Changes

no edit summary
Line 15: Line 15:     
==Gene Pages:==
 
==Gene Pages:==
'''''QUESTION:  Do we need to designate Genes as Drivers vs. Passengers?'''''
  −
   
You will be asked to choose the gene pages you wish to curate from this list: http://www.ccga.io/index.php/List_of_Gene_Pages.
 
You will be asked to choose the gene pages you wish to curate from this list: http://www.ccga.io/index.php/List_of_Gene_Pages.
 
A “Gene specific Template” has been added to these pages for you to use to add your curated information.
 
A “Gene specific Template” has been added to these pages for you to use to add your curated information.
Line 22: Line 20:  
Note: The gene pages template already has the required headers, links and other syntax.  Please do not change the syntax of the template so there is consistency between similar pages.
 
Note: The gene pages template already has the required headers, links and other syntax.  Please do not change the syntax of the template so there is consistency between similar pages.
   −
Note: Save edits to your page frequently or produce content in a Word format of the template and add it into the wiki site subsequently.  For a Word document template for authoring a <u>'''gene-specific page'''</u> before transferring content online please see [[File:Gene-Specific Template Word Version (8-2-20).docx|left|thumb]].
+
Note: Save edits to your page frequently or produce content in a Word format of the template and add it into the wiki site subsequently.  For a Word document template for authoring a <u>'''gene-specific page'''</u> before transferring content online please see [[File:Gene-Specific Template Word Version (9-28-21).docx|none|thumb|Gene-Specific Template]].  
    
NOTE:  When you do large edits on a Wiki page, the security makes sure you are a human with test at the top of the page and a simple mathematical formula you must complete, as below. YOU MUST answer the mathematical equation for your edits to be saved.
 
NOTE:  When you do large edits on a Wiki page, the security makes sure you are a human with test at the top of the page and a simple mathematical formula you must complete, as below. YOU MUST answer the mathematical equation for your edits to be saved.
Line 142: Line 140:  
The example of RUNX1 is shown below.
 
The example of RUNX1 is shown below.
   −
*'''[http://www.ccga.io/index.php/Acute_Myeloid_Leukemia_(AML)_and_Related_Precursor_Neoplasms Acute Myeloid Leukemia (AML) and Related Precursor Neoplasms]'''
+
*'''[http://www.ccga.io/index.php/HAEM4:Acute_Myeloid_Leukemia_(AML)_and_Related_Precursor_Neoplasms Acute Myeloid Leukemia (AML) and Related Precursor Neoplasms]'''
   −
--- '''[http://www.ccga.io/index.php/Acute_Myeloid_Leukemia_(AML)_with_t(8;21)(q22;q22.1);_RUNX1-RUNX1T1 Acute Myeloid Leukemia (AML) with t(8;21)(q22;q22.1); RUNX1-RUNX1T1]'''
+
--- '''[http://www.ccga.io/index.php/HAEM5:Acute_myeloid_leukaemia_with_RUNX1::RUNX1T1_fusion Acute Myeloid Leukemia (AML) with t(8;21)(q22;q22.1); RUNX1-RUNX1T1]'''
   −
--- '''[http://www.ccga.io/index.php/Acute_Myeloid_Leukemia_(AML)_with_Mutated_RUNX1 Acute Myeloid Leukemia (AML) with Mutated RUNX1]'''
+
--- '''[http://www.ccga.io/index.php/HAEM4:Acute_Myeloid_Leukemia_(AML)_with_Mutated_RUNX1 Acute Myeloid Leukemia (AML) with Mutated RUNX1]'''
    
