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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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BackgroundActivating Mutations of NOTCH1 in Human T Cell Acute Lymphoblastic Leukemia
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Self-citationEarly T-cell precursor leukaemia: a subtype of very high-risk acute lymphoblastic leukaemia
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“Published fusion partners include: PICALM (11q14) [31], XPO1 (2p15) [32], NAP1L1 (12q21) [11], NUP98 (11p15) [33], DDX3X (Xp11) [19], and HNRNPH1 (5q35) [19].”
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Self-citationEarly T-cell precursor leukemia/lymphoma in adults and children
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“The molecular landscape of ETP-ALL is also distinctive within T-ALL, characterized by a lower incidence of NOTCH1 mutations and frequent FLT3 and DNMT3A mutations (Neumann et al, 2012, 2013a,b; Zhang et al, 2012).”
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“…neoplasms, such as RAS family members, ETV6, MEF2C and EZH2, but whose mutations are rare in other T-ALL subtypes, (Homminga et al, 2011; Van Vlierberghe et al, 2011a; Zhang et al, ª 2018 John Wiley & Sons Ltd 921 British Journal of Haematology, 2018, 180, 919–924 2012; Zuurbier et al, 2014).”
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Self-citationPRC2 loss of function confers a targetable vulnerability to BET proteins in T-ALL
Andrieu, G. P., Kohn, M., Simonin, M., Smith, C. L., Cieślak, A., Dourthe, M.-É., Charbonnier, G., Graux, C., Huguet, F., Lhéritier, V., et al. (2021) · Blood · doi:10.1182/blood.2020010081 · Cited by 40
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Self-citationGATA-3 is a proto-oncogene in T-cell lymphoproliferative neoplasms
Geng, X., Wang, C., Gao, X., Chowdhury, P., Weiss, J., Villegas, J. A., Saed, B., Perera, T., Hu, Y., Reneau, J. C., et al. (2022) · Blood Cancer Journal · doi:10.1038/s41408-022-00745-y · Cited by 36
“1D), consistent with the demonstration of DNA methylation and epigenetic silencing of GATA-3 in ETP T-ALL [24], and recurrent loss-of-function GATA-3 mutations observed in this subset [25].”
NPMc+ cooperates with Flt3/ITD mutations to cause acute leukemia recapitulating human disease
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“By contrast, none of the 15 mice with either T cell ALL or mixed lineage T/ myeloid disease had LOH of the wild-type Flt3 allele (Figures 5A and 5B).”
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“A large and growing number of pathogenic chromosomal translocations have since been discovered in multiple solid tumors including breast cancer, lung cancer, prostate cancer, melanoma, hepatocellular carcinoma, pancreatic cancer, medulloblastoma and colorectal adenocarcinoma, and hematologic malignancies including ETP…”
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“(7) on ETP-ALL and from results of whole-genome sequencing studies (5).”
ResultRuxolitinib as potential targeted therapy for patients with JAK2 rearrangements
Chase, A., Bryant, C., Score, J., Haferlach, C., Grossmann, V., Schwaab, J., Hofmann, W. ‐., Reiter, A., & Cross, N. C. P. (2012) · Haematologica · doi:10.3324/haematol.2012.067959 · Cited by 35
“Cytogenetics revealed a complex karyotype (46,XY,der(5)t(3;5)(q26;q14)[1]/46,XY,der(5)t(3;5)(q26;q14), der(7)t(7;9)(q21;p24),r(9)(p13q34),der(12)t(12;18)(p12;p11),r(18)(p1 1q21)[19).”
Developmental origins shape the paediatric cancer genome
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“…genes encoding members of PRC2 complexes including enhancer of zeste homologue 2 ( EZH2 ), embryonic ectoderm development ( EED ) and SUZ12 in T-ALL 73 ; EZH2 , ASXL1 , ASXL2 and EED in AML with RUNX1–RUNX1T1 (also known as AML1 – ETO ) fusion 9 ; and at low frequency, EZH2 and ASXL1 in B-ALL 23 ;…”
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“In this regard, the processes we now describe could be mechanistically relevant to a number of recurrent interstitial oncogenic deletions associated with T- and B-cell acute lymphoblastic leukemias (27, 28) and with early T-cell precursor acute lymphoblastic leukemias (29).”
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“In addition to major cytogenetic alterations, genomic or expression profiling has recently identified the activation of several signal transduction pathways, including phosphoinositide 3-kinase (PI3K)/Akt/mammalian target of rapamycin (mTOR), Ras/Raf/MEK/Erk, Jak/STAT and others as driving features of leukemia [32–34].”
