436
edits
Changes
→1. PRIMARY AUTHORS section.
EG:
EG:
Steps in the curation process.
Steps in the curation process.
# After you have decided to become a curator, contact ???, read this tutorial, watch the tutorial and sign your Honor Agreement.
# Contact your editor and gain permission to the CCGA site
#After you have decided to become a curator, contact ???, read this tutorial, watch the tutorial and sign your Honor Agreement.
# Chose or be assigned a few GENE pages to curate
#Contact your editor and gain permission to the CCGA site
# Curate the page by reading suggested reading materials and authoring content on the GENE page (DO NOT PLAGIARIZE!)
#Chose or be assigned a few GENE pages to curate
# Contact Editor upon completion of GENE page curation.
#Curate the page by reading suggested reading materials and authoring content on the GENE page (DO NOT PLAGIARIZE!)
#Contact Editor upon completion of GENE page curation.
==Introduction:==
==Introduction:==
Note that the Template already has the markup language you will need for headers, links, and other syntax to be used in the Gene Paes. Please do not change the syntax of the template, so users of the CCGA pages will want to see the same format from page to page.
Note that the Template already has the markup language you will need for headers, links, and other syntax to be used in the Gene Paes. Please do not change the syntax of the template, so users of the CCGA pages will want to see the same format from page to page.
NOTE: When you do large edits on a Wiki page, the security makes sure yo are a human with test at the top of the page and a simple mathmatical formula you must complete, as below. YOU MUST answe the mathmatical equation for your edits to be saved.
NOTE: When you do large edits on a Wiki page, the security makes sure yo 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.
''Your edit includes new external links. To protect the wiki against automated spam, we kindly ask you to solve the following task below and enter the answer in the box in order to save your edit (more info): 45−1 =''
''Your edit includes new external links. To protect the wiki against automated spam, we kindly ask you to solve the following task below and enter the answer in the box in order to save your edit (more info): 45−1 =''
Sections:
Sections:
# Primary Authors
# Synonyms
#Primary Authors
# Genomic Location
#Synonyms
# Cancer Category/Type
#Genomic Location
# Gene Overview
#Cancer Category/Type
# Common Alteration Types
#Gene Overview
# Internal Pages
#Common Alteration Types
# External Links
#Internal Pages
# References
#External Links
#References
The sections of the Template are for ease of reading for the USER: HOWEVER, as a curator, you will want to curate and load information in the WIKI in a non-linear fashion. This is the suggested workflow:
The sections of the Template are for ease of reading for the USER: HOWEVER, as a curator, you will want to curate and load information in the WIKI in a non-linear fashion. This is the suggested workflow:
=== 1. PRIMARY AUTHORS section. ===
===1. PRIMARY AUTHORS section.===
By adding your name to the PRIMARY AUTHORS section you can make sure that no-one else is curating this gene now, and so you will get credit for curating this information by your peers.
By adding your name to the PRIMARY AUTHORS section you can make sure that no-one else is curating this gene now, and so you will get credit for curating this information by your peers. Please list your name and on the next line, type the phrase "Under Review" and the date you last edited it. When you are done editing and you think it is complete, please delete the "Under Review" and date.
