated with human leukemia (6, 40, 41).”
BackgroundJAK kinase inhibitors for the treatment of acute lymphoblastic leukemia
Degryse, S., & Cools, J. (2015) · Journal of Hematology & Oncology · doi:10.1186/s13045-015-0192-7 · Cited by 24
“These data indicate that JAK inhibitors are promising agents for the treatment of T-ALL, and that clinical trials to test these agents are warranted.”
BackgroundInfluentialSelf-citationDeletions of the long arm of chromosome 5 define subgroups of T-cell acute lymphoblastic leukemia
Starza, R. L., Barba, G., Demeyer, S., Pierini, V. E., Giacomo, D. D., Gianfelici, V., Schwab, C. J., Matteucci, C., Vicente, C., Cools, J., et al. (2016) · Haematologica · doi:10.3324/haematol.2016.143875 · Cited by 24
Self-citation3D Chromosomal Landscapes in Hematopoiesis and Immunity
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Multi-omic approaches to improve outcome for T-cell acute lymphoblastic leukemia patients
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Self-citationInactivation of theCdkn2alocus cooperates withHMGA1to drive T-cell leukemogenesis
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Self-citationDeregulation of polycomb repressor complex 1 modifier AUTS2 in T-cell leukemia
Nagel, S., Pommerenke, C., Meyer, C., Kaufmann, M., Drexler, H. G., & MacLeod, R. A. F. (2016) · Oncotarget · doi:10.18632/oncotarget.9982 · Cited by 24
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“…that show decent potency and selectivity against certain PKMTs. SETD2 specifically trimethylates H3K36 and has been identified as a tumor suppressor in p53-dependent gene regulation, transcription elongation, and intron–exon splicing (Duns et al., 2010; Varela et al., 2011; Zhang et al., 2012).”
BackgroundClonal conversion of B lymphoid leukemia reveals cross-lineage transfer of malignant statesPreprint
Somasundaram, R., Åhsberg, J., Okuyama, K., Ungerbäck, J., Lilljebjörn, H., Fioretos, T., Strid, T., & Sigvardsson, M. (2016) · Genes & Development · doi:10.1101/gad.285536.116 · Cited by 24
“Matching ATAC-seq data to ChIP-seq data of GATA3 binding in FLDN2b T-cell progenitors (GSE31235) (Zhang et al. 2012b) revealed a significantly increased epigenetic accessibility in the T-cell as compared with the original B-cell tumors (Fig.”
MethodResultInfluentialA Tumor Suppressor Enhancer of PTEN in T-cell Development and Leukemia
Tottone, L., Lancho, O., Loh, J.-W., Singh, A., Kimura, S., Roels, J., Kuchmiy, A. A., Strubbe, S., Lawlor, M. A., da Silva-Diz, V., et al. (2020) · Blood Cancer Discovery · doi:10.1158/2643-3230.bcd-20-0201 · Cited by 24
“gov/programs/ target), the database of Genotypes and Phenotypes (dbGaP), and the European Genome-phenome Archive, as previously described (64, 65).”
MethodSelf-citationFishman, H., Madiwale, S., Geron, I., Bari, V., Loocke, W. V., Kirschenbaum, Y., Ganmore, I., Kugler, E., Rein, A., Friedlander, G., et al. (2021) · Blood · doi:10.1182/blood.2020010405 · Cited by 23
Chromatin Regulators with Tumor Suppressor Properties and their Alterations in Human Cancers
Shu, X., Li, L., & Tao, Q. (2012) · Epigenomics · doi:10.2217/epi.12.50 · Cited by 23
McCole, R. B., Fonseka, C. Y., Koren, A., & Wu, C.-T. (2014) · PLoS Genetics · doi:10.1371/journal.pgen.1004646 · Cited by 23
“[88], Holmfeldt et al.”
Wong, J. C. Y., Weinfurtner, K. M., Alzamora, M. D. P., Kogan, S. C., Burgess, M. R., Zhang, Y., Nakitandwe, J., Ma, J., Cheng, J., Chen, S.-C., et al. (2015) · eLife · doi:10.7554/elife.07839 · Cited by 23
“The RNA-Seq paired-end reads were mapped to the mouse mm9 genome using an in-house mapping and quality assessment pipeline (Zhang et al., 2012).”
Self-citationGenetic alteration and misexpression of Polycomb group genes in hepatocellular carcinoma.