Patel, A. J., Warda, S., Mååg, J. L. V., Misra, R., Miranda-Román, M. A., Pachai, M. R., Lee, C. J., Li, D., Wang, N., Bayshtok, G., et al. (2022) · Cancer Discovery · doi:10.1158/2159-8290.cd-21-1671 · Cited by 36
Mechanisms of Epigenetic Regulation of Leukemia Onset and Progression
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Contribution of JAK2 mutations to T-cell lymphoblastic lymphoma development
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Transcriptional regulation of the Ikzf1 locus
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“Inactivating deletions and mutations in the IKZF1 locus have been reported as poor prognostic indicators in pre–B-cell progenitor acute lymphoblastic leukemia and early T-cell progenitor acute lymphoblastic leukemia in humans and mice.(12,13,15,36) Large deletions at the 7p BLOOD, 31 OCTOBER 2013 x VOLUME 122, NUMBER…”
BackgroundSelf-citationA CALM-derived nuclear export signal is essential for CALM-AF10–mediated leukemogenesis
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“When expressed in HEK293 cells, CALM(1-583)-AF10 and CALM(520-583)-AF10 are predominantly cytoplasmic, whereas CALM(1-552)-AF10 localizes to the nucleus (supplemental Figure 2A).”
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Self-citationAssessing telomeric DNA content in pediatric cancers using whole-genome sequencing data
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“It was launched in 2010 and WGS is complete for over 235 tumors from 15 different types of pediatric cancers with an average of 30fold haploid coverage [10], making it possible to carry out a comprehensive telomere analysis using WGS data [11-14].”
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“Likewise, in T-acute lymphoblastic leukemia, EZH2 and other PcG proteins are frequently mutated(123) with higher frequency of mutations in pediatric subtype of leukemia.(124)”
BackgroundPharmacogenomics in acute lymphoblastic leukemia
Lee, S. H. R., & Yang, J. J. J. (2017) · Best Practice & Research Clinical Haematology · doi:10.1016/j.beha.2017.07.007 · Cited by 32
“Via a multitude of both genome wide interrogation studies and candidate gen studies, there is increasing discovery of inherited germline variations associated with bo th early treatment response (minimal residual disease, MRD) and the risk of ALL relapse [6][7].”
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Genetic and Epigenetic Targeting Therapy for Pediatric Acute Lymphoblastic Leukemia
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“demonstrated that the rates of 5-year EFS and OS do not differ significantly between ETP-ALL and non-ETP-ALL in a study using a risk-adapted approach with intensified initial treatment [64].”
ResultThe epigenetic landscape of T-cell acute lymphoblastic leukemia
der Meulen, J. V., Roy, N. V., Vlierberghe, P. V., & Speleman, F. (2014) · The International Journal of Biochemistry & Cell Biology · doi:10.1016/j.biocel.2014.04.015 · Cited by 35
“In T-ALL, one ETV6-INO80D fusion (t(2;12)(q33;p13)) has been detected in an immature T-ALL case (Zhang et al., 2012), but, to date, no other recurrent genetic defects affecting ATPase remodeling complexes have been described.”
InfluentialHistone methyltransferase Setd2 is critical for the proliferation and differentiation of myoblasts
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“In support of our finding, activating mutations in KRAS have been identified in pediatric T-ALL patients (10, 25).”
BackgroundSelf-citationSomatic alterations and dysregulation of epigenetic modifiers in cancers
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“UTX, which encodes an enzyme which demethylates di- and trimethyl groups on H3K27 (H3K27me2/3), is frequently deleted and/or affected by loss-of-function mutations in multiple myeloma, T-ALL, and several epithelial carcinomas including renal cell carcinoma and bladder urothelial carcinoma.”
BackgroundInfluentialMolecular landscapes of human hematopoietic stem cells in health and leukemia
Vedi, A., Santoro, A., Dunant, C. F., Dick, J. E., & Laurenti, E. (2015) · Annals of the New York Academy of Sciences · doi:10.1111/nyas.12981 · Cited by 32
Self-citationTRIB2 regulates normal and stress-induced thymocyte proliferation
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“This is in accordance with LCK mRNA downregulation observed in ETP-ALL patients by Zhang et al.2 However, activated LCK (measured through SRC Y416) normalized on total LCK clearly indicated that LCK activity is significantly higher in ETP-ALL patients (Figure 1b).”
