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==Cancer Category/Type==
 
==Cancer Category/Type==
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'''[http://www.ccga.io/index.php/Acute_Myeloid_Leukemia_(AML)_and_Related_Precursor_Neoplasms  Acute Myeloid Leukemia (AML) and Related Precursor Neoplasms''']
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'''[http://www.ccga.io/index.php/Acute_Myeloid_Leukemia_(AML)_and_Related_Precursor_Neoplasms  Acute Myeloid Leukemia (AML) and Related Precursor Neoplasms]'''
    
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==Gene Overview==
 
==Gene Overview==
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This gene encodes a member of the myeloid translocation gene family which interact with DNA-bound transcription factors and recruit a range of corepressors to facilitate transcriptional repression. The translocation produces a chimeric gene made up of the 5'-region of the runt-related transcription factor 1 gene fused to the 3'-region of this gene. The chimeric protein is thought to associate with the nuclear corepressor/histone deacetylase complex to block hematopoietic differentiation.
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The RUNX1T1 gene is a member of the human myeloid translocation genes (MTGs).  The nuclear MTGs can mediate the formation of complex protein networks among nuclear corepressors (for example Sin3a, N-CoR, SMRT), chromatin-modifying enzymes (for example histone deacetylases), and DNA-binding transcription factors. Repression at target genes by MTG protein complexes is probably required for gene regulation during development and differentiation. Alterations in these genes can disrupt gene regulatory protein networks and can cause of cancers and neurodegeneration [8] The translocation t(8;21)(q22;q22.1);_RUNX1-RUNX1T1 produces a chimeric gene made up of the 5'-region of the runt-related transcription factor 1 (RUNX1) gene fused to the 3'-region of the RUNX1T1 gene. The chimeric protein is thought to associate with the nuclear corepressor/histone deacetylase complex to block hematopoietic differentiation.
    
==Common Alteration Types==
 
==Common Alteration Types==
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! Copy Number Loss  !! Copy Number Gain  !!  LOH  !!  Loss-of-Function Mutation  !!  Gain-of-Function Mutation  !!  Translocation/Fusion  
 
! Copy Number Loss  !! Copy Number Gain  !!  LOH  !!  Loss-of-Function Mutation  !!  Gain-of-Function Mutation  !!  Translocation/Fusion  
 
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==Internal Pages==
 
==Internal Pages==
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Put your text here
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'''[http://www.ccga.io/index.php/Acute_Myeloid_Leukemia_(AML)_and_Related_Precursor_Neoplasms Acute Myeloid Leukemia (AML) and Related Precursor Neoplasms]'''
   
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EXAMPLE [[Germline Cancer Predisposition Genes]]
      
==External Links==
 
==External Links==
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7. Arber DA, et al., (2017). Acute myeloid leukaemia with recurrent genetic abnormalities, in World Health Organization Classification of Tumours of Haematopoietic and Lymphoid Tissues, Revised 4th edition. Swerdlow SH, Campo E, Harris NL, Jaffe ES, Pileri SA, Stein H, Thiele J, Arber DA, Hasserjian RP, Le Beau MM, Orazi A, and Siebert R, Editors. Revised 4th Edition. IARC Press: Lyon, France, p140-141.
 
7. Arber DA, et al., (2017). Acute myeloid leukaemia with recurrent genetic abnormalities, in World Health Organization Classification of Tumours of Haematopoietic and Lymphoid Tissues, Revised 4th edition. Swerdlow SH, Campo E, Harris NL, Jaffe ES, Pileri SA, Stein H, Thiele J, Arber DA, Hasserjian RP, Le Beau MM, Orazi A, and Siebert R, Editors. Revised 4th Edition. IARC Press: Lyon, France, p140-141.
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8. Rossetti S. et al. (2004).  The MTG proteins: chromatin repression players with a passion for networking. Genomics 84:1-9.  PMID: 15203199 DOI 10.1016/j.ygeno.2004.02.011
    
== 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.
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