Gao, S.-B., Sun, S., Zheng, Q., Zhang, L., Zhu, Y., Jin, G., & Xue, L. (2015) · Europe PMC (PubMed Central) · Cited by 23
The clonal evolution of leukemic stem cells in T-cell acute lymphoblastic leukemia
Tremblay, C. S., & Curtis, D. J. (2014) · Current Opinion in Hematology · doi:10.1097/moh.0000000000000058 · Cited by 24
“Gene expression profiling shows that these oncogenes are associated with distinct T-ALL subgroups with the poor prognosis, immature T-ALL subgroup defined by high expression of LMO2, LYL1 and rearrangements of MEF2C [11].”
BackgroundInfluentialSilencing of GATA3 defines a novel stem cell-like subgroup of ETP-ALL
Fransecky, L. R., Neumann, M., Heesch, S., Schlee, C., Ortiz-Tánchez, J., Heller, S., Mossner, M., Schwartz, S., Mochmann, L. H., Isaakidis, K., et al. (2016) · Journal of Hematology & Oncology · doi:10.1186/s13045-016-0324-8 · Cited by 23
“For gene set enrichment analysis (GSEA), GATA3-supervised GEPs were examined for enrichment of curated gene sets representing ETP-ALL [19], HSC [30], T cell differentiation [30], granulocyte/macrophage progenitors (GMP) [30], and myeloid/lymphoid progenitors (MLP) [31]”
BackgroundMethodChen, Z., Raghoonundun, C.-D., Chen, W., Zhang, Y., Tang, W., Fan, X., & Shi, X. (2018) · Biochemical and Biophysical Research Communications · doi:10.1016/j.bbrc.2018.03.022 · Cited by 26
Siekmann, I., Dierck, K., Prall, S., Klokow, M., Strauß, J., Buhs, S., Wrzeszcz, A., Bockmayr, M. L., Beck, F., Trochimiuk, M., et al. (2018) · Blood Advances · doi:10.1182/bloodadvances.2018020693 · Cited by 22
Roy, U., & Raghavan, S. C. (2021) · International Journal of Cancer · doi:10.1002/ijc.33527 · Cited by 26
Kong, J., Chen, N., Li, M., Zhang, J., Wu, X., Zong, L., Wu, D., Song, B., & Qiu, H. (2021) · Annals of Hematology · doi:10.1007/s00277-021-04530-y · Cited by 22
Self-citationJAK/BCL2 inhibition acts synergistically with LSD1 inhibitors to selectively target ETP-ALL
Benyoucef, A., Haigh, K., Cuddihy, A. R., & Haigh, J. J. (2022) · Leukemia · doi:10.1038/s41375-022-01716-9 · Cited by 22
“In addition, comparison of the gene expression profile of ETP-ALL with normal hematopoietic cells and acute myeloid leukemia demonstrated enrichment for a leukemic stem-cell signature associated with poor outcome in acute myeloid leukemia (AML) [4, 5].”
BackgroundMethodResultInfluentialThe Killer’s Web: Interconnection between Inflammation, Epigenetics and Nutrition in Cancer
Mecca, M., Picerno, S., & Cortellino, S. (2024) · International Journal of Molecular Sciences · doi:10.3390/ijms25052750 · Cited by 24
“In contrast, loss-of-function mutations in EZH2, which confer a poor prognosis, have been described in myeloid malignancies, T-ALL, suggesting a tumor-suppressive role for EZH2 in these cell lineages [261,262].”
BackgroundDanis, E., Yamauchi, T., Echanique, K. A., Haladyna, J. N., Kalkur, R. S., Riedel, S. S., Zhu, N., Xie, H.-F., Bernt, K., Orkin, S., et al. (2015) · Experimental Hematology · doi:10.1016/j.exphem.2015.06.005 · Cited by 25
“In mice, genetic inactivation of Ezh2 leads to T-ALL [1] and MDS/MPN [2], which is in keeping with PRC2 alterations in human T-lineage ALL [3, 4] and in myeloid neoplasms [5-7].”
BackgroundGenome instability mechanisms and the structure of cancer genomes
Cassidy, L. D., & Venkitaraman, A. R. (2012) · Current Opinion in Genetics & Development · doi:10.1016/j.gde.2012.02.003 · Cited by 22
Identification of a tumor suppressor network in T-cell leukemia
Nagel, S., Pommerenke, C., Meyer, C., Kaufmann, M., MacLeod, R. A. F., & Drexler, H. G. (2017) · Leukemia & lymphoma/Leukemia and lymphoma · doi:10.1080/10428194.2017.1283029 · Cited by 21
“Additional expression analysis of FOXN2 and FOXN3 in both early T-cell progenitor (ETP) ALL and T-ALL patient samples (GSE28703) [54] showed significantly higher levels in ETP-ALL (Supplementary Figure 3(A,B)), supporting their observed aberrant downregulation in T-ALL.”
