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https://en.wikipedia.org/wiki/Fusion_gene

Oncogenes

It has been known for 30 years that the corresponding gene fusion plays an important role in tumorigenesis.[5] Fusion genes can contribute to tumor formation because fusion genes can produce much more active abnormal protein than non-fusion genes. Often, fusion genes are oncogenes that cause cancer; these include BCR-ABL,[6] 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.[7] The fusion of the genes ERG and TMPRSS2 is the most common for this cancer. By disrupting the androgen receptor (AR) signaling and inhibiting the AR expression by an oncogenic ETS transcription factor, the fusion product regulates the prostate cancer.[8] The other not as common fusions also are affected by the androgen receptor and occur in the prostate as well. Most fusion genes are found from hematological cancers, sarcomas, and prostate cancer.[9][10] BCAM-AKT2 is a fusion gene that is specific and unique to high-grade serous ovarian cancer.[11] 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 (which can produce lots of gene product), 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.[12] Oncogenic fusion transcripts may also be caused by trans-splicing or read-through events.[13] Since chromosomal translocations play such a significant role in neoplasia (abnormal growth), a specialized database of chromosomal aberrations and gene fusions in cancer has been created. This database is called Mitelman Database of Chromosome Aberrations and Gene Fusions in Cancer.

https://www.ncbi.nlm.nih.gov/pubmed/24659477#:~:text=