BackgroundResultInfluentialSelf-citationJamalpour, M., Li, X., Gustafsson, K. U., Tyner, J. W., & Welsh, M. (2018) · Tumor Biology · doi:10.1177/1010428318771472 · Cited by 31
“Oncogenic Kras is primarily found in human myeloid and T-cell leukemias.20 In addition, the elevated level of rat sarcoma (RAS) signaling has been observed in AML and T-ALL.21,22 Oncogenic mutations in the Ras genes result in constitutive activation of RAS proteins.23 RAS is an essential factor for the signaling pathw…”
BackgroundJDP2: An oncogenic bZIP transcription factor in T cell acute lymphoblastic leukemia
Mansour, M. R., He, S., Li, Z., Lobbardi, R., Abraham, B. J., Hug, C. B., Rahman, S., León, T. E., Kuang, Y., Zimmerman, M. W., et al. (2018) · The Journal of Experimental Medicine · doi:10.1084/jem.20170484 · Cited by 32
“One other factor that could potentially impact the transcriptional activity of JDP2 is that approximately half of ETP-ALL cases have inactivating mutations of members of the PRC2 complex (Zhang et al., 2012).”
BackgroundA decade with whole exome sequencing in haematology
Hansen, M. H., Haferlach, T., & Nyvold, C. G. (2019) · British Journal of Haematology · doi:10.1111/bjh.16249 · Cited by 32
The evolution of relapse of adult T cell acute lymphoblastic leukemia
Sentís, I., González, S., Genescà, E., García‐Hernández, V., Muiños, F., González‐Gil, C., López‐Arribillaga, E., González, J., Fernández‐Ibarrondo, L., Mularoni, L., et al. (2020) · Genome biology · doi:10.1186/s13059-020-02192-z · Cited by 35
“We have used only samples of which we could recover clinical information from the associated publications [5, 8, 10, 38, 39].”
MethodHistone H3.3 and cancer: A potential reader connection
Lan, F., & Shi, Y. (2014) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1418996111 · Cited by 32
Bonn, B. R., Huge, A., Rohde, M., Oschlies, I., Klapper, W., Voß, R., Makarova, O., Rössig, C., Jürgens, H., Seggewiß, J., et al. (2014) · British Journal of Haematology · doi:10.1111/bjh.13105 · Cited by 31
Lajoie, M., Drouin, S., Caron, M., St-Onge, P., Ouimet, M., Gioia, R., Lafond, M.-H., Vidal, R. O., Richer, C., Oualkacha, K., et al. (2017) · PLoS ONE · doi:10.1371/journal.pone.0174124 · Cited by 31
Polycomb repressive complex 2 (PRC2) suppresses Eμ-myc lymphoma
Lee, S. C.-W., Phipson, B., Hyland, C. D., Leong, H. S., Allan, R. S., Lun, A. T. L., Hilton, D. J., Nutt, S. L., Blewitt, M. E., Smyth, G. K., et al. (2013) · Blood · doi:10.1182/blood-2013-02-484055 · Cited by 29
“Cells were stained with monoclonal antibodies to B220 [RA3-6B2], CD19 [1D3], CD25 [PC61], c-Kit [2B8], IgM [II/41], IgD [11-26], Mac-1 [M1- 5 70], Gr-1 [RB6-8C5], Ter119 [Ter119], CD4 [GK1.”
MethodAn epigenetic therapy for diffuse intrinsic pontine gliomas
Ramaswamy, V., Remke, M., & Taylor, M. D. (2014) · Nature Medicine · doi:10.1038/nm.3769 · Cited by 30
Brown, N. A., & Elenitoba‐Johnson, K. S. J. (2017) · Head and Neck Pathology · doi:10.1007/s12105-017-0802-5 · Cited by 30
Recent Advances in Adult Acute Lymphoblastic Leukemia
Richard‐Carpentier, G., Kantarjian, H. M., & Jabbour, E. J. (2019) · Current Hematologic Malignancy Reports · doi:10.1007/s11899-019-00503-1 · Cited by 31
Targeting steroid resistance in T-cell acute lymphoblastic leukemia
Smedt, R. D., Morscio, J., Goossens, S., & Vlierberghe, P. V. (2019) · Blood Reviews · doi:10.1016/j.blre.2019.100591 · Cited by 30
Deleterious and Oncogenic Mutations in the IL7RA
Campos, L. W., Pissinato, L. G., & Yunes, J. A. (2019) · Cancers · doi:10.3390/cancers11121952 · Cited by 30
“LL242-243>SPCI RTPEINNSSGEMDPISPC ITISILSFFSVALLVILACVLW KKRIK ETP-ALL [67]”
BackgroundInfluentialGonzález‐Gil, C., Ribera, J., Ribera, J., & Genescà, E. (2021) · Genes · doi:10.3390/genes12010079 · Cited by 32
“Therefore, the CDKN2A/B deletion is a common alteration in cortical/mature T-ALL subtypes characterized by the overexpression of TLX1 and TLX3 [48,50,53,71,74,75], whereas the frequency in immature subtypes is significantly lower [48,84].”