CAR T-cell therapy for glioblastoma: ready for the next round of clinical testing?
Prinzing, B. L., Gottschalk, S. M., & Krenciute, G. (2018) · Expert Review of Anticancer Therapy · doi:10.1080/14737140.2018.1451749 · Cited by 22
“Another group completely circumnavigated the necessity of providing a pro-survival cytokine and expressed a constitutively active IL-7 receptor (C7R) that homodimerizes without its ligand IL-7, once again producing constitutive STAT5 activation [95,96].”
BackgroundTargeted genome editing in acute lymphoblastic leukemia: a review
Montaño, A., Forero‐Castro, M., Hernández‐Rivas, J. M., García‐Tuñón, I., & Benito, R. (2018) · BMC Biotechnology · doi:10.1186/s12896-018-0455-9 · Cited by 23
Acute Leukemias of Ambiguous Lineage
Kurzer, J. H., & Weinberg, O. K. (2019) · Surgical pathology clinics · doi:10.1016/j.path.2019.03.008 · Cited by 22
The Longevity-Associated SH2B3 (LNK) Genetic Variant: Selected Aging Phenotypes in 379,758 Subjects
Kuo, C., Joaquim, M., Kuchel, G. A., Ferrucci, L., Harries, L. W., Pilling, L. C., & Melzer, D. R. (2019) · The Journals of Gerontology Series A · doi:10.1093/gerona/glz191 · Cited by 22
“Several other links have been shown between SH2B3 and cancers, including the presence of activating mutations in acute lymphoblastic leukemia cells (30,31).”
BackgroundRegulatory network of GATA3 in pediatric acute lymphoblastic leukemia
Hou, Q., Liao, F., Zhang, S., Zhang, D., Zhang, Y., Zhou, X., Xia, X., Ye, Y., Yang, H., Li, Z., et al. (2017) · Oncotarget · doi:10.18632/oncotarget.16424 · Cited by 24
“Expression microarray datasets searching and association analyses Expression level of all genes in B-ALL patients were obtained from Gene Expression Omnibus (GSE7440 [44], GSE11877 [45], GSE10792 [46], GSE13351 [47], GSE13425 [47], GSE635 [48], GSE10255 [49], GSE4698 [50], GSE33315 [51], and GSE13204 [52]).”
MethodInfluentialMutational landscape of adult ETP-ALL
Neumann, M., Greif, P. A., & Baldus, C. D. (2013) · Oncotarget · doi:10.18632/oncotarget.1106 · Cited by 22
Regulatory Network and Prognostic Effect Investigation of PIP4K2A in Leukemia and Solid Cancers
Zhang, S., Li, Z., Yan, X., Li, B., Deng, Y., Zeng, F., Wang, P., Zhu, J., Yin, D., Liao, F., et al. (2019) · Frontiers in Genetics · doi:10.3389/fgene.2018.00721 · Cited by 21
“Datasets analyzed for this study are available in GEO repository (http://www.ncbi.nlm.nih.gov/gds): GSE635, GSE10792, GSE13351, GSE13425, GSE10255, GSE4698, GSE33315, GSE7440, GSE11877, and GSE13204, and TCGA database (https://cancergenome.nih.gov/).”
Govaerts, I., Jacobs, K., Vandepoel, R., & Cools, J. (2019) · HemaSphere · doi:10.1097/hs9.0000000000000313 · Cited by 21
Self-citationKužílková, D., Bugarin, C., Rejlová, K., Schulz, A. R., Mei, H. E., Paganin, M., Biffi, A., Biondi, A., Kalina, T., & Gaipa, G. (2021) · Haematologica · doi:10.3324/haematol.2021.278796 · Cited by 20
Gene mutation profiles and prognostic implications in Korean patients with T-lymphoblastic leukemia
Huh, H. J., Lee, S. H., Yoo, K. H., Sung, K. W., Koo, H. H., Jang, J. H., Kım, K., Kim, S. J., Kim, W. S., Jung, C. W., et al. (2013) · Annals of Hematology · doi:10.1007/s00277-012-1664-2 · Cited by 21
Variation in Dicer Gene Is Associated with Increased Survival in T-Cell Lymphoma
Li, X., Tian, X., Zhang, B., Zhang, Y., & Chen, J. (2012) · PLoS ONE · doi:10.1371/journal.pone.0051640 · Cited by 21
Winter, S. S., Ricci, J., Luo, L., Lovato, D. M., Khawaja, H. M., Serna-Gallegos, T. R., DeBassige, N., & Larson, R. A. (2013) · Health · doi:10.4236/health.2013.55a005 · Cited by 21
“These findings suggest that ETP patients have a variety of molecular aberrations, as recently extensively documented by Zhang and co-workers [37].”
