Archive for Research Update

An editorial in today’s edition of Urotoday, “Exploring Causes for Declining Prostate Cancer Mortality Rates in the United States” (1/5/09), looks at possible explanations for the the reduction in deaths from prostate cancer in recent years (’93-’03).  The authors relied on information from a a study reported recently in the journal Urologic Oncology (Nov-Dec).

The researchers  found that the following correlated with decreased PC mortality in *white men*:

  • PSA screening; and
  • High cholesterol

 The widespread use of statins to treat high cholesterol appears to benefit men, especially those with advanced or fatal PC.

In black men, access to health care and insurance coverage were the only factors correlated with a decrease in PC deaths.

These findings lend credibility to those who favor prostate screening for all men over 50 (or in certain cases, younger).

Here are some excerpts from the story in Urotoday:

Editor’s Pick:  “BERKELEY, CA (UroToday.com) – A question that has never been clearly answered is, following the introduction of PSA screening in the US in 1989, why prostate cancer deaths increased between 1989 and 1993, then decreased from 1993 to 2003. . . .

“In the Nov-Dec issue of Urologic Oncology, Drs. Janet Colli and Christopher Amling compared declining prostate cancer mortality rates with levels of PSA screening, health insurance coverage, obesity, physical inactivity, diabetes, and high cholesterol.

“The investigators studied men over age 50 included from 1979 to 2003 in the National Vital Statistic System database at the National Center for Health Statistics of the Centers for Disease Control and Prevention. . . .

“Declining prostate cancer mortality rates for white males correlated with high cholesterol levels and PSA screening levels. No other independent variable for white males correlated with declining PCa mortality rates. . . . Among black males, declining prostate cancer mortality rates correlated with health insurance coverage. . . .

“The authors point out that while cholesterol is considered a risk factor for PCa, the extensive use of statins in this population is associated with a decreased risk in this population. This relationship has been especially suggested between statin use and advanced and fatal PCa. Health insurance coverage and access to health care was not a factor in white men, but appeared to be so in black men.”

Urol Oncol. 2008 Nov-Dec;26(6):627-33
10.1016/j.urolonc.2007.05.016

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Jul
06

Consider Adding Radiation to Surgery

Posted by: Leah | Comments (0)

Dear All,

I have been revisiting the issue of salvage radiation therapy (RT) since Ted just began this treatment last week.  There isn’t a lot of good data (only “retrospective” data) about this, so when I first tackled this subject a few months ago I decided I was better off “reading the tea leaves”.  But it seems that I may have overlooked some things (been too pessimistic!).

One thing that shocked me about reading this was: We know there’s a lot of stuff about PC that we don’t know.  But I realize that there is critical info that we do know about, which, for some reason, is not being incorporated into clinical practice.

What I’ve found out is:

* Experts agree that post-RP radiotherapy is “underutilized”

* There is some evidence that RT may be effective even in men with advanced disease.

* Post-op RT should be started ASAP.  It can make a big difference if the patient starts radiotherapy when their PSA is at .5 vs. 1.0, vs. 2.0.  The differences can be really significant.

Also, the factors that have previously been considered critical for RT success may in fact not be so.  MSK has recently developed a nomogram that is supposed to accurately predict the success of salvage radiotherapy (in the med lit they call this “sRT”).  (Journal of Clinical Oncology, 2006 ASCO Annual Mtg.  “Predicting the outcome of sRT for recurrent PC after RP”, by Stephenson, Scardino et al.)

And maybe “prophylactic RT” (adjuvant), should be done as a matter of course on high- and even medium-risk men.  Salvage RT is also thought to work, but the results are not that clear.

There is a consensus that if RT is going to be given, it should be started sooner than later.  *So why is it standard medical advice after a positive PSA to advise the patient to wait 6 mos. before doing anything?  It just doesn’t make sense.

When Ted’s PSA started to rise back in January, I was advised by some “elders” online to seek help immediately, i.e., to visit some oncologists.  We did this, even though it was “AMA” (Against Medical Advice).  I am glad for that insider info, but not everybody has access to it.  And even though we started early, it took 5 mos. until T. actually got the RT.  (Getting records, consultations, switching his insurance, etc.)

The first person we saw was Dr. Peter Schiff at Columbia Presb., a highly-rated radiation oncologist.  I was surprised when he told Ted, who had a PSA of .14 at the time, that he should begin RT as soon as possible.  Not this minute, necessarily, but within a couple of weeks.  Well, I thought I was smarter than the doctor: it seemed that he was “rushing to judgment”.  Turns out he was right.

I have a stack of papers on this subject in front of me, which I have reviewed carefully, but mostly I will quote from Endotext.org, a medical reference source, which I know to be reliable and current.  Also, what they say is consistent with what I’ve read. 

“Treatment of Post-Prostatectomy Recurrences”:

A number of retrospective comparative series have examined the potential benefit to adjuvant radiotherapy.

*Unselected series have suggested biochemical control rates in the combined surgery plus adjuvant radiotherapy cases of 52-93%, compared to surgery only rates of 25-74%. More concordant results were seen in two published matched pair analyses which showed surgery only freedom from biochemical failure (FFbF) of 55-59% which was increased to 88-89% with the addition of radiotherapy.”

Also noted: “Grade 3 toxicity” and urinary incontinence problems were not increased by the addition of RT.

This combination of randomised trial data (amounting to level 1 evidence) suggest that there is an unequivocal capacity for post-RRP adjuvant radiotherapy to approximately halve the chance of having a future PSA-detectable tumour recurrence in pT3 / margin positive patients, while maintaining a low level of toxicity. More maturity to the data is awaited to determine the overall impact this has on distant metastases or survival.

Salvage radiotherapy

The role of salvage radiotherapy is far less clearly defined, with no prospective studies of efficacy or toxicity to guide decisions. Retrospective analyses suggest that the PSA level prior to initiating the salvage radiotherapy is strongly predictive of outcome, with some series suggesting that treatment at PSA levels below 1 ng/mL do substantially better than those above this level. This PSA effect has been shown to be independent of the PSA doubling time, potentially indicating that these patients benefit from early referral for treatment regardless of PSA dynamics.”

Indeed, one series demonstrated an independent benefit to the use of immediate adjuvant therapy rather than waiting until requiring salvage.

Larger series typically show a 5 year biochemical control rate in the order of 50% typically (501, 505), and over 70% for those with a pre-treatment PSA of less than 1 ng/mL and an operative Gleason score of 7 or lower (502).”

“Despite the apparent ability to provide a substantial chance for long-term control in relapsed men, there is concerning data that post-RRP radiotherapy may be under-utilised. Only 55% and the 38% of the biochemical failures in the observation arms of the EORTC and SWOG randomised trials respectively underwent potentially curative salvage radiotherapy . . . 

Take care and bear with me while I learn to blog.

Leah

Jul
05

Step Ahead for Vaccine Therapy

Posted by: Leah | Comments (0)

Dendritic cells are replenished from blood

 Dendritic cells help direct the body’s immune response by presenting invading antigens to T cells so they know what to attack. But an ongoing debate exists about where dendritic cells originate and how they multiply, especially in the spleen and lymph system. Now, in a paper published in this month’s issue of Nature Immunology, Rockefeller University scientists have come a step closer to understanding the origins of the spleen and lymph node dendritic cells, findings that are especially important for researchers developing immune-cell-targeted vaccines.