BackgroundCurrent and emerging therapeutic approaches for T‐cell acute lymphoblastic leukaemia
Pocock, R., Farah, N., Richardson, S. E., & Mansour, M. R. (2021) · British Journal of Haematology · doi:10.1111/bjh.17310 · Cited by 30
Klein, K., Stoiber, D., Sexl, V., & Witalisz‐Siepracka, A. (2021) · Cancers · doi:10.3390/cancers13112611 · Cited by 30
Polycomb Directed Cell Fate Decisions in Development and Cancer
German, B., & Ellis, L. (2022) · Epigenomes · doi:10.3390/epigenomes6030028 · Cited by 34
“In addition, 25% of the T-ALL present global epigenetic remodeling towards H3K27ac, which activates mutations of the JAK/STAT signaling pathway [238].”
BackgroundPre-T cell receptor self-MHC sampling restricts thymocyte dedifferentiation
Duke‐Cohan, J. S., Akitsu, A., Mallis, R. J., Messier, C. M., Lizotte, P. H., Aster, J. C., Hwang, W., Lang, M. J., & Reinherz, E. L. (2022) · Nature · doi:10.1038/s41586-022-05555-7 · Cited by 36
Lu, B. Y., Thanawala, S. U., Zochowski, K. C., Burke, M. J., Carroll, W. L., & Bhatla, T. (2016) · Leukemia & lymphoma/Leukemia and lymphoma · doi:10.3109/10428194.2015.1110747 · Cited by 30
“However, despite significant scientific rationale favoring the role of epigenetic dysregulation in T-ALL biology [3,4], we did not observe robust chemosensitization in the T-ALL cell lines Jurkat and Molt-4 [Table I].”
BackgroundMessina, M., Chiaretti, S., Wang, J., Fedullo, A. L., Peragine, N., Gianfelici, V., Piciocchi, A., Brugnoletti, F., Giacomo, F. D., Pauselli, S., et al. (2016) · Oncotarget · doi:10.18632/oncotarget.7356 · Cited by 30
“Given the low number of recurrently mutated genes detected in the discovery panel, WES was broadened to 68 additional B-NEG cases (screening panel 1) and the bioinformatic analysis focused on the genes mutated in the discovery panel and/or reported as affected by mutations or CNAs in published ALL series [25-29].”
BackgroundSelf-citationGe, Z., Gu, Y., Han, Q., Zhao, G., Li, M., Li, J., Chen, B., Sun, T., Dovat, S., Gale, R. P., et al. (2016) · Scientific Reports · doi:10.1038/srep38004 · Cited by 30
Borssén, M., Nordlund, J., Haider, Z., Landfors, M., Larsson, P. G., Kanerva, J. A., Schmiegelow, K., Flægstad, T., Jónsson, Ó. G., Frost, B., et al. (2018) · Clinical Epigenetics · doi:10.1186/s13148-018-0466-3 · Cited by 30
“mutations in genes involved in epigenetic regulation have been reported [16, 17].”
BackgroundThe multi-faceted role of Gata3 in developmental haematopoiesis
Zaidan, N. M., & Ottersbach, K. (2018) · Open Biology · doi:10.1098/rsob.180152 · Cited by 31
“In addition, whole genome sequencing of patients with early T-cell precursor acute lymphoblastic leukaemia (ETP-ALL), an aggressive subtype of T-ALL, has revealed GATA3 inactivating lesions disrupting haematopoietic development [50].”
