Methylation-associated silencing of BASP1 contributes to leukemogenesis in t(8;21) acute myeloid leukemia
2018
Lei Zhou | Lin Fu | Na Lv | Jing Liu | Yan Li | Xiaosu Chen | Qingyu Xu | Guofeng Chen | Baoxu Pang | Lili Wang | Yonghui Li | Xiaodong Zhang | Li Yu
Cancer: Mismatched molecules unleash leukemia cell proliferation A chromosomal rearrangement commonly observed in certain leukemias selectively inactivates a gene that otherwise thwarts cancerous growth. Between 7 and 12% of acute myeloid leukemia cases exhibit a dramatic alteration in chromosomal structure that results in the production of an abnormal fusion protein. Researchers led by Li Yu at the General Hospital of Shenzen University in China have learned that this protein promotes disease progression by switching off an important tumor suppressor. Yu and colleagues showed that it binds a genomic sequence that regulates the gene encoding a second protein called BASP1, dramatically reducing its production. This gene silencing facilitates tumor growth. Chemicals that reactivated BASP1 production slowed proliferation and initiated ‘self-destruct’ mechanisms in leukemia cells. These findings suggest that BASP1-oriented therapies could offer a fruitful avenue of treatment for some patients.
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