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Leukemia occurs with stained weight row and additional molecular fractures, but the mechanism of cooperation between the two remains unclear.
recently published in the journal Blood, researchers sequenced all-exoscopic twins from children with inconsistent fusion of ETV6-RUNX1 (E/R) genes in the paper "Dentification of functional cooperative mutations of GNAO1 in human acute lymphoblastic leukemia."
sequencing results found that the R209C mutation of G protein alpha subchio1 is a new risk point for ALL.
addition, GNAO1 error mutations occur only in ALL patients and are associated with E/R fusion.
expression GNAO1 R209C mutant can increase its GTPase activity, promote cell proliferation and cell tumor transformation.
E/R fusion, the GNAO1 R209C mutation promotes leukemia by activating the PI3K/Akt/mTOR signal.
, activated mTORC1 phosphorylation p300 acetyl transferase, which in turn makes E/R acetylation, thereby enhancing the E/R transcription activity of GNAO1 R209C.
, the study provides clinical evidence for functional collaboration between GNAO1 mutations and E/R fusion, suggesting that GNAO1 may be a potential therapeutic target for human leukemia.
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