Pearson, J. C., Lemons, D. & McGinnis, W. Modulating Hox gene features throughout animal physique patterning. Nat. Rev. Genet 6, 893–904 (2005).
Innis, J. W. Function of HOX genes in human improvement. Curr. Opin. Pediatr. 9, 617–622 (1997).
Krumlauf, R. Hox genes in vertebrate improvement. Cell 78, 191–201 (1994).
Lawrence, H. J., Sauvageau, G., Humphries, R. Ok. & Largman, C. The function of HOX homeobox genes in regular and leukemic hematopoiesis. Stem Cells 14, 281–291 (1996).
van Oostveen, J., Bijl, J., Raaphorst, F., Walboomers, J. & Meijer, C. The function of homeobox genes in regular hematopoiesis and hematological malignancies. Leukemia 13, 1675–1690 (1999).
Argiropoulos, B. & Humphries, R. Ok. Hox genes in hematopoiesis and leukemogenesis. Oncogene 26, 6766–6776 (2007).
Lawrence, H. J. et al. Mice bearing a focused interruption of the homeobox gene HOXA9 have defects in myeloid, erythroid, and lymphoid hematopoiesis. Blood 89, 1922–1930 (1997).
Alharbi, R. A., Pettengell, R., Pandha, H. S. & Morgan, R. The function of HOX genes in regular hematopoiesis and acute leukemia. Leukemia 27, 1000–1008 (2013).
Andreeff, M. et al. HOX expression patterns determine a typical signature for favorable AML. Leukemia 22, 2041–2047 (2008).
Drabkin, H. A. et al. Quantitative HOX expression in chromosomally outlined subsets of acute myelogenous leukemia. Leukemia 16, 186–195 (2002).
Gao, L., Solar, J., Liu, F., Zhang, H. & Ma, Y. Increased expression ranges of the HOXA9 gene, intently related to MLL-PTD and EZH2 mutations, predict inferior end result in acute myeloid leukemia. Onco Targets Ther. 9, 711–722 (2016).
Kroon, E., Thorsteinsdottir, U., Mayotte, N., Nakamura, T. & Sauvageau, G. NUP98-HOXA9 expression in hemopoietic stem cells induces power and acute myeloid leukemias in mice. EMBO J. 20, 350–361 (2001).
Faber, J. et al. HOXA9 is required for survival in human MLL-rearranged acute leukemias. Blood 113, 2375–2385 (2009).
Milne, T. A. et al. A number of interactions recruit MLL1 and MLL1 fusion proteins to the HOXA9 locus in leukemogenesis. Mol. Cell 38, 853–863 (2010).
Rozovskaia, T. et al. Upregulation of Meis1 and HoxA9 in acute lymphocytic leukemias with the t(4: 11) abnormality. Oncogene 20, 874–878 (2001).
Ferrando, A. A. et al. Gene expression signatures in MLL-rearranged T-lineage and B-precursor acute leukemias: dominance of HOX dysregulation. Blood 102, 262–268 (2003).
Ayton, P. M. & Cleary, M. L. Transformation of myeloid progenitors by MLL oncoproteins relies on Hoxa7 and Hoxa9. Genes Dev. 17, 2298–2307 (2003).
Bernt, Ok. M. et al. MLL-Rearranged Leukemia Is Depending on Aberrant H3K79 Methylation by DOT1L. Most cancers Cell 20, 66–78 (2011).
Chen, W. L. et al. Proton pump inhibitors selectively suppress MLL rearranged leukemia cells by way of disrupting MLL1-WDR5 protein-protein interplay. Eur. J. Med. Chem. 188, 112027 (2020).
Yokoyama, A., Somervaille, T. & Cleary, M. L. The menin tumor suppressor protein is a vital oncogenic cofactor for MLL-associated leukemogenesis. Blood 106, 196a–196a (2005).
Mereau, H. et al. Impairing MLL-fusion gene-mediated transformation by dissecting crucial interactions with the lens epithelium-derived development issue (LEDGF/p75). Leukemia 27, 1245–1253 (2013).
Daigle, S. R. et al. Potent inhibition of DOT1L as remedy of MLL-fusion leukemia. Blood 122, 1017–1025 (2013).
Shi, A. et al. Structural insights into inhibition of the bivalent menin-MLL interplay by small molecules in leukemia. Blood 120, 4461–4469 (2012).
Borkin, D. et al. Pharmacologic inhibition of the Menin-MLL interplay blocks development of MLL leukemia in vivo. Most cancers Cell 27, 589–602 (2015).
Hyle, J. et al. Acute depletion of CTCF straight impacts MYC regulation by lack of enhancer-promoter looping. Nucleic Acids Res. 47, 6699–6713 (2019).
Zhang, H. et al. Practical interrogation of HOXA9 regulome in MLLr leukemia by way of reporter-based CRISPR/Cas9 display screen. Elife 9. https://doi.org/10.7554/eLife.57858 (2020).
