RE: FW: Catalona's response to the Stamey article.

[Guest guest]

Kathy

Thanks for this one

I found it well worth reading

[Guest guest]

Thank you Kathy this was very interesting... Brad

> >Reply-To: ProstateCancerSupport >To: <ProstateCancerSupport > >Subject: FW: Catalona's response to the Stamey article. >Date: Mon, 13 Sep 2004 17:42:27 -0400 > > >Q: Would you discuss new Stamey study? Source >URL:http://mednews.stanford.edu/releases/2004/September/stamey.htm >A: I believe the new Stamey study has some flaws in it and the message >is misleading to men concerning prostate cancer. > >I have written a response to this that will soon appear in a journal. A >draft of that response appears below.Prostate Cancer Screening > > J. Catalona, M.D. >Professor of Urology, Director, Clinical Prostate Cancer Program, >H. Lurie Comprehensive Cancer Center, Feinberg School of Medicine, >Northwestern University, Chicago, Illinois, USA > >Screening for prostate cancer is controversial. The pro side of the >controversy holds that: (1) prostate cancer is the most common visceral >cancer in (US) men and the second-leading cause of cancer death; (2) >since there is no cure for advanced prostate cancer and no known means >of preventing prostate cancer, the only hope for reducing suffering and >death from prostate cancer is to detect it early and treat it >effectively; and (3) since prostate cancer usually produces no symptoms >until it is too late, it is necessary to pro-actively screen for and >detect it when it is curable. The con side is that: (1) there are other >important needs for health care resources; (2) the benefits of prostate >cancer screening have not yet been conclusively demonstrated; (3) there >are risks associated with treatment; and (4) screening should not be >implemented until there is proof that it does more good than harm. The >goals of screening are to reduce prostate cancer-related suffering and >death by detecting and treating potentially harmful cancers while they >are curable while avoiding causing excessive side effects and having >reasonable economic costs. However, if there were no effective treatment >for prostate cancer, screening could not achieve these goals. Recently, >a randomized trial has demonstrated that radical prostatectomy reduces >metastasis and death rates from prostate cancer as compared with >watchful waiting.1 If screening and treatment were effective, one would >expect an initial increase in incidence rates, as previously >undetectable cancers are detected; a subsequent decline in incidence, as >previously occult cancers are culled from the population; a higher new >baseline incidence rate, because more of the prevalent cases are >detected; detection of earlier stage disease; a decrease in mortality >rates from advanced cancer; an increase in the "relative" survival rate >(survival relative to other causes of death); detection of cancer at a >younger age and lower PSA levels. All of these trends have been >observed. To prove conclusively that screening is effective, either a >randomized trial or a sustained reduction in national cancer-specific >mortality rates would be required. Even if there were proof, there would >remain questions about which patients benefit; how many cancers must be >detected to save one life; what is the risk-benefit ratio in relation to >side effects; and what are the economic costs in relation to the >benefits? The great majority of PSA-detected tumors have the >histological characteristics of clinically important cancers, and most >are organ confined. PSA screening advances the date of diagnosis by 5 >to13 years, and the US prostate cancer-specific mortality rates have >decreased by more than 20% since 1995 in the PSA screening era.2 There >are large ongoing randomized clinical trials, and some smaller studies >have suggested a mortality benefit from screening. These trends have >been interpreted by some cancer epidemiologists as showing the influence >of PSA screening: ".there is little uncertainty that PSA testing has >left its mark on the vital statistics for prostate cancer. Several >factors, especially the decline in the incidence of and mortality from >distant stage disease, hold out the promise that PSA testing may lead to >a sustained decline in prostate cancer mortality."2 >Certainly, screening causes some instances of "over detection" of >cancer; however, very few harmless, so-called "autopsy" cancers can be >detected with prostate biopsies. In the US, 17% of men are diagnosed >with prostate cancer during their lifetime and of these men with >prostate cancer, 16% die of their disease. Thus, overall, approximately >3% of US men die of prostate cancer. It has been implied that this >disparity indicates that most prostate cancers are harmless. The fact >that a man does not die of his cancer does not necessarily mean that the >cancer was harmless. Some patients are cured of virulent cancers, and >others suffer from advanced disease but die of other causes. >Possible alternative explanations for the current favorable prostate >cancer incidence and mortality trends are lead-time and length-time >bias, improved treatments, the earlier use of hormonal therapy; >misclassification of cause of death, and diet or environmental factors. >However, it is difficult to discount the importance of early detection. >With widespread screening, tumors are smaller at the time of diagnosis >now than in the past. With smaller tumors, the "noise" >(BPH/prostatitis)-to-"signal" (cancer) ratio of the PSA level in the >blood increases, and PSA performs less well as a screening test for >cancer. This is especially true in older men. This is the main reason a >decreasing correlation has been reported between the PSA level and the >volume of the "index" tumor in the prostate gland. However, with early >prostate cancer, the tumor cells are frequently scattered throughout the >prostate in microscopic foci, and, if one measures only the volume of >the largest "index" tumor, one might miss the correlation between total >tumor volume and the serum PSA level. However, a direct association has >been demonstrated between the serum PSA level and the likelihood of >prostate cancer, even at low PSA levels.3 A recent study reported that >15% of men with a normal prostate examination and a PSA less than 4 >ng/ml have cancer detected on systematic needle biopsies, 3 raising >questions about the