=== 8. EXTERNAL LINKS Section. ===
===8. EXTERNAL LINKS Section.===
To familiarize yourself with the latest information on the Gene you are curating, “Your Gene of Interest” (designated YGI throughout), please start with one of the last sections of the Template, the EXTERNAL LINKS Section. The listed resources will provide exhaustive (but not necessarily recent) molecular information about YGI, its mutations and its place in disease and cancer and treatment. The resources suggested as EXTERNAL LINKS as of Dec 2018 are as follows:
To familiarize yourself with the latest information on the Gene you are curating, “Your Gene of Interest” (designated YGI throughout), please start with one of the last sections of the Template, the EXTERNAL LINKS Section. The listed resources will provide exhaustive (but not necessarily recent) molecular information about YGI, its mutations and its place in disease and cancer and treatment. The resources suggested as EXTERNAL LINKS as of Dec 2018 are as follows:
# Atlas of Genetics and Cytogenetics in Oncology and Haematology
#Atlas of Genetics and Cytogenetics in Oncology and Haematology
# COSMIC
#COSMIC
# CIViC
#CIViC
# St. Jude ProteinPaint
#St. Jude ProteinPaint
# Precision Medicine Knowledgebase (Weill Cornell)
#Precision Medicine Knowledgebase (Weill Cornell)
# Cancer Index
#Cancer Index
# OncoKB
#OncoKB
# NCBI Gene
#NCBI Gene
# My Cancer Genome
#My Cancer Genome
# UniProt
#UniProt
# Pfam
#Pfam
# GeneCards
#GeneCards
# OMIM
#OMIM
# LOVD(3)
#LOVD(3)
# TICdb
#TICdb
# In some cases, a specialized source that may be available for some genes, for example '''[http://p53.iarc.fr/ ''TP53'' by IARC]''' - ''TP53'' a database with reference sequences and mutational landscapes
#In some cases, a specialized source that may be available for some genes, for example '''[http://p53.iarc.fr/ ''TP53'' by IARC]''' - ''TP53'' a database with reference sequences and mutational landscapes
Please note that some genes may have special resources devoted to them. An example is the International Agency for Research on Cancer page devoted to TP53 (see http://p53.iarc.fr/). This is unusual, but P53 is the most studied gene and protein on earth, so in this case, a specialized resource is justified. TO find if there are any special resources for YGI, perform a google search on YGI and include words like "database" or "resource". Ask your Editor.
Please note that some genes may have special resources devoted to them. An example is the International Agency for Research on Cancer page devoted to TP53 (see http://p53.iarc.fr/). This is unusual, but P53 is the most studied gene and protein on earth, so in this case, a specialized resource is justified. TO find if there are any special resources for YGI, perform a google search on YGI and include words like "database" or "resource". Ask your Editor.
<big>'''''PLEASE NOTE: DO NOT PLAGIARIZE. You can borrow phrases here or there without attribution. Yo can even use a sentence here and there if you attribute the quote directly ( eg: "From NCBI"). However, you CANNOT cut and paste whole paragraphs from other resources into the CCGA pages.'''''</big>
<big>'''''PLEASE NOTE: DO NOT PLAGIARIZE. You can borrow phrases here or there without attribution. Yo can even use a sentence here and there if you attribute the quote directly ( eg: "From NCBI"). However, you CANNOT cut and paste whole paragraphs from other resources into the CCGA pages.'''''</big>
=== 2. SYNONYMS Section ===
===2. SYNONYMS Section===
As you read though the EXTERNAL LINKS resources, you will find many of them have lists of synonyms, esp. NCBI Gene and GeneCards. Please italicize the alternative gene names (synonyms).
As you read though the EXTERNAL LINKS resources, you will find many of them have lists of synonyms, esp. NCBI Gene and GeneCards. Please italicize the alternative gene names (synonyms). Please source your information, for example by putting "(from GeneCards and NCBI Gene)" after the information.
=== 3. GENOMIC LOCATION Section. ===
===3. GENOMIC LOCATION Section.===
This information is most easily obtained from GeneCards, in the GeneCards section "Genomics" and subsection "Genomic Locations for YFG" and subsection "Genomic View for YFG"and sub-subsection "Cytogenetic band"
This information is most easily obtained from GeneCards, in the GeneCards section "Genomics" and subsection "Genomic Locations for YFG" and subsection "Genomic View for YFG"and sub-subsection "Cytogenetic band". Please source your information, for example by putting "(from GeneCards)" after the information.
