Changes

==== 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 yo will be finding information that will fit in other sections of the gene template, like CANCER CATEGORY TYPE and COMMON ALTERATION TYPES.  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

# the molecular function of the gene/protein

# its normal cellular role

# its normal cellular role

The ''ABL1'' gene encodes a non-receptor tyrosine kinase that is ubiquitously expressed and involved in a large number of cellular processes (see '''[https://www.ncbi.nlm.nih.gov/gene/25#reference-sequences "NCBI Gene]''').  By far the most prevalent ''ABL1'' alteration associated with cancer are the fusions of the ''ABL1'' gene with a number of partners, but especially with the ''BCR'' gene in CML [1,2] and to a lesser extent in B-ALL and T-ALL.  The head to tail arrangement of the BCR-ABL1 fusion gene results in an activated tyrosine kinase activity [6].  It appears that the N-terminal domain of ''BCR'' can cause oligomerization of the BCR-ABL1 protein product, thus activating the ''ABL1'' tyrosine kinase domain of the fusion protein [6,10,11].  The ''ABL1'' and ''ABL2'' genes encode tyrosine kinases which share overlapping physiological roles, and ''ABL2'' somatic or amplification mutations are more common than similar mutations in ''ABL1'' [6].

The ''ABL1'' gene encodes a non-receptor tyrosine kinase that is ubiquitously expressed and involved in a large number of cellular processes (see '''[https://www.ncbi.nlm.nih.gov/gene/25#reference-sequences "NCBI Gene]''').  By far the most prevalent ''ABL1'' alteration associated with cancer are the fusions of the ''ABL1'' gene with a number of partners, but especially with the ''BCR'' gene in CML [1,2] and to a lesser extent in B-ALL and T-ALL.  The head to tail arrangement of the BCR-ABL1 fusion gene results in an activated tyrosine kinase activity [6].  It appears that the N-terminal domain of ''BCR'' can cause oligomerization of the BCR-ABL1 protein product, thus activating the ''ABL1'' tyrosine kinase domain of the fusion protein [6,10,11].  The ''ABL1'' and ''ABL2'' genes encode tyrosine kinases which share overlapping physiological roles, and ''ABL2'' somatic or amplification mutations are more common than similar mutations in ''ABL1'' [6]. 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.

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:

# Pfam

# 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

# Atlas of Genetics and Cytogenetics in Oncology and Haematology

# COSMIC  

# COSMIC  

Note that in this section, you mauch

Note that in this section, you mauch

== <big>Appendix</big> ==

== <big>Appendix</big> ==