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t(6;12)(q22;q24) NCOR2/ROS1

Written2019-09Tatiana Gindina
R.M. Gorbacheva Memorial Institute of Children Oncology, Hematology and Transplantation at Pavlov First Saint-Petersburg State Medical University, Saint-Petersburg, Russian Federation / e-mail: tatgindina@gmail.com

Abstract Review on t(6;12)(q22;q24), with data on the genes involved.

Keywords Chromosome 6; Chromosome 12; t(6;12)(q22;q24); Anaplastic large cell lymphoma, ALK negative 

(Note : for Links provided by Atlas : click)

Identity

ICD-Topo C420,C421,C424
ICD-Morpho 9702/3 Peripheral T-cell lymphoma, NOS; Anaplastic large cell lymphoma, ALK negative
Atlas_Id 1765

Clinics and Pathology

Disease Anaplastic large cell lymphoma, ALK negative
Note Two available cases of t(6;12)(q22;q24) to date (Barbieri et al., 1984; Crescenzo et al., 2015). One case was a 39 year old patient (Barbieri et al., 1984).
Prognosis No data

Genes involved and Proteins

Note In one case of t(6;12)(q22;q24) a hybrid NCOR2/ROS1 was found (Crescenzo et al., 2015).
Gene NameNCOR2
Location 12q24.31
Protein This gene encodes a nuclear receptor co-repressor that mediates transcriptional silencing of certain nuclear receptors by promoting chromatin condensation, thus preventing access of the basal transcription. Aberrant expression of NCOR2 is associated with certain cancers.
Gene NameROS1
Location 6q22.1
Protein This proto-oncogene belongs to the subfamily of tyrosine kinase insulin receptor genes and expresses in a variety of tumor cell lines. ROS1 is an integral membrane protein with tyrosine kinase activity, that may function as a growth or differentiation factor receptor.

Result of the chromosomal anomaly

Hybrid gene
Note NCOR2/ROS1
  
Fusion Protein
 
  Schematic of the structure of the NCOR2/ROS1 fusion. The N-term region of NCOR2 is fused to the intracytoplasmic region of ROS1.
Description EXPRESSION_LOCALISATION
Oncogenesis The chimeric NCOR2/ROS1 fusion may influence the transcriptional activity of the partner genes, perturbing transcription repression. This, in turn, may lead to a widespread derangement of several metabolic and signaling pathways ( STAT3), which concur to tumor transformation [Crescenzo et al, 2015; Tabbo et al, 2016].
  

To be noted

Additional cases are needed to delineate the epidemiology of this rare entity:
you are welcome to submit a paper to our new Case Report section.

Bibliography

Cytogenetic evaluation of bone marrow involvement in non-Hodgkin's lymphomas. A survey of 94 cases.
Barbieri D, Michaux JL, Bosly A, van Hove W, Noens L, Drochmans A, Louwagie A, Tricot G, Boogaerts M, Vermaelen K, et al.
Haematologica. 1984 May-Jun;69(3):285-96.
PMID 6432640
 
Convergent mutations and kinase fusions lead to oncogenic STAT3 activation in anaplastic large cell lymphoma.
Crescenzo R, Abate F, Lasorsa E, Tabbo F, Gaudiano M, et al.
Cancer Cell. 2015; 27(4):516-532
PMID 25873174
 
Oncogenic kinase fusions: an evolving arens with innovative clinical opportunities.
Tabbo F, Pizzi M, Kyriakides PW, Ruggeri B, Inghirami G.
Oncotarget. 2016; 7(18):25064-25086
PMID 26943776
 

Citation

This paper should be referenced as such :
Gindina T
t(6;12)(q22;q24) NCOR2/ROS1;
Atlas Genet Cytogenet Oncol Haematol. in press
On line version : http://AtlasGeneticsOncology.org/Anomalies/t0612q22q24NCOR2_ROS1ID1765.html


Translocations implicated (Data extracted from papers in the Atlas)

 t(6;12)(q22;q24) NCOR2/ROS1

External links

Mitelman databaset(6;12)(q22;q24) [Case List]    t(6;12)(q22;q24) [Transloc-MCList] NCOR2/ROS1 [Fusion-MCList]
arrayMap (UZH-SIB Zurich)Morph ( 9702/3) -   [auto + random 100 samples .. if exist ]   [tabulated segments]
 
 
REVIEW articlesautomatic search in PubMed
Last year articlesautomatic search in PubMed
All articlesautomatic search in PubMed


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indexed on : Wed Nov 13 22:14:09 CET 2019


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