Oestrogen breakthrough gives hope to inoperable prostate cancer victims

Deadly therapy-resistant prostate cancer could be overcome with a treatment based on the female hormone oestrogen.

The secret is to target a particular tumour molecule that responds to the hormone, tests reveal.

Growth of prostate cancer is usually associated with androgen male hormones, such as testosterone.

Hope: The breakthrough is great news for the thousands of men battling prostate cancer

But men carry a certain amount of oestrogen, the female sex hormone. The new research indicates that biological pathways involving oestrogen can be used to combat prostate cancer.

Oestrogen binds to specific receptors on the surfaces of cells - molecules that trigger biochemical effects when stimulated. Prostate tumours are known to carry two oestrogen receptors. One of them, the beta oestrogen receptor, causes cancer cells to commit suicide when activated, the research shows.

Conventional hormone treatment for prostate cancer that has not been cured by surgery or radiotherapy involves blocking the effects of androgens, or cutting off their supply.

Australian scientists carrying out the new research developed a drug that selectively targets beta oestrogen receptors.

Professor Gail Risbridger, from Monash University in Victoria, which co-led the study, said: 'It not only inhibits the growth of prostate cancer but also kills off cancer cells that are resistant to conventional treatment such as androgen deprivation therapy, more commonly known as castration therapy, and does so using a mechanism that is different to castration.

'The team at Monash University has discovered how this compound working through the beta receptors targets a small, but very important, population of cells in the tumour. It is a significant piece of the puzzle that will help medical research in this field - an achievement that could eventually enhance treatment options for patients around the world with advanced prostate cancer.'

After making the discovery in animals, the scientists repeated the results using human cells and tissues from prostate cancer patients.

The findings were published last month in the journal Proceedings of the National Academy of Sciences.

Each year around 35,000 men in the UK are diagnosed with prostate cancer and 10,000 die from the disease.

Breakthrough: Professor Gail Risbridger from Victoria's Monash University led the research

'This research.. provides me with the imperative to conduct basic biomedical research where the fundamental outcomes such as those we describe may ultimately translate into more effective ways to treat prostate cancer,' Prof. Risbridger added.

Dr Helen Rippon, head of research management at The Prostate Cancer Charity, said: 'Hormone therapy to block the actions of androgens, or male hormones, is the mainstay of treatment for men with advanced prostate cancer that has spread beyond the confines of the prostate.

'Although hormone therapy can control the cancer for many years, prostate tumours eventually stop responding and resume growth. This is thought to be because small groups of cancer cells emerge within the tumour that are no longer dependent on androgens to survive and thrive.

'This study looks specifically at new ways to kill prostate cancer cells once they have become androgen resistant. It identifies another hormone pathway, controlled by oestrogens, which could be a promising target for the development of new treatments. This research shows that 'switching this pathway on' can force the androgen-resistant cells to 'commit suicide'.

'Although this research is still at a comparatively early stage, it does suggest that oestrogen-based drugs could be developed and tested specifically for late-stage prostate cancer treatment.

'We are pleased to see researchers taking on this important issue because, sadly, once prostate cancer has become resistant to anti-androgen therapy, there is a dearth of effective treatments available. Men with later stages of the disease can be left feeling that they have very few options left and this needs to change - as rapidly as possible.'