The frequency of ''RUNX1'' mutations is between 5-18% of all AML patients tested [3]. The most common chromosomal translocation is t(8;21)(q22;q22)resulting in RUNX1-RUNX1T1 fusion in ''de novo'' AML, at approximately 7% [2,6].  This translocation confers a favorable prognosis in AML and other neoplasms [2,5,6].  Another ''RUNX1'' alteration is the t(3;21)(q26;q22), in which the RUNT domain of ''RUNX1'' is fused to the entire ''EVI1'' gene.  This translocation is rarely found in patients diagnosed with ''de novo'' AML and is more common in those with therapy-related myelodysplastic syndrome (MDS)/AML [9].  Other mutations in ''RUNX1'' include deletions, missense, splicing, frameshift, and nonsense alterations (mostly loss-of-function or decreased function), and occur at a frequency of approximately 10% in AML patients [6]. These mutations are mechanistically distinct from the chromosomal translocations and confer a worse prognosis [2,5,6].
 
The frequency of ''RUNX1'' mutations is between 5-18% of all AML patients tested [3]. The most common chromosomal translocation is t(8;21)(q22;q22)resulting in RUNX1-RUNX1T1 fusion in ''de novo'' AML, at approximately 7% [2,6].  This translocation confers a favorable prognosis in AML and other neoplasms [2,5,6].  Another ''RUNX1'' alteration is the t(3;21)(q26;q22), in which the RUNT domain of ''RUNX1'' is fused to the entire ''EVI1'' gene.  This translocation is rarely found in patients diagnosed with ''de novo'' AML and is more common in those with therapy-related myelodysplastic syndrome (MDS)/AML [9].  Other mutations in ''RUNX1'' include deletions, missense, splicing, frameshift, and nonsense alterations (mostly loss-of-function or decreased function), and occur at a frequency of approximately 10% in AML patients [6]. These mutations are mechanistically distinct from the chromosomal translocations and confer a worse prognosis [2,5,6].
Line 234: Line 232:  
'''[http://www.ccga.io/index.php/Acute_lymphoblastic_leukaemia_(ALL) Acute Lymphoblastic Leukemia]'''
 
'''[http://www.ccga.io/index.php/Acute_lymphoblastic_leukaemia_(ALL) Acute Lymphoblastic Leukemia]'''
   −
'''[http://www.ccga.io/index.php/Acute_Myeloid_Leukemia_(AML)_with_BCR-ABL1 Acute Myeloid Leukemia (AML) with BCR-ABL1]'''
+
'''[http://www.ccga.io/index.php/HAEM5:Acute_myeloid_leukaemia_with_BCR::ABL1_fusion Acute Myeloid Leukemia (AML) with BCR-ABL1]'''
   −
'''[http://www.ccga.io/index.php/Mixed_Phenotype_Acute_Leukemia_(MPAL)_with_t(9;22)(q34.1;q11.2);_BCR-ABL1 Mixed Phenotype Acute Leukemia (MPAL) with t(9;22)(q34.1;q11.2); BCR-ABL1]'''
+
'''[http://www.ccga.io/index.php/HAEM5:Mixed-phenotype_acute_leukaemia_with_BCR::ABL1_fusion Mixed Phenotype Acute Leukemia (MPAL) with t(9;22)(q34.1;q11.2); BCR-ABL1]'''
    
See the '''[http://www.ccga.io/index.php/BCR "BCR gene"]''' for additional details of the BCR-ABL1 gene fusion.
 
See the '''[http://www.ccga.io/index.php/BCR "BCR gene"]''' for additional details of the BCR-ABL1 gene fusion.
Line 254: Line 252:  
#“WHO Classification of Tumours of Haematopoietic and Lymphoid Tissues.pdf” Download from http://publications.iarc.fr/_publications/media/download/1511/700ac655d7f248cf1044efd985275086ed4f341f.pdf
 
#“WHO Classification of Tumours of Haematopoietic and Lymphoid Tissues.pdf” Download from http://publications.iarc.fr/_publications/media/download/1511/700ac655d7f248cf1044efd985275086ed4f341f.pdf
    +
==<big>FAQ (Frequently Asked Questions)</big>==
   −
+
'''''QUESTION:  Do we need to designate Genes as Drivers vs. Passengers?'''''
==<big>FAQ (Frequently Asked Questions)</big>==