usefulness of PSA testing. Another study reported >that PSA in the range below 10 ng/ml is primarily a marker for BPH >(article by Stamey). These reports, along with concerns about >unnecessary biopsies, the "costs" of screening, and possible over >treatment, have been the topics of public debate in the lay media and >have created more confusion and controversy than the information >warrants. They could result in men thinking they do not need to have >annual PSA testing or timely treatment after a prostate cancer >diagnosis. Nothing could be further from the truth. I believe that >several changes should be considered for the future prostate cancer >screening. In 1991, I published the first study demonstrating that PSA >could be used as a first-line screening test for prostate cancer, using >a PSA cutoff of 4 ng/ml. 4 From preliminary research, it was clear that >no PSA cutoff could completely separate men with curable prostate cancer >from those with benign enlargement or inflammation. Therefore, I >initially selected the 4-ng/ml cutoff because I believed it would detect >many of the dangerous, yet curable, cancers while limiting the number of >unnecessary biopsies in men without cancer. My PSA study enrolled 36,000 >men for screening and lasted for 12 years. After a few years, it became >apparent that nearly half of the men whose PSA was in the 2.5 to 4 ng/ml >range progressed to PSA levels above 4 ng/ml within four years. In >nearly one-third of these men with rapidly rising PSA values, the cancer >had spread to the margins of the prostate or beyond by the time the PSA >had reached 4 ng/ml. We have subsequently demonstrated that a PSA cutoff >of 4 ng/ml is too high5 and that PSA velocity during the year before the >diagnosis of cancer is strongly associated with the risk for prostate >cancer-specific death.6 These results indicate that PSA trends are more >important than any single PSA value in assessing the risk for >life-threatening prostate cancer. >Some prostate cancers are highly aggressive but do not produce much PSA. >They can spread beyond the prostate before the PSA reaches 4 ng/ml. >Catching them in time is a challenge, and the only practical strategy is >annual screening beginning at an early age with PSA testing and a >digital rectal examination. Therefore, in 1995, I decided to lower the >PSA cutoff for biopsy to 2.5 ng/ml in my PSA study (and personal >practice) and since have demonstrated the usefulness of the 2.5 ng/ml >cutoff. Approximately 25% of men have cancer detected, and the cancer is >more often organ confined without over detecting harmless cancers.7 Some >have protested that this cutoff means more unnecessary biopsies, but, in >fact, in many cases it simply means that the biopsy is performed at an >earlier time. The current American Cancer Society and the 2004 National >Comprehensive Cancer Center Network guidelines also recommend >consideration of a biopsy for a PSA above 2.5 ng/ml. >Here is what I recommend for prostate cancer screening: annual PSA and >digital rectal examination beginning at age 40, or earlier in men with a >family history of early age-at-onset prostate cancer (PSA levels should >be 0.6 to 0.7 ng/ml in men in their 40s and 50s without prostate >disease); prospectively monitoring PSA velocity; biopsies for men with a >suspicious digital rectal examination, PSA higher than 2.5 ng/ml, or a >PSA velocity higher than 0.75 ng/ml per year, using 12 core biopsy >protocols under local prostate anesthesia; considering measuring >androgen levels in interpreting PSA results; and using percent free PSA, >percent complexed PSA, PSA density, and PSA velocity measurements to >determine the need for repeat biopsies. >The most effective and acceptable treatments eradicate the tumor at a >very early stage before it has a chance to spread. Every man hopes to be >cured with primary treatment without additional therapy. No one wants to >hear about long-term hormonal therapy, chemotherapy, or harsh >experimental treatments. The risk of unnecessary treatment is low when >good clinical judgment is exercised. > > > >References > >1. Holmberg L, Bill-Axelson A, Helgesen F, Salo JO, Folmerz P, Haggman >M, Andersson SO, Spangberg A, Busch C, Nordling S, Palmgren J, Adami HO, >Johansson JE, Norlen BJ; Scandinavian Prostatic Cancer Group Study >Number 4. A randomized trial comparing radical prostatectomy with >watchful waiting in early prostate cancer. N Engl J Med. 2002; >347:781-9. 2. Hankey BF, Feuer EJ, Clegg LX, RB, Legler JM, Prorok >PC, Ries LA, Merrill RM, Kaplan RS. Cancer surveillance series: >interpreting trends in prostate cancer--part I: Evidence of the effects >of screening in recent prostate cancer incidence, mortality, and >survival rates. J Natl Cancer Inst. 1999; 91:1017-24. >3. IM, er DK, Goodman PJ, Tangen CM, Lucia MS, Parnes HL, >Minasian LM, Ford LG, Lippman SM, Crawford ED, Crowley JJ, Coltman CA >Jr. Prevalence of prostate cancer among men with a prostate-specific >antigen level < or =4.0 ng per milliliter. N Engl J Med. 2004; >350:2239-46. 4. Catalona WJ, DS, Ratliff TL, Dodds KM, Coplen DE, >Yuan JJ, Petros JA, Andriole GL. Measurement of prostate-specific >antigen in serum as a screening test for prostate cancer. N Engl J Med. >1991; 324:1156-61. 5. Punglia RS, D'Amico AV, Catalona WJ, Roehl KA, >Kuntz KM. Effect of verification bias on screening for prostate cancer >by measurement of prostate-specific antigen. N Engl J Med. 2003; 3494): >335-42. 6. D'Amico AV, Chen MH, Roehl KA, Catalona WJ. Preoperative PSA >velocity and the risk of death from prostate cancer after radical >prostatectomy. N Engl J Med. 2004; 351:125-35. 7. Krumholtz JS, >Carvalhal GF, Ramos CG, DS, Thorson P, Yan Y, Humphrey PA, Roehl >KA, Catalona WJ. Prostate-specific antigen cutoff of 2.6 ng/mL for >prostate cancer screening is associated with favorable pathologic tumor >features. Urology. 2002 60:469-73. > >http://www.drcatalona.com/qa.asp > > >Kathy Meade >http://www.vapcacoalition.org/ >Arlington Educational Consulting >phone >fax > >There can be no knowledge without emotion. We may be aware of a truth, >yet until we have felt its force, it is not ours. To the cognition of >the brain must be added the experience of the soul. >Arnold (1867-1931), British novelist. The Journals of Arnold > (1932), entry for 18 March 1897 > > On the road to retirement? Check out MSN Life Events for advice on how to get there!

