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Screening of the PSA

VascodaGama's picture
VascodaGama
Posts: 3205
Joined: Nov 2010

I believe many survivors are familiar with the name Paul Lange MD. Not just for his published papers on cancer researches, or his book "Prostate Cancer for Dummies", but also from being one of the pioneers of the PSA assay. Interestingly he also belonged to the group of urologists that at beginning did not believe in the PSA’s practical significance, but he decided to begin testing his own PSA in his 50s ("It started to go up, so I got a biopsy") and was diagnosed with PCa. Thomas Stamey, MD was the one that originally found and published his findings about the correlation between increased PSA serum levels to prostate cancer, back in 1987. Later this doctor started the controversy in regards to the value of the PSA in the screening for prostate cancer.
Thomas Stamey said prostate cancer is a disease “all men get if we live long enough. All you need is an excuse to biopsy the prostate and you are going to find cancer.”

Initially many involved in the “manufacture” of feasible assays for PSA confronted constant errors so that this test did not become imperative as a screening tool and it took some time to become “popular” among urologists. It was in 1994 that FDA approved finally the PSA (together with DRE) to screen asymptomatic men for prostate cancer. My doctor belonged to the group of the “disbelievers” and instead of the PSA he used PAP to screen PCa, since I become 45 years old (1994). Unfortunately my first PSA done at 50 years of age (22.4) proved how he was mistaken.

Recently Dr. Paul Lange was interviewed by Prostate Forum where he comments about his findings in regards to the progression of the disease. I found this article very instructive and I believe that we all should read it, particularly the newbies and those that depend much on the PSA as a marker. How much trust can we lay in this test?

Here is the link;

https://askdrmyers.wordpress.com/2014/10/30/dr-paul-lange-on-lymph-node-disease/?mc_cid=27c942c5c4&mc_eid=179dca884e

 

In regards to Dr. Thomas Stamey views, you can read details in this link;
http://www.medscape.com/viewarticle/489474

All about the PSA;
http://www.cancer.gov/cancertopics/factsheet/detection/PSA

 

Best wishes to all comrades,

VGama

 

Old Salt
Posts: 720
Joined: Aug 2014

Good reading; recommended

hopeful and opt...
Posts: 2249
Joined: Apr 2009

Thanks for posting.

 

I found the information that Dr. Lange presented to by very informative.... 

 

Thanks again,

H & Optimistic

Max Former Hodgkins Stage 3's picture
Max Former Hodg...
Posts: 3446
Joined: May 2012

Vasco,

I will study each of these links Monday, since I work ten-hour nights all weekend.

My family doctor has discussed some of this history with me over the last two years, and he is in the "PSA is overused" camp of thought.  My long-term follower at my cancer center (a Nurse Practioner) is who recommended that I get a biopsy after my 4.6 PSA result a few months ago. I am pretty certain my doctor would have said it was "unnecessary."

Based on what you know now, with an initial PSA of 22.4, would your first choice for first-line (initial) therapy be PS or RT ?

 

I was a fast attack submarine sailor in the US Navy for many years. In the Atlantic Fleet, boats were specialized in either "Northern Runs" (under the Arctic ice) or "Med Runs" (Mediterranean Sea).  I was an under ice guy, and never got to see the Med, where the guys used to get liberty stops in Southern France (Toulon, mostly), Italy (La Maddalena, mostly) and ports elsewhere. Would love to have see those warmer climes, and especially Portugal, but never did.

max

VascodaGama's picture
VascodaGama
Posts: 3205
Joined: Nov 2010

Max

As of today, I would not base my choice of a radical treatment on the fact of a high PSA but with the consensus of the overall exams. In fact there are many high risk cases with aggressive (poorly differentiated) forms of cancer that produce very little amounts of PSA. On the contrary, high PSA seems to be related to well differentiate cells (low Gleason rates) with a tendency of being indolent. Surely, “low or high risk” is important in the judgement and many researchers define risk and make decisions based on PSA thresholds, but in my lay opinion the most significant piece of information in the diagnosis is the location of the cancer. The aggressivity factor provided by the Gleason is good when judging “indolence” or dormancy. The decision on a treatment needs assurance that the whole cancerous tumour is addressed, so that we would need to see it in image studies, otherwise we have to guess its location based on the available data that is correlated with past experiences.

If my diagnosis were obtained today I would try obtaining “pictures” using the latest techniques in image studies. I also would map my risks with basis on my gens to evaluate indolence. I would try getting the real percentage of Gleason patterns including those grades of 1 and 2 because these relate to extended survival but are now grouped homogeneously as 3 (prune to unneeded treatment just for avoiding possible errors if analysed by inexperienced pathologists). I also would consider palliative treatments (with lesser side effects), if the cancer were less voluminous and not aggressive.

14 years ago I did prostatectomy because the cancer seemed to be contained. The clinical stage was B (T2). The biopsy was the traditional sextant, typical of those times. I was diagnosed with low risk Gleason 5 (2+3), negative DRE and negative image studies. The scans involved the traditional MRI, Scintigraphy bone scan (Gama machine) colour Doppler and localized X-rays. The prime worry focuses in the volume of cancer found by the biopsy (all needles positive, 4x Gs4, 2x Gs5). These were verified in a second laboratory and one of them was later rechecked at MSKCC (Gleason 5 is not typical in Japan). After surgery my pathological stage became pT3apN0, with positive margins, positive ECE but negative lymph nodes (9 numbers taken). The prostate was of normal size and the cancer occupied 2/3.

My story started on May 1st, 2000, with a PSA and a biopsy on May 12th. The surgery was performed in August 15th. The SRT was done in November 2006 and IADT started in November 2010. I am fully continent and manage erections at the 4 o’clock direction with a shorter penis (less 1.5cm). SRT made me partial loss of sensation when passing stool but I am continent. While on ADT I experienced loss of libido and felt tired most of the time. I have been all these years asymptomatic and never got a “picture” of the bandit. The PSA has been the only marker identifying progression.

Best

VG

 

Max Former Hodgkins Stage 3's picture
Max Former Hodg...
Posts: 3446
Joined: May 2012

Detailed and thoughtful as always....

 

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