医学
乳腺癌
突变体
抗药性
癌症研究
酪氨酸激酶
内科学
癌症
突变
后天抵抗
药品
药理学
遗传学
基因
生物
受体
标识
DOI:10.1056/nejmcibr2110552
摘要
A recent study suggests that HER2-mutated breast cancer may develop resistance to drugs that inhibit the tyrosine kinase domain of HER2 through developing mutations in HER3, which enhance the dimerization between HER2 and HER3. The HER3 mutations augment signaling. This study supports a specific approach to overcoming mutant-HER3–mediated resistance.
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