=== 5. GENE OVERVIEW Section ===
===5. GENE OVERVIEW Section===
This is where you will be compelled to find and read journal articles and book text. You may have found some relevant articles listed at some of the EXTERNAL LINKS sites (esp. Uniprot and NCBI Gene), but you will have to search for new, relevant articles in PubMed and also from the Hematological Cancer resource "WHO Classification of Tumours of Haematopoietic and Lymphoid Tissues (download from http://publications.iarc.fr/_publications/media/download/1511/700ac655d7f248cf1044efd985275086ed4f341f.pdf). Note that you will be finding information that will fit in other sections of the gene template, like CANCER CATEGORY TYPE and COMMON ALTERATION TYPES and REFERENCES. This section should describe in 1 paragraph (approx 5-7 sentences):
This is where you will be compelled to find and read journal articles and book text. You may have found some relevant articles listed at some of the EXTERNAL LINKS sites (esp. Uniprot and NCBI Gene), but you will have to search for new, relevant articles in PubMed and also from the Hematological Cancer resource "WHO Classification of Tumours of Haematopoietic and Lymphoid Tissues (download from http://publications.iarc.fr/_publications/media/download/1511/700ac655d7f248cf1044efd985275086ed4f341f.pdf). Note that you will be finding information that will fit in other sections of the gene template, like CANCER CATEGORY TYPE and COMMON ALTERATION TYPES and REFERENCES. This section should describe in 1 paragraph (approx 5-7 sentences):
# the molecular function of the gene/protein
# its normal cellular role, for example in cellular processes or cellular pathways.
#the molecular function of the gene/protein
# its role in diseases, esp. cancer diseases in the CCGA.
#its normal cellular role, for example in cellular processes or cellular pathways.
# interesting or frequent mutations and their effects on specific cancers.
#its role in diseases, esp. cancer diseases in the CCGA.
# role in drug resistance, if any.
#interesting or frequent mutations and their effects on specific cancers.
# diagnostic or prognostic value, if any.
#role in drug resistance, if any.
#diagnostic or prognostic value, if any.
A few examples are shown below.
A few examples are shown below.
For molecular information and some disease and mutation information, this section is most informed by reading the EXTERNAL LINKS resources of:
For molecular information and some disease and mutation information, this section is most informed by reading the EXTERNAL LINKS resources of:
# UniProt (by far the best)
# GeneCards
#UniProt (by far the best)
# NCBI Gene
#GeneCards
# CIViC
#NCBI Gene
# Cancer Index
#CIViC
# My Cancer Genome
#Cancer Index
# Pfam
#My Cancer Genome
#Pfam
For mutational information, this section is most informed by:
For mutational information, this section is most informed by:
# Atlas of Genetics and Cytogenetics in Oncology and Haematology
# COSMIC
#Atlas of Genetics and Cytogenetics in Oncology and Haematology
# LOVD(3)
#COSMIC
# TICdb
#LOVD(3)
# St. Jude ProteinPaint
#TICdb
# Precision Medicine Knowledgebase (Weill Cornell)
#St. Jude ProteinPaint
# OncoKB
#Precision Medicine Knowledgebase (Weill Cornell)
#OncoKB
For Disease information, the best resources are:
For Disease information, the best resources are:
# OMIM
# WHO Classification of Tumours of Haematopoietic and Lymphoid Tissues (download from http://publications.iarc.fr/_publications/media/download/1511/700ac655d7f248cf1044efd985275086ed4f341f.pdf)
#OMIM
# Pubmed (search for YFG, esp. in context of "cancer" or specific cancers)
#WHO Classification of Tumours of Haematopoietic and Lymphoid Tissues (download from http://publications.iarc.fr/_publications/media/download/1511/700ac655d7f248cf1044efd985275086ed4f341f.pdf)
#Pubmed (search for YFG, esp. in context of "cancer" or specific cancers)
Note that in this section, you must also go to PubMed (https://www.ncbi.nlm.nih.gov/pubmed/) and search for articles about YGI and cancer or specific cancers. The best articles to read are usually the most recent and should be are freely available to the public (eg, PubMed Central). If you are new to YGI and some of these cancers, then a recent review article may be helpful. Also very helpful is to use the book "WHO Classification of Tumours of Haematopoietic and Lymphoid Tissues" (download from http://publications.iarc.fr/_publications/media/download/1511/700ac655d7f248cf1044efd985275086ed4f341f.pdf) Search through the PDF file for YGI and read those sections where YGI is mentioned.
