Like any of the 80,000 or so men in this country suffering from advanced – meaning incurable – prostate cancer, I was gripped by the headlines last week about the development of a new, allegedly wonderful, if not wonder, drug. According to early trial results, something called abiraterone can shrink prostate tumours that have ceased to respond to all other known treatments.

As things stand at present, men diagnosed with an early cancer that is “still in the capsule” – the tumour confined within the prostate gland, in other words – have a good chance of recovery. Those like me, whose cancer has spread, have a much more bleak outlook.

Once the conventional quartet of surgery and the hormone, radio and chemo therapies have been tried and failed – which they will do, sooner or later, as the cancer gradually mutates and outsmarts them prior to embarking on its final rampage – the only remaining option for the terminal prostate cancer patient is repeated doses of heavy opioid painkillers.

Then, in no more than a year or so, it’s lights out. My cancer hasn’t reached the uncontrollable stage yet, thank God. It’s still responding, more or less, to the traditional treatments; but over the past month it’s really started to hurt.

Waking up last Tuesday morning with that vice-like, nerve-frazzling ache in my hip and lower back – the usual sign that the disease is grimly following its classic path and forming secondary growths, or “metastases”, in the bones – the news burbling out of my bedside radio to the effect that there was now this pill which, swallowed once daily, could swiftly eradicate the pain without inflicting any serious side effects sounded almost too good to be true.

The cynic in me soon piped up: maybe that’s exactly what it was – too good to be true. In the six years that I’ve been grappling with this wretched illness, I’ve lost count of the new drugs, herbal remedies and dietary regimes purporting to treat, even cure, prostate cancer which have received effusive and largely uncritical media attention.

It sometimes feels as though the silence and neglect that surrounded the prostate gland for centuries – it was the only one of the human organs which da Vinci never bothered to draw in his anatomical studies – have flipped into an overcompensating cacophony of concern that is, in its own way, just as confusing.

On a slow news day in the silly season, nothing brightens up a front page better, it seems, than some supposed remedy for the most common cancer among men in this country. I’m not immune to quackish charms either.

Among the putatively therapeutic groceries I’ve been encouraged to add to my shopping list of late are pomegranate juice, turmeric and old-fashioned tomato sauce. According to newspaper reports of research, usually carried out in American university hospitals, all these foodstuffs – and several others which have slipped my mind – have severely clobbered prostate tumours in rats and mice.

Sadly, they don’t seem to have affected mine. A naturally occurring form of oestrogen, PC-Spes – subsequently withdrawn after a row about mis-labelling – and a set of herbal medicines known collectively as the Pfeifer protocol, have both been suggested to me as more effective and less punishing alternatives to the big pharma-produced drug packages which I have mostly resorted to.

Ben Pfeifer, the American doctor who devised the protocol, isn’t some beardy, sandal-wearing naturopath, by the way; he’s an impeccably qualified member of the US medical establishment. The trouble is, his herbs don’t come cheap (several grand a month) and my medical insurance won’t cover them.

Please don’t talk to me about cancer diets. I’ve listened to eminent nutritionists telling me it’s vital that I cut down on my sugar intake, and particularly alcohol, on the grounds that tumours thrive on anything sweet; and I’ve been assured on the contrary by senior oncologists that cancers are far too clever to care what I put away and have been strongly advised not to waste the time I have left depriving myself of life’s few remaining pleasures.

If there’s one thing I’ve learnt from my experience, it’s that there is remarkably little consensus and clarity on anything. So when I heard the ostensibly fantastic news about abiraterone – hailed last week by one British tabloid as a cure, no less, for prostate cancer – I assumed that I probably wasn’t getting quite the full story.

I was right. When I spoke to Dr Johann de Bono, the research scientist based at the Royal Marsden hospital in Sutton who is leading the team developing abiraterone for the Institute of Cancer Research, he was in a tizz about how his preliminary findings had been misrepresented. “Some parts of the press have hyped this drug way beyond what I said about it,” he complained.

“This is not a cure, let me correct that. I believe this drug definitely works – but it works much better with some patients than it does with others.”

He could not enlarge on that caveat at present, he said, for reasons of medical confidentiality. He also pointed out that his was not a revolutionary pharmaceutical discovery: another drug, MDV3100, which operates along similar lines, is being tested by a company in San Francisco. What sparked last week’s storm of interest was an article de Bono published in the Journal of Clinical Oncology, Britain’s leading cancer journal. In it he disclosed the results of a small trial, known as a phase 1 study, in which 21 patients with advanced, untreatable prostate cancer and an average life expectancy of two years, were given abiraterone.

