We may soon have a new class of drugs that could help us in our fight against resistant cancer, a new study has revealed.
While the drug will not enter production phase for quite a few years, scientists are optimistic that if clinical trials are successful, the drug will help us tackle a variety of treatment-resistant cancers.
Patients with breast cancer for example frequently become resistant to existing hormone-based treatments, leading to the disease becoming fatal.
Early lab-based tests of ICEC0942 were successful in targeting resistant breast cancers and indicated minimal side effects, according to the results published in the journal Molecular Cancer Therapeutics. ICEC0942 was then licenced to Carrick Therapeutics, who developed it into a molecule named CT7001, which they have taken to early-stage clinical trials in less than two years.
“Treatment-resistant tumours represent a significant threat for patients, as once a cancer stops responding to treatments there is increasingly little clinicians can do,” said Charles Coombes, a professor at Imperial College London. “Drugs such as these could help to shift the balance back in favour of the patients, potentially providing a new option to patients for who existing treatments no longer work.”
The drug targets an enzyme called CDK7, involved in directing cells through their life cycle, which consists of growth, DNA replication and cell division. CDK7 is also involved in the process of transcription, a vital step in gene expression – the creation of proteins to carry out cell functions.
Particular cancers, such as treatment-resistant breast cancers, have a unique dependence on transcription, meaning targeting CDK7 may be particularly effective.
By inhibiting transcription, ICEC0942 shuts down the ability of the cancer to spread.
As well as breast cancers, cancers such as acute myeloid leukaemia and small-cell lung cancer are particularly transcription-dependent, so ICEC0942 may work well for these too, especially where they have become resistant to other treatments.