Note that in this section, you must also go to PubMed (https://www.ncbi.nlm.nih.gov/pubmed/) and search for articles about YGI and cancer or specific cancers. The best articles to read are usually the most recent and should be are freely available to the public (eg, PubMed Central). If you are new to YGI and some of these cancers, then a recent review article may be helpful. Also very helpful is to use the book "WHO Classification of Tumours of Haematopoietic and Lymphoid Tissues" (download from http://publications.iarc.fr/_publications/media/download/1511/700ac655d7f248cf1044efd985275086ed4f341f.pdf) Search through the PDF file for YGI and read those sections where YGI is mentioned.
We suggest when writing in the wiki, that you use a reference "placeholder" in the text you are writing. For example, use the first author's last name and year as a placeholder in the text, at the end of a sentence. Then, write the full reference into the REFERENCE Section (section 9) using the proper syntax suggested for either book, article or internet source. Then, when you are done with all sections and the reference section, you can replace the "placeholders" with the the numbered reference.
We suggest when writing in the wiki, that you use a reference "placeholder" in the text you are writing. For example, use the first author's last name and year as a placeholder in the text, at the end of a sentence. Then, write the full reference into the REFERENCE Section (section 9) using the proper syntax suggested for either book, article or internet source. Then, when you are done with all sections and the reference section, you can replace the "placeholders" with the the numbered reference.
=== 4. CANCER CATEGORY/TYPE Section ===
===4. CANCER CATEGORY/TYPE Section===
'''''Question: how many links to diseases in CCGA should we do? And how do we find the links. Eg, look at how many "sub diseae pages there are for AML, but the RUNX1 Gene page does not link to them all.'''''
'''''Question: how many links to diseases in CCGA should we do? And how do we find the links. Eg, look at how many "sub diseae pages there are for AML, but the RUNX1 Gene page does not link to them all.'''''
The extent of the content should be a short paragraph for each cancer type (1-7 sentences). The content should include:
The extent of the content should be a short paragraph for each cancer type (1-7 sentences). The content should include:
# Frequency of YGI mutations or fusion genes associated to patients with that specific disease,
# Whether the mutation is a common mutation in that specific disease (if it is uncommon, you are likely NOT to reference that fact, because you would end up referencing dozens or hundreds of mutations and diseases),
#Frequency of YGI mutations or fusion genes associated to patients with that specific disease,
# Whether the gene or mutation is a target of drugs
#Whether the mutation is a common mutation in that specific disease (if it is uncommon, you are likely NOT to reference that fact, because you would end up referencing dozens or hundreds of mutations and diseases),
# Whether there is diagnostic value in this gene or mutation(s)
#Whether the gene or mutation is a target of drugs
# Whether there is prognostic value in this gene or mutation(s)
#Whether there is diagnostic value in this gene or mutation(s)
# Whether there are companion diagnostics (with certain therapies) based on this gene or mutation(s)
#Whether there is prognostic value in this gene or mutation(s)
#Whether there are companion diagnostics (with certain therapies) based on this gene or mutation(s)
In some cases, you will find that some CCGA Diseases/Cancer Types have not yet been created. Please DO NOT create a disease page. Instead, within the Gene page, simply curate that information in a heading and contact your editor. As CCGA grows, we will add new Diseases/Cancer types and link to the Gene pages later (see example of CML, below).
In some cases, you will find that some CCGA Diseases/Cancer Types have not yet been created. Please DO NOT create a disease page. Instead, within the Gene page, simply curate that information in a heading and contact your editor. As CCGA grows, we will add new Diseases/Cancer types and link to the Gene pages later (see example of CML, below).
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/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/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/Acute_lymphoblastic_leukaemia_(ALL) Acute Lymphocytic Leukemia (ALL)]'''
*'''[http://www.ccga.io/index.php/Acute_lymphoblastic_leukaemia_(ALL) Acute Lymphocytic Leukemia (ALL)]'''
iAMP21 is an intrachromosomal amplification of chromosome 21, which includes the genes ''RUNX1'' and ''miR-802'' among others. This amplification occurs in about 1.5-2% of all Acute Lymphocytic Leukemia cases tested and is associated with poor prognostication [5].
iAMP21 is an intrachromosomal amplification of chromosome 21, which includes the genes ''RUNX1'' and ''miR-802'' among others. This amplification occurs in about 1.5-2% of all Acute Lymphocytic Leukemia cases tested and is associated with poor prognostication [5].