Li, W. et al. MAGeCK allows strong identification of important genes from genome-scale CRISPR/Cas9 knockout screens. Genome Biol. 15, 554 (2014).
Yang, M. J. et al. 13q12.2 deletions in acute lymphoblastic leukemia result in upregulation of FLT3 by enhancer hijacking. Blood 136, 946–956 (2020).
Stam, R. W. et al. Prognostic significance of high-level FLT3 expression in MLL-rearranged toddler acute lymphoblastic leukemia. Blood 110, 2774–2775 (2007).
Fedders, H. et al. Constitutive Activation of FLT3 Is a Optimistic Prognostic Consider Infants with MLL-Rearranged Acute Lymphoblastic Leukemia. Blood 126. https://doi.org/10.1182/blood.V126.23.2681.2681 (2015).
Stam, R. W. et al. Focusing on FLT3 in major MLL-gene-rearranged toddler acute lymphoblastic leukemia. Blood 106, 2484–2490 (2005).
Wang, G. G., Pasillas, M. P. & Kamps, M. P. Persistent transactivation by Meis1 replaces Hox operate in myeloid leukemogenesis fashions: Proof for co-occupancy of Meis1-Pbx and Hox-Pbx complexes on promoters of leukemia-associated genes. Mol. Cell Biol. 26, 3902–3916 (2006).
Gwin, Ok., Frank, E., Bossou, A. & Medina, Ok. L. Hoxa9 regulates Flt3 in lymphohematopoietic progenitors. J. Immunol. 185, 6572–6583 (2010).
Corces, M. R. et al. Lineage-specific and single-cell chromatin accessibility charts human hematopoiesis and leukemia evolution. Nat. Genet 48, 1193–1203 (2016).
Wan, L. et al. ENL hyperlinks histone acetylation to oncogenic gene expression in acute myeloid leukaemia. Nature 543, 265–269 (2017).
Pelish, H. E. et al. Mediator kinase inhibition additional prompts super-enhancer-associated genes in AML. Nature 526, 273 (2015).
Brunetti, L. et al. Mutant NPM1 Maintains the Leukemic State by HOX Expression. Most cancers Cell 34, 499 (2018).
Armstrong, S. A. et al. Inhibition of FLT3 in MLL. Validation of a therapeutic goal recognized by gene expression based mostly classification. Most cancers Cell 3, 173–183 (2003).
Brown, P. et al. FLT3 inhibition selectively kills childhood acute lymphoblastic leukemia cells with excessive ranges of FLT3 expression. Blood 105, 812–820 (2005).
Stam, R. W. & Pieters, R. FLT3 Inhibitors as Therapeutic Brokers in MLL Rearranged Acute Lymphoblastic Leukemia. New Brokers for the Remedy of Acute Lymphoblastic Leukemia, 189–202. https://doi.org/10.1007/978-1-4419-8459-3_10 (2011).
Shimada, Ok., Bachman, J. A., Muhlich, J. L. & Mitchison, T. J. shinyDepMap, a device to determine targetable most cancers genes and their practical connections from Most cancers Dependency Map information. Elife 10. https://doi.org/10.7554/eLife.57116 (2021).
Friskes, A. et al. Double-strand break toxicity is chromatin context impartial. Nucleic Acids Res. 50, 9930–9947 (2022).
Liu, S. C. et al. Goal residence of Cas9-sgRNA influences DNA double-strand break restore pathway selections in CRISPR/Cas9 genome enhancing. Genome Biol. 23, 165 (2022).
Zhou, J. et al. Tremendous-enhancer panorama reveals leukemia stem cell reliance on X-box binding protein 1 as a therapeutic vulnerability. Sci. Transl. Med. 13, eabh3462 (2021).
Chavez, A. et al. Extremely environment friendly Cas9-mediated transcriptional programming. Nat. Strategies 12, 326–328 (2015).
Konermann, S. et al. Genome-scale transcriptional activation by an engineered CRISPR-Cas9 complicated. Nature 517, 583–588 (2015).
Zhao, X. et al. Molecular Mechanisms of ARID5B-Mediated Genetic Susceptibility to Acute Lymphoblastic Leukemia. J. Natl Most cancers Inst. 114, 1287–1295 (2022).
Huang, Y. et al. Identification and characterization of Hoxa9 binding websites in hematopoietic cells. Blood 119, 388–398 (2012).
Solar, Y. et al. HOXA9 Reprograms the Enhancer Panorama to Promote Leukemogenesis. Most cancers Cell 34, 643–658 e645 (2018).
Armstrong, S. A. et al. MLL translocations specify a definite gene expression profile that distinguishes a novel leukemia. Nat. Genet 30, 41–47 (2002).