This drug is a hormone suppressant with a difference. Unlike conventional drugs which stop the testicles generating the male hormone that feeds prostate cancer, abiraterone suppresses the testosterone which, de Bono and others believe, is created by the cancer itself.

The key scientific insight here concerns the way that secondary prostate tumours behave once they are deprived of their initial, naturally occurring supply of testosterone. In its early stages, a tumour feeds and grows on testosterone produced by the body and, up to now, treatments for prostate cancer have largely been hormone suppressants, a form of chemical castration, designed to switch off that supply.

Once the body stopped producing testosterone, it was thought that prostate cancers mutated, adapted and learnt to live on other nutrients in their final, “hormone refractory” phase. But now it seems that the tumour may actually somehow “learn” to produce its own supply of testosterone.

Having observed that many prostate tumours continued to contain high levels of the male hormone until the very end, some American oncologists, led by Howard Scher at the Memorial Sloane-Kettering Cancer Center in New York, identified the tumorous enzyme responsible for creating it.

De Bono and his team then set about devising a drug that would block the process by which the cancer produces its own-brand testosterone. De Bono modestly pointed out that in this he was only following an analogous development in the treatment of breast cancer in women (breast cancer research is far more advanced than research into prostate cancer). Abiraterone mirrors the behaviour of so-called aromatase inhibitors which suppress the production of oestrogen within breast tumours.

In the wake of all the media hoo-hah, de Bono sounded slightly regretful that he had published the eye-catching results of his early research last week.

Yes of course he was gratified that all 21 of the patients treated at the Marsden with abiraterone were still alive and had mostly seen their tumours shrink, in line with a dramatic drop in their levels of prostate specific antigens (PSA), the blood marker of the cancer.

The story of one of them, a retired banker who had been given less than a year to live and was last week shown whacking a drum kit was, for many of us, an inspiring image. Having worked for 25 years on developing cancer treatments, de Bono was understandably keen to flag up what may be the prelude to his biggest success yet. However, the $100m (£50m) study into the safety and effectiveness of the new drug had barely begun, he said, and it would take another four years to reach a conclusion and acquire a licence.

A total of 1,200 patients, mostly British or North American, will be taking part. Even if it meets all the regulatory criteria, abiraterone will not be available, de Bono said, before 2011 at the earliest. Well, with a potentially life-changing, if not life-saving, drug in the offing and the chap who invented it on the end of the telephone, I had to ask. Would it be possible for an advanced prostate cancer sufferer such as, er, myself to take part in the trial? The answer perfectly illustrated just how too good to be true the premature reporting of this wonder drug really was, not just for me but for all the other incurables whose hopes may have been raised by what they read and heard last week.

De Bono thought that I most likely would be eligible to take part but, he added ominously, “this trial is not something you or I would probably like or choose”.

The reason, he explained, was that this was “a placebo randomised trial” in which one third of the participants would, unknown to themselves or the trial organisers, be issued with a dud pill in order to assess the relative effectiveness of the real thing. More depressing was the clinical requirement to prove that abiraterone extended survival rather than simply relieving symptoms.

In order to elucidate that point, quite a few, possibly all, of the 400 terminally ill trial subjects who drew the short straw of the placebo stood to die during the nearly four years that the trial lasted. In order to take part I would have to give up the hormone-suppressant therapy I am on. So I was swiftly disinclined to pursue de Bono on fast-tracking me into his research programme.

“We have to wait far too long to get these prostate-cancer drugs approved,” de Bono said, sympathetically registering my guttering interest. “There is no doubt in my mind that this one is effective, but these cancers are smart, too. They are always finding ways to spring back.”

Equally resilient, I felt like saying, is my irrational urge to hope against hope that one day, one of these stories of breakthroughs in the battle against prostate cancer might actually lead to something. I suppose that for other men out there, or for others in the future, this might well be a help in the latter stages, although it is far from a cure. As for me? Well, maybe next week . . .

GROUNDS FOR HOPE

After years of being the “hidden” cancer – the one that men were too embarrassed to talk about – prostate cancer is finally on the global researchers’ agenda and some of the most hopeful therapies are under trial in Britain.

At University College hospital in London, doctors are perfecting photodynamic therapy, in which a drug the cancer cells are vulnerable to is administered, then activated by a light, destroying the cells.

High-frequency ultrasound works in a similar fashion, focusing on the cancer cells and leaving the rest of the prostate intact, thereby avoiding debilitating surgery which can cause impotence and incontinence.

Earlier this year a team at the Institute of Cancer Research discovered seven genes involved in prostate cancer which it is hoped will lead to a better understanding of who will get the disease and the development of early screening.

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