Google gives quite a few hits, but other than a vague sky news item on
the lines of "could help up to 80%" I didn't find any useful detail. I
guess new trial data gets so diffused over so many categories and
parameters it becomes impossible to pin down an overall figure which
is meaningful.  But the harbingers (that always sounds like a surname
to me) are good.

Just a couple of hits I found at random:-

http://tinyurl.com/5owedz

http://tinyurl.com/5jegkx

Indeed

http://www.timesonline.co.uk/tol/news/uk/health/article4405767.ece
July 27, 2008
This new drug is no magic bullet
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.

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.

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.

http://prostatecancerinfolink.net/2008/06/02/asco-meeting-update-no-4/

ASCO annual meeting update no. 4
Posted on June 2, 2008 by E. Michael D. ("Mike") Scott

A session this morning reported on an additional group of drugs in
potential development for the treatment of hormone refractory prostate
cancer. (Actually it is notable that the term “castration-resistant
prostate cancer” appears to be the politically correct term for this stage
of disease in the oncology community today. The older term
“androgen-independent prostate cancer”  seems to be outmoded.)

Beer et al. reported on a Phase I trial of the monoclonal antibody
ipilimumab alone and in combination with radiotherapy in treatment of 33
patients with metastatic castration-resistant prostate cancer. While the
drug alone and the drug in combination with radiotherapy appeared to have
some impact on PSA, and a very small number of the patinets appeared to
show some degree of actual disease remission, The “New” Prostate Cancer
InfoLink got the strong impression that the cost in terms of adverse events
was extremely high, including one patient death and many grade 3 and grade
4 side effects. We would not currently recommend that patients participate
in this trial given what appear to be other clinical trial options with
apparently superior responses to date and a lower risk for adverse events.

De Bono et al. provided a detailed report on Phase I and Phase II trials of
abiraterone acetate, an innovative CYP17 inhibitor of androgen synthesis,
in chemotherapy-naive and docetaxel pre-treated castration-resistant
prostate cancer patients.

These trials appeared to suggest a significant potential impact of
abiraterone in combination with steriod therapy (prednisone or
dexamethasone), with > 50 percent declines in PSA in more than 70 percent
of patients, clear responses of metastases to therapy, and a relatively
modest adverse reaction profile. It would appear from the data presented
that patients either do or definitively don’t respond to abiraterone. This
may reflect the continuing degree of hormone-responsiveness of the
individual patients, with some patient having minimal response to hormone
therapy, and others maintaining a significant level of hormone response.

De Bono stated that a randomized, double blind, multicenter Phase III
clinical trial of abiraterone + prednisone vs placebo + prednisone is now
in development, and it will be interesting to see if this trial can show
definitive impact on progression-free and overall survival.

Sher et al. provided an overview of Phase I/II trial data on the
investigational agent MDV3100 in patients with progressive
castration-resistant prostate cancer. MDV3100 is a novel molecule that
inhibits androgen receptor function. This drug again shows highly
significant reductions in PSA levels in some patients, and at the time of
this presentation, the maximal therapeutic dose had still not been
established. Patient recruitment to this trial is still ongoing, but it
should be noted that there was a relatrively high drop-out rate from this
trial, and we may again be seeing a situation in which one set of patinets
may respond well to this agent and another group is not able to tolerate
treatment. Further data will be necessary before the potential benefits of
MDV3100 can be clearly established.

Finally, Pili et al. reported on a novel tumor vascular disrupting agent
(known as DMXAA or ASA404) in combination with docetaxel for treatment of
castration-resistant prostate cancer. This Phase II trial compared 33
patients receiving DMXAA + docetaxel to 38 patients receiving docetaxel
alone. There are suggestions from this trial of superior outcomes on the
combination arm, but The “New” Prostate Cancer InfoLink did not feel that
the data were sufficiently mature at this point in time be able to
establish a clear benefit for the combination therapy over docetaxel.

We would conclude by noting that the real take-away from ASCO is the
increasing number of new agents that are being tested for their potential
in late stage prostate cancer, and our increasing appreciation of the
potential of new therapies in this stage of disease. It seems likely that,
at some point relatively soon, at least one (and perhaps more than one) of
these new agents or new combinations will show a truly significant impact
on late stage disease — prior to, in combination with, or following
chemotherapy with the current standard therapy of docetaxel and
prednisone."

I had another link that said some/many? dropped out after 2 treatments due
to side effects.
I will try to refind it.
J