Schmittgen, T. D. & Livak, Ok. J. Analyzing real-time PCR information by the comparative C(T) technique. Nat. Protoc. 3, 1101–1108 (2008).
Dobin, A. et al. STAR: ultrafast common RNA-seq aligner. Bioinformatics 29, 15–21 (2013).
Li, B. & Dewey, C. N. RSEM: correct transcript quantification from RNA-Seq information with or with out a reference genome. BMC Bioinforma. 12, 323 (2011).
Harrow, J. et al. GENCODE: the reference human genome annotation for The ENCODE Undertaking. Genome Res. 22, 1760–1774 (2012).
Regulation, C. W., Chen, Y., Shi, W. & Smyth, G. Ok. voom: Precision weights unlock linear mannequin evaluation instruments for RNA-seq learn counts. Genome Biol. 15, R29 (2014).
Liberzon, A. et al. The Molecular Signatures Database (MSigDB) hallmark gene set assortment. Cell Syst. 1, 417–425 (2015).
Liberzon, A. et al. Molecular signatures database (MSigDB) 3.0. Bioinformatics 27, 1739–1740 (2011).
Zhao, L. Z. et al. Transcription issue MEF2D is required for the upkeep of MLL-rearranged acute myeloid leukemia. Blood Adv. 5, 4727–4740 (2021).
Yang, X. et al. Differentiation of human pluripotent stem cells into neurons or cortical organoids requires transcriptional co-regulation by UTX and 53BP1. Nat. Neurosci. 22, 362–373 (2019).
Landt, S. G. et al. ChIP-seq tips and practices of the ENCODE and modENCODE consortia. Genome Res. 22, 1813–1831 (2012).
Heinz, S. et al. Easy Mixtures of Lineage-Figuring out Transcription Elements Prime cis-Regulatory Components Required for Macrophage and B Cell Identities. Mol. Cell 38, 576–589 (2010).
Martin, M. Cutadapt removes adapter sequences from high-throughput sequencing reads. EMBnet. J. 17, 10–12 (2011).
Langmead, B. & Salzberg, S. L. Quick gapped-read alignment with Bowtie 2. Nat. Strategies 9, 357–U354 (2012).
Zhang, Y. et al. Mannequin-based Evaluation of ChIP-Seq (MACS). Genome Biol. 9. https://doi.org/10.1186/gb-2008-9-9-r137 (2008).
Quinlan, A. R. & Corridor, I. M. BEDTools: a versatile suite of utilities for evaluating genomic options. Bioinformatics 26, 841–842 (2010).
Yang, W. T., Rosenstiel, P. C. & Schulenburg, H. ABSSeq: a brand new RNA-Seq evaluation technique based mostly on modelling absolute expression variations. Bmc Genomics 17. https://doi.org/10.1186/s12864-016-2848-2 (2016).
Anders, S., Pyl, P. T. & Huber, W. HTSeq-a Python framework to work with high-throughput sequencing information. Bioinformatics 31, 166–169 (2015).
Barnett, Ok. R. et al. Epigenomic mapping in B-cell acute lymphoblastic leukemia identifies transcriptional regulators and noncoding variants selling distinct chromatin architectures. bioRxiv. https://doi.org/10.1101/2023.02.14.528493 (2023).
Xu, B. et al. Acute depletion of CTCF rewires genome-wide chromatin accessibility. Genome Biol. 22, 244 (2021).
Godfrey, L. et al. DOT1L inhibition reveals a definite subset of enhancers depending on H3K79 methylation. Nat. Commun. 10, 2803 (2019).
Bernstein, B. E. et al. The NIH Roadmap Epigenomics Mapping Consortium. Nat. Biotechnol. 28, 1045–1048 (2010).
Prange, Ok. H. M. et al. MLL-AF9 and MLL-AF4 oncofusion proteins bind a definite enhancer repertoire and goal the RUNX1 program in 11q23 acute myeloid leukemia. Oncogene 36, 3346–3356 (2017).
Tarumoto, Y. et al. LKB1, Salt-Inducible Kinases, and MEF2C Are Linked Dependencies in Acute Myeloid Leukemia. Mol. Cell 69, 1017–1027 e1016 (2018).
Li, Ok. et al. Noncoding Variants Join Enhancer Dysregulation with Nuclear Receptor Signaling in Hematopoietic Malignancies. Most cancers Discov. 10, 724–745 (2020).
Blagitko-Dorfs, N. et al. Mixture remedy of acute myeloid leukemia cells with DNMT and HDAC inhibitors: predominant synergistic gene downregulation related to gene physique demethylation. Leukemia 33, 945–956 (2019).
Oka, M. et al. Chromatin-bound CRM1 recruits SET-Nup214 and NPM1c onto HOX clusters inflicting aberrant HOX expression in leukemia cells. Elife 8. https://doi.org/10.7554/eLife.46667 (2019).