* '''[http://www.ccga.io/index.php/T-ALL T-cell Acute Lymphocytic Leukemia (T-ALL)]'''
*'''[http://www.ccga.io/index.php/T-ALL T-cell Acute Lymphocytic Leukemia (T-ALL)]'''
''RUNX1'' mutations have been described in 20% of patients with early T-cell precursor acute lymphoblastic leukemia (ETP-ALL) [6].
''RUNX1'' mutations have been described in 20% of patients with early T-cell precursor acute lymphoblastic leukemia (ETP-ALL) [6].
* '''[http://www.ccga.io/index.php?title=B_lymphoblastic_leukaemia/lymphoma_with_t(12;21)(p13;q22);_TEL-AML1_(ETV6-RUNX1)_positive&redirect=no B-cell Acute Lymphocytic Leukemia (B-ALL)]'''
*'''[http://www.ccga.io/index.php?title=B_lymphoblastic_leukaemia/lymphoma_with_t(12;21)(p13;q22);_TEL-AML1_(ETV6-RUNX1)_positive&redirect=no B-cell Acute Lymphocytic Leukemia (B-ALL)]'''
The most common chromosomal translocation is t(12;21)(p13;q22) resulting in ETV6-RUNX1 fusion in B-cell acute lymphocytic leukemia (B-ALL) [2]. This translocation occurs in 25% of Pediatric B-ALL but only 2% of Adult B-ALL [5, 6], and confers a favorable prognosis in B-ALL and other neoplasms [2,5,6]. iAMP21 is an intrachromosomal amplification of chromosome 21 which includes the genes ''RUNX1'' and ''miR-802'' among others. This amplification occurs in about 2% of all B-cell Acute Lymphocytic Leukemia cases tested and is associated with poor prognostication [6].
The most common chromosomal translocation is t(12;21)(p13;q22) resulting in ETV6-RUNX1 fusion in B-cell acute lymphocytic leukemia (B-ALL) [2]. This translocation occurs in 25% of Pediatric B-ALL but only 2% of Adult B-ALL [5, 6], and confers a favorable prognosis in B-ALL and other neoplasms [2,5,6]. iAMP21 is an intrachromosomal amplification of chromosome 21 which includes the genes ''RUNX1'' and ''miR-802'' among others. This amplification occurs in about 2% of all B-cell Acute Lymphocytic Leukemia cases tested and is associated with poor prognostication [6].
* '''Chronic Myeloid Leukemia (CML)'''
*'''Chronic Myeloid Leukemia (CML)'''
A number of simple mutations in ''RUNX1'' have been reported in CML patients, and these mutations may be in part responsible for progression from the chronic phase to blast crisis (BC) [7].
A number of simple mutations in ''RUNX1'' have been reported in CML patients, and these mutations may be in part responsible for progression from the chronic phase to blast crisis (BC) [7].
* '''[http://www.ccga.io/index.php/MDS Myelodysplastic Syndrome (MDS)]'''
*'''[http://www.ccga.io/index.php/MDS Myelodysplastic Syndrome (MDS)]'''
A high frequency (42%) of ''RUNX1'' mutations has been reported among radiation-associated and therapy-related Myelodysplastic Syndrome (MDS) patients [8].
A high frequency (42%) of ''RUNX1'' mutations has been reported among radiation-associated and therapy-related Myelodysplastic Syndrome (MDS) patients [8].
* '''CCUS (Clonal cytopenia of undetermined significance) or ICUS (Idiopathic cytopenia of undetermined significance )'''
*'''CCUS (Clonal cytopenia of undetermined significance) or ICUS (Idiopathic cytopenia of undetermined significance )'''
''RUNX1'' mutations are more common in clonal cytopenia of undetermined significance (CCUS) [2].
''RUNX1'' mutations are more common in clonal cytopenia of undetermined significance (CCUS) [2].
* '''Familial platelet disorder with predisposition to acute myeloid leukemia (FPD/AML)'''
*'''Familial platelet disorder with predisposition to acute myeloid leukemia (FPD/AML)'''
Germline mutations of ''RUNX1'' have been reported in the rare autosomal dominant Familial platelet disorder with predisposition to acute myeloid leukemia (FPD/AML) [8].
