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From Wikipedia, the free encyclopedia

A fusion gene is a hybrid gene formed from two previously separate genes. It can occur as the result of a translocation, interstitial deletion, or chromosomal inversion. Often, fusion genes are oncogenes; examples include BCR-ABL,[1] TEL-AML1 (ALL with t(12 ; 21)), AML1-ETO (M2 AML with t(8 ; 21)) and TMPRSS2-ERG with an interstitial deletion on chromosome 21, often occurring in prostate cancer.[2] Most fusion genes are found from hematological cancers, sarcomas and prostate cancer.[3][4]

Oncogenic fusion genes may lead to a gene product with a new or different function from the two fusion partners. Alternatively, a proto-oncogene is fused to a strong promoter, and thereby the oncogenic function is set to function by an upregulation caused by the strong promoter of the upstream fusion partner. The latter is common in lymphomas, where oncogenes are juxtaposed to the promoters of the immunoglobulin genes.[5] Oncogenic fusion transcripts may also be caused by trans-splicing.

Presence of certain chromosomal aberrations and their resulting fusion genes is commonly used within cancer diagnostics in order to set a precise diagnosis. In routine diagnostic laboratories the following methods are most commonly used: chromosome banding analysis, fluorescence in situ hybridisation, and RT-PCR. These methods all have their distinct shortcomings due to the very complex nature of cancer genomes. Recent developments such as high-throughput sequencing[6] and custom-designed DNA microarrays[7] bear promise of introduction of more efficient methods.

Biologists may also deliberately create fusion genes for research purposes. For example, by creating a fusion gene of a protein of interest and green fluorescent protein,[8] the protein of interest may be observed in cells or tissue using fluorescence microscopy. The protein synthesized when a fusion gene is expressed is called a fusion protein.

References

  1. ^ Nowell, PC; Hungerford, DA (1960). "A minute chromosome in chronic granulocytic leukemia". Science.  
  2. ^ Tomlins, SA; Rhodes; Perner; Dhanasekaran; Mehra; Sun; Varambally; Cao et al. (2005). "Recurrent fusion of TMPRSS2 and ETS transcription factor genes in prostate cancer". Science 310 (5748): 644–8. doi:10.1126/science.1117679. PMID 16254181.  
  3. ^ Mitelman, F; Johansson; Mertens (2007). "The impact of translocations and gene fusions on cancer causation". Nature reviews. Cancer 7 (4): 233–45. doi:10.1038/nrc2091. PMID 17361217.  
  4. ^ Teixeira, MR (2006). "Recurrent fusion oncogenes in carcinomas.". Critical reviews in oncogenesis 12 (3-4): 257–71. PMID 17425505.  
  5. ^ Vega, F; Medeiros (2003). "Chromosomal translocations involved in non-Hodgkin lymphomas". Archives of pathology & laboratory medicine 127 (9): 1148–60. PMID 12946230.  
  6. ^ Maher, CA; Kumar-Sinha; Cao; Kalyana-Sundaram; Han; Jing; Sam; Barrette et al. (2009). "Transcriptome sequencing to detect gene fusions in cancer". Nature 458 (7234): 97–101. doi:10.1038/nature07638. PMID 19136943.  
  7. ^ Skotheim, RI; Thomassen; Eken; Lind; Micci; Ribeiro; Cerveira; Teixeira et al. (2009). "A universal assay for detection of oncogenic fusion transcripts by oligo microarray analysis". Molecular cancer 8: 5. doi:10.1186/1476-4598-8-5. PMID 19152679.  
  8. ^ Prendergast, FG; Mann (1978). "Chemical and physical properties of aequorin and the green fluorescent protein isolated from Aequorea forskålea". Biochemistry 17 (17): 3448–53. PMID 28749.  
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