[Guest guest]

Terry,

My sentiments exactly about Catalona. In the words of Mandy Rice Davies "Well, he would say that wouldn't he?"

PS Have a nice trip down-under

So I'll limit my comments to this about Dr Catalona's paper. As the 'father'

of PSA testing he obviously has an emotional attachment to the test, despite

its shortfalls

[Guest guest]

I have been itching to join in this discussion, but time has not permitted

it. I am off on Thursday for a six week trip to Australia. We are going to

see our son and his wife and our ten week old granddaughter. As usual my

clients have all come up with problems to be dealt with before I leave.

So I'll limit my comments to this about Dr Catalona's paper. As the 'father'

of PSA testing he obviously has an emotional attachment to the test, despite

its shortfalls (he may even have a financial attachment, although I believe

that I read somewhere that the substantial royalties accruing from the test

are diverted to a Trust of some sort) and because of this he interprets what

data there is in a w y that differs markedly from that of Dr Stamey. Dr

Stamey of course has no vested interest in PSA testing, but is developing an

alternative test, so it might be said that he has a vested interest in

discrediting PSA, and interpreting data accordingly.

We could argue forever about what the data really means, but the key to this

whole puzzle is in the last sentence:

<snip> The risk of unnecessary treatment is low when good clinical judgment

is exercised.<snip>

If only there was a way of educating doctors all the way down the line to

exercise good clinical judgement: to understand that it is possible (with an

accuracy of about 90% according to Dr Scardino) to distinguish between the

dangerous and the indolent variants of this disease: to counsel newly

diagnosed men not to rush into treatment without considering all options.

People like Donna Pogliano are trying to push this aspect of diagnosis - see

her proposed protocol at http://www.yananow.net/DonnasDoctor.html but it

seems at times that it is like trying to push water uphill.

All the best

Terry Herbert

in sunny Kalk Bay, South Africa

Diagnosed '96: Age 54: Stage T2b: PSA 7.2: Gleason 3+3=6: No treatment. June

'04: TURP. Sep '04 PSA 7.45 fPSA 42%

My site is at www.prostatecancerwatchfulwaiting.co.za

It is a tragedy of the world that no one knows what he doesn't know, and the

less a man knows, the more sure he is that he knows everything. Joyce

Carey