BackgroundWhole-genome sequencing of a malignant granular cell tumor with metabolic response to pazopanibPreprint
Wei, L., Liu, S., Conroy, J. M., Wang, J., Papanicolau‐Sengos, A., Glenn, S. T., Murakami, M., Liu, L., Hu, Q., Conroy, J., et al. (2015) · Molecular Case Studies · doi:10.1101/mcs.a000380 · Cited by 30
“Using a previous definition (Zhang et al. 2012b), the current WGS analysis identified 17 tier-1 mutations in gene coding regions, splice sites or noncoding RNA; 81 tier-2mutations in regulatory or evolutionarily conserved regions of the genome; and 541 tier-3 mutations in other nonrepetitive…”
MethodSelf-citationGenomic Characterization of Acute Leukemias
Chiaretti, S., Gianfelici, V., Ceglie, G., & Foà, R. (2014) · Medical Principles and Practice · doi:10.1159/000362793 · Cited by 32
Epigenetic Modifiers in Normal and Malignant Hematopoiesis
Haladyna, J. N., Yamauchi, T., Neff, T., & Bernt, K. M. (2015) · Epigenomics · doi:10.2217/epi.14.88 · Cited by 30
A novel transmembrane protein defines the endoplasmic reticulum stress-induced cell death pathway
Tamaki, T., Kamatsuka, K., Sato, T., Morooka, S., Otsuka, K., Hattori, M., & Sugiyama, T. (2017) · Biochemical and Biophysical Research Communications · doi:10.1016/j.bbrc.2017.03.017 · Cited by 29
Ferrando, A. A. (2018) · Best Practice & Research Clinical Haematology · doi:10.1016/j.beha.2018.10.001 · Cited by 29
“In addition, ETP T-ALL has a lower frequency of mutations in NOTCH1 and loss of the short arm of chromosome 9 [4].”
BackgroundUltraconserved Elements Occupy Specific Arenas of Three-Dimensional Mammalian Genome Organization
McCole, R. B., Erceg, J., Saylor, W., & Wu, C.-T. (2018) · Cell Reports · doi:10.1016/j.celrep.2018.06.031 · Cited by 30
A novel algorithm comprehensively characterizes human RH genes using whole-genome sequencing data
Chang, T., Haupfear, K., Yu, J. H., Rampersaud, E., Sheehan, V., Flanagan, J. M., Hankins, J. S., Weiss, M. J., Wu, G., Vege, S., et al. (2020) · Blood Advances · doi:10.1182/bloodadvances.2020002148 · Cited by 29
“WGS and RH SNP array genotyping Genomic DNA was extracted from peripheral blood mononuclear cells by standardmethods, andWGSwas performed at HudsonAlpha Institute for Biotechnology, as previously described.(18,19) Pairedend reads were aligned against the human genome build GRCh38 (hg38) with the Burrows-Wheeler Aligne…”
MethodSelf-citationChang, Y.-H., Yu, C., Jou, S., Lin, C., Lin, K., Lu, M., Wu, K., Chang, H., Lin, D., Lin, S., et al. (2021) · Scientific Reports · doi:10.1038/s41598-020-80613-6 · Cited by 29
Zhou, Y., Petrovic, J., Zhao, J., Zhang, W., Bigdeli, A., Zhang, Z., Berger, S. L., Pear, W. S., & Faryabi, R. B. (2022) · Molecular Cell · doi:10.1016/j.molcel.2022.01.015 · Cited by 28
Yan, J., Chen, Y., Patel, A. J., Warda, S., Lee, C. J., Nixon, B. G., Wong, E. W. P., Miranda-Román, M. A., Yang, N., Wang, Y., et al. (2022) · Journal of Clinical Investigation · doi:10.1172/jci153437 · Cited by 30
“PRC2 is a context-dependent tumor suppressor, whose core components are frequently inactivated genetically or epigenetically in various cancer types, including malignant peripheral nerve sheath tumors (MPNSTs) (2, 3), melanoma (2), myeloid disorders (4, 5), T cell acute lymphocytic leukemia (ALL) (6), early T cell pre…”
BackgroundMughal, T. I., Girnius, S. K., Rosen, S. T., Kumar, S. K., Wiestner, A. U., Abdel-Wahab, O. I., Kiladjian, J., Wilson, W. H., & Etten, R. A. V. (2013) · Leukemia & lymphoma/Leukemia and lymphoma · doi:10.3109/10428194.2013.863307 · Cited by 29
Liu, X., Rothe, K., Yen, R., Fruhstorfer, C., Maetzig, T., Chen, M., Forrest, D. L., Humphries, R. K., & Jiang, X. (2017) · Leukemia · doi:10.1038/leu.2017.108 · Cited by 28
