Development and Cancer Group

Dr Amanda Swain’s group is investigating how the molecular processes that form the prostate, gonad and adrenal glands can contribute to tumour formation and progression.

Research, projects and publications in this group

We are studying the molecular and cellular processes that contribute to tumour formation and progression with an aim to provide information that will contribute to improving cancer patient therapy.

Dr Amanda Swain

Group Leader:

Development and Cancer AmandaSwain, head of the Tumour Profiling Unit

Dr Amanda Swain is studying how organs such as the prostate, gonads and adrenal gland form normally and the role of these processes in cancer development and progression. As well as running her own research group, Dr Swain is head of the Tumour Profiling Unit.

Researchers in this group

.

Phone: +44 20 3437 7443

Email: [email protected]

Location: Chelsea

.

Phone: +44 20 3437 3623

Email: [email protected]

Location: Chelsea

Dr Amanda Swain's group have written 62 publications

Most recent new publication 11/2024

See all their publications

We develop and use a combination of preclinical models to address our functional and therapeutic questions including 3D self organising organoids, patient derived xenografts and genetically modified mouse models.
We have a current focus on three cancers, prostate adenocarcinoma, salivary gland adenoid cystic carcinoma and adrenal cortical carcinoma.

Recent discoveries from this group

16/01/13

A protein called β-catenin appears to play an important role in the growth and spread of prostate cancer and the researchers are increasingly confident that the protein could be an effective target for treatment of the disease.

The new study, published in the journal PLoS Genetics, looked initially at the role of the protein in the healthy prostate. The team showed that it is important in the development of the gland, but does not play a significant role when it is fully formed.

They then looked at its involvement in prostate cancer. They looked, in particular, at how β-catenin interacts with a gene called PTEN which, when mutated or deleted, is involved in a high proportion of metastatic prostate cancers. They found that prostates with a PTEN deletion and a mutant form of b-catenin with increased activity have an aggressive form of cancer. They showed that this is likely to be due to switching on genes that enable prostate cancer cells to grow.

They also showed that prostate cancers which had increased β-catenin activity were independent of the prostate and highly invasive, meaning these tumours are those which spread to other parts of the body. They suggest that novel drugs which stop β-catenin from working, such as a class of drugs called tankyrase inhibitors, could be effective in the treatment of prostate cancer for these patients.

Study author, Dr Amanda Swain, a team leader in the Division of Cancer Biology at The Institute of Cancer Research, said: “Due to advances over the past decades, we can now successfully treat many prostate cancers. But there remain a significant proportion which grow aggressively and are hard to treat. This research gives crucial information about how some of those cancers grow and spread and indicates how we might be able to treat them.”

This research was carried out by studying the protein in mice. Now it has been shown to have promise as a possible target for treatment, the next step is to look at how β-catenin functions in samples from prostate cancer patients.

Dr Swain added: “We want to try to refine this work and identify which patients’ prostate cancer is driven by β-catenin. The future of cancer treatment will be about finding the right treatment for the right patient so this work is crucial to discovering if this protein can become a tool in the fight against the disease.”