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Many mutations in one clinical-trial basket

When abnormality in a gene is linked to cancer and a drug targets the encoded protein, how can the patients who will respond to the drug be identified if the gene is mutated in many different ways in many different cancers?
  1. Elaine Mardis

    1. Elaine R. Mardis is in the Institute for Genomic Medicine, Nationwide Children’s Hospital, Columbus, Ohio 43205, USA.

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Cancer usually arises from genomic abnormalities. However, the number and complexity of genetic alterations in tumours can make it difficult to predict whether, and in which tissues, a particular mutation in a specific cancer-linked gene will drive tumour growth. This poses a challenge when trying to identify effective treatments. For example, if a drug that targets a specific protein can treat a person with breast cancer who has a mutation in the gene encoding the protein, could the drug treat another patient who has a different mutation in that gene? And could it treat a person with a mutation in the same gene, but in a tumour that has developed in a different tissue? In a paper in Nature, Hyman et al.1 report the outcome of a clinical trial testing the ability of the drug neratinib, which inhibits HER2 and HER3 tyrosine kinase enzymes, to reduce or eliminate tumours. The drug was tested on 21 types of cancer in 141 people who had a total of 42 different mutations affecting one of the enzymes.

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Nature 554, 173-175 (2018)

doi: https://doi.org/10.1038/d41586-018-01312-x

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