Germline mutations of ''RUNX1'' have been reported in the rare autosomal dominant Familial platelet disorder with predisposition to acute myeloid leukemia (FPD/AML) [8].
=== 6. COMMON ALTERATION TYPES Section ===
===6. COMMON ALTERATION TYPES Section===
This section should be completed in concert with the GENE OVERVIEW Section and CANCER CATEGORY/TYPE Section. It is meant to be an "At a Glance" section for the type of alteration that ARE MOST COMMON ACROSS ALL CANCERS. The types of alterations are:
This section should be completed in concert with the GENE OVERVIEW Section and CANCER CATEGORY/TYPE Section. It is meant to be an "At a Glance" section for the type of alteration that ARE MOST COMMON ACROSS ALL CANCERS. The types of alterations are:
* Copy Number Loss
* Copy Number Gain
*Copy Number Loss
* LOH (Loss of Heterozygosity)
*Copy Number Gain
* Loss-of-Function Mutation
*LOH (Loss of Heterozygosity)
* Gain-of-Function Mutation
*Loss-of-Function Mutation
* Translocation/Fusion
*Gain-of-Function Mutation
*Translocation/Fusion
In an example for TP53, there are two short paragraphs followed by a table. This is appropriate, because TP53 is found in a vast number of different cancers.
In an example for TP53, there are two short paragraphs followed by a table. This is appropriate, because TP53 is found in a vast number of different cancers.
{| class="wikitable sortable"
{| class="wikitable sortable"
|-
|-
! 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
|-
|-
| X || || X || X || X ||
|X|| ||X||X||X||
|}
|}
{| class="wikitable sortable"
{| class="wikitable sortable"
|-
|-
! 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
|-
|-
| || || || X || || X
| || || ||X|| ||X
|}
|}
=== 7. INTERNAL PAGES Section ===
===7. INTERNAL PAGES Section===
After you have completed the GENE OVERVIEW, CANCER CATEGORY/TYPE and COMMON ALTERATION TYPES, you will be more knowledgeable about the other INTERNAL PAGES that are relevant to information on YGI page. These will include links to diseases, and links to fusion partner genes. In fact, these links will essentially collect all the related INTERNAL PAGES from the GENE OVERVIEW, CANCER CATEGORY/TYPE and COMMON ALTERATION TYPES sections, all in one place.
After you have completed the GENE OVERVIEW, CANCER CATEGORY/TYPE and COMMON ALTERATION TYPES, you will be more knowledgeable about the other INTERNAL PAGES that are relevant to information on YGI page. These will include links to diseases, and links to fusion partner genes. In fact, these links will essentially collect all the related INTERNAL PAGES from the GENE OVERVIEW, CANCER CATEGORY/TYPE and COMMON ALTERATION TYPES sections, all in one place.
A good example is the ABL1 page INTERNAL PAGES Section.
A good example is the ABL1 page INTERNAL PAGES Section.
'''''[http://www.ccga.io/index.php/Chronic_Myeloid_Leukemia_(CML)_with_t(9;22)(q34.1;q11.2);_BCR-ABL1 Chronic Myeloid Leukemia]'''
'''''[http://www.ccga.io/index.php/Chronic_Myeloid_Leukemia_(CML)_with_t(9;22)(q34.1;q11.2);_BCR-ABL1 Chronic Myeloid Leukemia]'''''
'''[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/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/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]'''
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.
=== 9. REFERENCES section ===
===9. REFERENCES section===
When you are done with all sections and the reference section, you can then replace the "placeholders" authors last name with the the numbered reference in the relevant sections.
When you are done with all sections and the reference section, you can then replace the "placeholders" authors last name with the the numbered reference in the relevant sections.
== <big>Appendix</big> ==
==<big>Appendix</big>==
==Resources:==
==Resources:==
#The CCGA web site is here : http://www.ccga.io/index.php/Main_Page
#The CCGA web site is here : http://www.ccga.io/index.php/Main_Page
#“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> ==
==<big>FAQ (Frequently Asked Questions)</big>==