The Institute of Cancer Research finds that combining existing breast and blood cancer drugs could halt the growth of tumours in the prostate
Prostate cancer patients who are diagnosed late could get years more with loved ones by taking drugs designed for other cancers.
New research by the Institute of Cancer Research (ICR) in London has found that combining existing breast and blood cancer drugs could halt the growth of tumours in the prostate. Scientists say the double-pronged attack on advanced prostate cancer could help treat as many as two in five patients with late-stage disease.
It can take 10 to 15 years for new cancer drugs to get from development, through human clinical trials and to be approved for use on the NHS.
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Hormone therapy works against prostate cancer by lowering the levels of testosterone in the body, which fuels the cancer’s growth. However for some this doesn’t work and scientists are often unsure why some patients are resistant.
This group of patients have much worse survival chances so ICR scientists conducted a series of lab tests on drugs already in development, or used to treat other cancers. Dr Adam Sharp, leader of the Translational Therapeutics Group at the ICR, said: “For men with advanced prostate cancer, once hormone therapies stop working, the outcomes are bleak.
“Researchers are constantly searching for new treatment options, but discovering and developing a new drug from scratch is a lengthy process. In this work, we screened a large number of drugs that are in development, or already being used to treat cancers.
“We identified a particularly promising pairing that could help patients with advanced prostate cancer, and our data suggests that up to 40% of people with this disease could benefit. Excitingly, we found that the treatment doesn’t just slow tumour growth – it actually kills cancer cells. We’re cautiously optimistic that this approach may better prevent resistance to treatment from occurring.”
Researchers set out to find a combination of drugs which attack proteins in the body which promote cancer cell survival. MCL1 is a protein that promotes cancer cell survival and protein AKT plays a key role in a mechanism that many cancer cells rely on to survive, grow and resist treatment.
The research, published in the journal Nature Communications, found that inhibiting MCL1 and AKT at the same time triggered prostate cancer cell death in lab samples. Follow up tests in mice showed the combination significantly slowed cancer growth.
Professor Kristian Helin, ICR chief executive, said: “Finding new ways to overcome treatment resistance is a key priority in cancer research. This study highlights how progress can come from re-assessing existing drugs in innovative ways. By identifying the most effective combinations – and, crucially, the patients most likely to benefit – we hope to halt cancer’s progression and give patients more time with their loved ones.”
Scientists used the blood cancer drug fadraciclib to indirectly target the protein by inhibiting another protein that regulates MCL1 levels. The team inhibited AKT using either a drug called ipatasertib, which is being investigated as a potential treatment for a number of different cancers, or another called capivasertib – used to treat certain types of breast cancer. Combining fadraciclib with either capivasertib or ipatasertib triggered prostate cancer cell death.
Specifically, they found that prostate cancer cells which had a certain type of tumour which affected 40% of patients, known as PTEN-loss/PI3K-activated, responded best to the combinations.