Double sword role of EZH2 in leukemia
Safaei, S., Baradaran, B., Hagh, M. F., Alivand, M. R., Talebi, M., Gharibi, T., & Solali, S. (2017) · Biomedicine & Pharmacotherapy · doi:10.1016/j.biopha.2017.12.059 · Cited by 29
Tumors of Lymphoid and Hematopoietic Tissues
Leventaki, V., Khoury, J. D., & Voss, S. D. (2014) · Springer eBooks · doi:10.1007/978-1-4939-1729-7_5 · Cited by 29
The roles of Polycomb group proteins in hematopoietic stem cells and hematological malignancies
Takamatsu-Ichihara, E., & Kitabayashi, I. (2016) · International Journal of Hematology · doi:10.1007/s12185-016-2011-5 · Cited by 28
Defective K-Ras oncoproteins overcome impaired effector activation to initiate leukemia in vivo
Shieh, A., Ward, A. F., Donlan, K. L., Harding-Theobald, E. R., Xu, J., Mullighan, C. G., Zhang, C., Chen, S.-C., Su, X., Downing, J. R., et al. (2013) · Blood · doi:10.1182/blood-2012-05-432252 · Cited by 29
Self-citationGowda, C. S., Soliman, M., Kapadia, M. A., Ding, Y., Payne, K. J., & Dovat, S. (2017) · Advances in Biological Regulation · doi:10.1016/j.jbior.2017.06.001 · Cited by 30
“The overexpression of CK2 is becoming a hallmark of ALL and therefore serves as an important therapeutic target, via CK2-specific inhibitors, in T-cell and B-cell ALL (Buontempo et al., 2014; Ge et al., 2017; Gowda, C. et al., 2017a; Li et al., 2012; Song et al., 2015).”
BackgroundInfluentialAli, T., Bednarska, J., Vassilopoulos, S., Tran, M., Diakonov, I. A., Ziyadeh-Isleem, A., Guicheney, P., Gorelik, J., Korchev, Y. E., Reilly, M. M., et al. (2019) · The FASEB Journal · doi:10.1096/fj.201802635r · Cited by 27
Starza, R. L., Pierini, V., Pierini, T., Nofrini, V., Matteucci, C., Arniani, S., Moretti, M., Fernandez, A. G. L., Pellanera, F., Giacomo, D. D., et al. (2020) · Journal of Molecular Diagnostics · doi:10.1016/j.jmoldx.2020.02.004 · Cited by 28
“The panel of genes involved in T-ALL were inferred from available gene expression profile, molecular cytogenetics, and sequencing data.(4-6,9,10) CI-FISH studies were performed in a two-step diagnostic algorithm (Figure 1).”
BackgroundMethodInfluentialSelf-citationEarly precursor T-cell acute lymphoblastic leukemia: current paradigms and evolving concepts
Puglianini, O. A. C., & Papadantonakis, N. (2020) · Therapeutic Advances in Hematology · doi:10.1177/2040620720929475 · Cited by 29
Deregulation of the Interleukin-7 Signaling Pathway in Lymphoid Malignancies
Lodewijckx, I., & Cools, J. (2021) · Pharmaceuticals · doi:10.3390/ph14050443 · Cited by 28
“Genetic alterations in DNM2 are identified in around 10% of adult T-ALL and up to 20% of the ETP subtype of T-ALL and are heterozygous, with frameshifts, non-sense, missense and splice mutations and deletions throughout the whole gene [67,120].”
BackgroundInfluentialSelf-citationD’Angelo, V., Iannotta, A., Ramaglia, M., Lombardi, A., Zarone, M. R., Desiderio, V., Affinita, M. C., Pecoraro, G., Martino, M. D., Indolfi, P., et al. (2015) · Journal of Experimental & Clinical Cancer Research · doi:10.1186/s13046-015-0191-0 · Cited by 28
Meng, T., Yao, Y., Xu, Y., Xue, S., Han, Y., Tang, X., Qiu, H., Sun, A., Wu, D., Zhang, Y., et al. (2020) · Hematological Oncology · doi:10.1002/hon.2783 · Cited by 27
“The mutation and global transcriptional profiles of ETP‐ALL are similar to myeloid neoplasms, providing the rationale to explore myeloid‐based therapies in the treatment of ETP‐ALL.(2,7) In previous studies, CAG regimen (aclarubicin, cytarabine [Ara‐C], and granulocyte colony‐stimulating factor [G‐CSF]), a widely used…”
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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