Research press release




HER2遺伝子とHER3遺伝子のさまざまな変異が、広範な種類のがんに見つかっている。これらの変異の一部はHER2タンパク質の過剰発現を引き起こし、発がんに至るが、その他多くの変異の特徴は解明されていない。今回、David Hymanたちの研究グループは、HER2遺伝子とHER3遺伝子に種々の変異を有する乳がん、肺がん、膀胱がん、大腸がんの患者(合計141人)に対するネラチニブ(HER2タンパク質の活性を阻害する医薬品)の有効性を検討した。その結果、ネラチニブに対する反応は変異と組織の種類によって決まり、HER2遺伝子に変異のあるがんに限られることが分かった。


The efficacy of a cancer drug that targets a particular class of mutations depends on the tumour tissue type and the exact nature of the mutation, reports a clinical trial published online in Nature. The research highlights how molecularly driven clinical trials can be used to enhance our understanding of the effects of genetic mutations, a finding that could aid the development of personalized cancer therapies.

Various mutations in the HER2 and HER3 genes are found in a wide range of cancers. Some of these mutations cause overexpression of the HER2 protein, leading to cancer, but most are uncharacterized. David Hyman and colleagues tested the efficacy of neratinib, a drug that blocks the activity of HER proteins, in 141 patients with a variety of cancers, including breast, lung, bladder and colorectal, and a variety of different mutations in the HER2 and HER3 genes. They found that the response to treatment was determined by mutation and tissue type, and was restricted to cancers with HER2 mutants.

The move towards personalized cancer therapies has been hampered because the clinical and biological importance of most genomic variants is unknown. This study helps to change that, providing new insights that were not predicted by preclinical models. It also highlights the value of so-called ‘basket’ trials, which focus on a mutation type, such as those found in the HER genes, rather than the tissue in which the cancer appears.

doi: 10.1038/nature25475

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