Currently working on an oncology presentation. Our professor assigned us a chemotherapy and we have to do in-depth research on it (indications, mechanism of action, etc). The drug I was assigned specifically is used for FGFR2 fusions. I’ve scoured through Pubmed, BioMed, and various oncology journals and I cannot get a straight answer as to what an FGFR fusion even is. All I’m getting is that it can amplify FGFR signaling, leading to proliferation, which I understand. I just don’t want to get to my presentation and my professor ask what an FGFR fusion is and I have no idea how to respond
Hopefully someone here is knowledgeable on this! Thanks!
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A fusion gene is essentially what you get when a piece of one gene ends up fused to another following some manner of translocation.
The textbook example is BCR-ABL, which is a hallmark of chronic myeloid leukemia. The result is a tyrosine kinase with very strong proliferative signaling, with its usual regulatory bits swapped to something that’s always on.
Reading through [this paper](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7555921) about FGFR fusion, it’s actually very similar — the common factor to the described type I and II fusions is FGFR’s tyrosine kinase domain being disconnected from its normal regulation.
Good luck!
A fusion gene is essentially what you get when a piece of one gene ends up fused to another following some manner of translocation.
The textbook example is BCR-ABL, which is a hallmark of chronic myeloid leukemia. The result is a tyrosine kinase with very strong proliferative signaling, with its usual regulatory bits swapped to something that’s always on.
Reading through [this paper](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7555921) about FGFR fusion, it’s actually very similar — the common factor to the described type I and II fusions is FGFR’s tyrosine kinase domain being disconnected from its normal regulation.
Good luck!
A fusion gene is essentially what you get when a piece of one gene ends up fused to another following some manner of translocation.
The textbook example is BCR-ABL, which is a hallmark of chronic myeloid leukemia. The result is a tyrosine kinase with very strong proliferative signaling, with its usual regulatory bits swapped to something that’s always on.
Reading through [this paper](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7555921) about FGFR fusion, it’s actually very similar — the common factor to the described type I and II fusions is FGFR’s tyrosine kinase domain being disconnected from its normal regulation.
Good luck!
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