Self-citationTargeting IRAK1 in T-Cell acute lymphoblastic leukemia
Dussiau, C., Trinquand, A., Lhermitte, L., Latiri, M., Simonin, M., Cieślak, A., Bedjaoui, N., Villarèse, P., Verhoeyen, E., Dombret, H., et al. (2015) · Oncotarget · doi:10.18632/oncotarget.4150 · Cited by 21
“Indeed, kinases play a key role in signaling pathways downstream to cytokine receptors that are important in T-ALL and central to ETP ALL oncogenesis [3].”
BackgroundNRAS Mutant Melanoma: An Overview for the Clinician for Melanoma Management
Jenkins, R. W., & Sullivan, R. J. (2016) · Melanoma Management · doi:10.2217/mmt.15.40 · Cited by 24
Melão, A., Spit, M., Cardoso, B. A., & Barata, J. T. (2016) · Haematologica · doi:10.3324/haematol.2015.141143 · Cited by 21
“The pro-oncogenic role of IL7 and IL-7R in human T-ALL has been clearly highlighted by recent data, revealing that IL-7 significantly accelerates T-ALL disease progression in vivo(11) and that gain-of-function mutations in the IL-7R exist in T-ALL patients, including in poor prognosis cases.(12,13,40) On the other han…”
BackgroundTrentin, L., Bresolin, S., Giarin, E., Bardini, M., Serafin, V., Accordi, B., Fais, F., Tenca, C., Lorenzo, P. D., Valsecchi, M. G., et al. (2016) · Scientific Reports · doi:10.1038/srep34449 · Cited by 20
“…nature of KRAS and NRAS activating mutations is not just an unusual feature in cancer; low RAS mutation load was reported in colorectal cancer biopsies 42 , early T-cell precursor acute lymphoblastic leukaemia (ETP-ALL) 43 and also in acute myeloid leukaemia (AML) with MLL rearrangements 44 .”
Self-citationColomer‐Lahiguera, S., Pisecker, M., König, M., Nebral, K., Pickl, W. F., Kauer, M. O., Haas, O. A., Ullmann, R., Attarbaschi, A., Dworzak, M. N., et al. (2017) · Leukemia & lymphoma/Leukemia and lymphoma · doi:10.1080/10428194.2017.1312383 · Cited by 21
“Generally, ETP-like or early immature T-ALL shows lower frequencies of prototypical T-ALL-specific genetic lesions such as CDKN2A/B deletions and NOTCH1 pathway activating mutations but higher incidences of mutations typically found in acute myeloid leukemia [7,41,42].”
BackgroundResultLeón‐González, A. J., Sharif, T., Auger, C., Abbas, M., Fuhrmann, G., & Schini‐Kerth, V. B. (2018) · Journal of Functional Foods · doi:10.1016/j.jff.2018.03.013 · Cited by 21
DNA mismatch repair in the context of chromatin
Huang, Y., & Li, G. (2020) · Cell & Bioscience · doi:10.1186/s13578-020-0379-7 · Cited by 21
Kaito, S., & Iwama, A. (2020) · International Journal of Molecular Sciences · doi:10.3390/ijms22010074 · Cited by 21
Hhex regulates Kit to promote radioresistance of self-renewing thymocytes in Lmo2-transgenic mice
Shields, B., Alserihi, R. F., Nasa, C., Bogue, C. W., Alexander, W. S., & McCormack, M. P. (2014) · Leukemia · doi:10.1038/leu.2014.292 · Cited by 23
Metzeler, K. H., & Bloomfield, C. D. (2017) · Advances in experimental medicine and biology · doi:10.1007/978-981-10-3233-2_12 · Cited by 22
Mixed phenotype acute leukemia
Borowitz, M. J. (2014) · Cytometry Part B Clinical Cytometry · doi:10.1002/cyto.b.21155 · Cited by 21
“A unique feature of ETP ALL, in addition to its phenotype and poor outcome, is that it has many genetic features in common with myeloid leukemias (4).”
BackgroundPerspectives and future directions for epigenetics in hematology
Goodell, M. A., & Godley, L. A. (2013) · Blood · doi:10.1182/blood-2013-04-427724 · Cited by 20
Thillo, Q. V., Bie, J. D., Seneviratne, J. A., Demeyer, S., Omari, S. A., Balachandran, A., Zhai, V., Tam, W. L., Sweron, B., Geerdens, E., et al. (2021) · Nature Communications · doi:10.1038/s41467-021-24442-9 · Cited by 20
Self-citation
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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