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==References==
 
==References==
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=== EXAMPLE Book ===
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1. Yang L, et al., (2015). DNMT3A in haematological malignancies. Nat Rev Cancer 15(3):152-165, PMID 25693834.  
#Arber DA, et al., (2008). Acute myeloid leukaemia with recurrent genetic abnormalities, in World Health Organization Classification of Tumours of Haematopoietic and Lymphoid Tissues, 4th edition. Swerdlow SH, Campo E, Harris NL, Jaffe ES, Pileri SA, Stein H, Thiele J, Vardiman JW, Editors. IARC Press: Lyon, France, p117-118.
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=== EXAMPLE Journal Article ===
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2. Wienholz BL, et al., (2010). DNMT3L modulates significant and distinct flanking sequence preference for DNA methylation by DNMT3A and DNMT3B in vivo. PLoS Genet 6(9):e1001106, PMID 20838592.
#Li Y, et al., (2001). Fusion of two novel genes, RBM15 and MKL1, in the t(1;22)(p13;q13) of acute megakaryoblastic leukemia. Nat Genet 28:220-221, PMID 11431691.
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3. Kaneda M, et al., (2004). Essential role for de novo DNA methyltransferase Dnmt3a in paternal and maternal imprinting. Nature 429(6994):900-903, PMID 15215868.
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4. Xu F, et al., (2010). Molecular and enzymatic profiles of mammalian DNA methyltransferases: structures and targets for drugs. Curr Med Chem 17(33):4052-4071, PMID 20939822.
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5. Tahiliani M, et al., (2009). Conversion of 5-methylcytosine to 5-hydroxymethylcytosine in mammalian DNA by MLL partner TET1. Science 324(5929):930-935, PMID 19372391. 
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6. Challen GA, et al., (2011). Dnmt3a is essential for hematopoietic stem cell differentiation. Nat Genet 44(1):23-31, PMID 22138693.
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7. Mayle A, et al., (2015). Dnmt3a loss predisposes murine hematopoietic stem cells to malignant transformation. Blood 125(4):629-638, PMID 25416277.
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8. Ley TJ, et al., (2010). DNMT3A mutations in acute myeloid leukemia. N Engl J Med 363(25):2424-2433, PMID 21067377. 
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9. Patel JP, et al., (2012). Prognostic relevance of integrated genetic profiling in acute myeloid leukemia. N Eng J Med 366(12):1079-1089, PMID 22417203.
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10. Spencer DH, et al., (2017). CpG island hypermethylation mediated by DNMT3A is a consequence of AML progression. Cell 168(5):801-816, PMID 28215704.
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11. Spencer D, et al., (2016). DNMT3A-dependent DNA methylation may act as a tumor suppressor – not a tumor promoter – during AML progression. Blood 128(22):1050.
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12. Walter MJ, et al., (2011). Recurrent DNMT3A mutations in patients with myelodysplastic syndromes. Leukemia 25(7):1153-1158, PMID 21415852.
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13. Bejar R, et al., (2012). Validation of a prognostic model and the impact of mutations in patients with lower-risk myelodysplastic syndromes. J Clin Oncol 30(27):3376-3382, PMID 22869879.
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14. Roller A, et al., (2013). Landmark analysis of DNMT3A mutations in hematological malignancies. Leukemia 27(7):1573-1578, PMID 23519389.
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15. Grossmann V, et al., (2013). The molecular profile of adult T-cell acute lymphoblastic leukemia: mutations in RUNX1 and DNMT3A are associated with poor prognosis in T-ALL. Genes Chromosomes Cancer 52(4):410-422, PMID 23341344.
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16. Tan M, et al., (2017). Clinical implications of DNMT3A mutations in a Southeast Asian cohort leukaemia patients. J Clin Pathol 70(8):669-676, PMID 28100593.
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17. LaRochelle O, et al., (2011). Do AML patients with DNMT3A exon 23 mutations benefit from idarubicin as compared to daunorubicin? A single center experience. Oncotarget 2(11):850-861, PMID 22081665.
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18. Toyota M, et al., (2001). Methylation profiling in acute myeloid leukemia. Blood 97(9):2823-2829, PMID 11313277.
    
== Notes ==
 
== Notes ==
 
<nowiki>*</nowiki>Primary authors will typically be those that initially create and complete the content of a page.  If a subsequent user modifies the content and feels the effort put forth is of high enough significance to warrant listing in the authorship section, please contact the CCGA coordinators (contact information provided on the homepage).  Additional global feedback or concerns are also welcome.
 
<nowiki>*</nowiki>Primary authors will typically be those that initially create and complete the content of a page.  If a subsequent user modifies the content and feels the effort put forth is of high enough significance to warrant listing in the authorship section, please contact the CCGA coordinators (contact information provided on the homepage).  Additional global feedback or concerns are also welcome.