[Hopespringpcsg] FW: [PPML] Does "bi-lobal" inherently mean "multi-focal"?

[Glen Tolhurst]

Hi all:
Below is an interesting post from a US PCa blog.
Thx.
Glen

-----Original Message-----

Subject: [PPML] Does "bi-lobal" inherently mean "multi-focal"?

Clearly not all prostate cancer is inherently 'multi-focal'.
With increasingly accurate imaging the initial number of foci can be determined.
Generally if there is cancer in both lobes, it is not a single tumor spanning both lobes but rather spatially independent cancer sites.

An initial diagnosis of a single core Gleason 3+3 can indeed be found to be, or not be, multi focal when the entire organ is surgically removed an sliced an diced for a whole-prostate pathology.  Especially if the original biopsy was a traditional spatially distributed 12- or 13-core needle biopsy.  However, the downside of a surgically removed prostate found to have only pattern 3 tissue confined within the prostate is that 'Congratulations Mr. Brown, you didn't need to have the prostate out'.

Current excellent imaging by excellent practitioners should be able to more accurately target biopsies with more accurate mapping of the tumors. In those cases, one can have some confidence that a targeted biopsy finding only a single small tumor probably is accurate in finding that the cancer is not multi-focal.

Can an initial Gleason 3+3 tumor become more aggressive?  So far research suggests that Gleason 3+3 cells do not progress into 3+4 or
4+3.  In other words, a true Gleason pattern 3 tissue is very unlikely
to progress to pattern 4.  However the issue is we cannot yet 'guarantee' that even an accurately  targeted biopsy has not missed some Gleason pattern 4 tissue that will grow and be more aggressive.

In my own case an initial 'random' biopsy finding one core of 13 with less than 5% Gleason 3+3, on the right side, was followed for seven years by Active Surveillance with imaging-- color Doppler (CDU) by Dr.
Bahn (Ventura. CA) and endorectal MRIs at UCSF.  The MRI's never found anything other than a single 'suspicious' area on the right side.
Over time the CDU imaging with targeted biopsies found the original site to be slowly growing but still 3+3.  Three years into AS two other very small 3+3 tumors with no connection to the original tumor were found on the right.  5 years out another very small 3+3 was found on the left.  Finally a targeted biopsy in year 6 took two cores through the larger 'index tumor' on the right and found about 50% of each core to be Gleason 3+4, with about 20% of those being pattern 4 tissue.

So, the CDU imaging found more tumors developing over 6 years and clearly showed them to be spatially independent.  Repeat targeted sampling of the largest 'index' tumor found in year 6 pattern 4 tissue
(3+4) .  Did that mean that the Gleason pattern 3 tissue morphed into pattern 4 over time? We don't think so.  Rather the higher probability is that small clusters of pattern 4 cells missed even by the targeted sampling grew larger over time and were finally found.

Summary of my case-- what was originally diagnosed as a very small single Gleason 3+3 was found over time with accurate CDU targeting to become multi-focal with the foci spatially independent. The site of the growing 'index' tumor was found after 6 years to have small amount of pattern 4 tissue (Gleason 3+4).  So, at the time of moving from Active Surveillance to treatment the prostate cancer was still by most measures to be of low 'intermediate risk', with the odds of ultimate recurrence after treatment not significantly increased by the treatment delay.

Is any of this 'typical'?  After dealing with our disease for 10 years I don't think there is anything like a 'typical' prostate cancer.  I so think there is strong evidence, including my own experience, that a initially diagnosed 'low risk' prostate cancer can, with repeat targeted biopsies, be monitored by Active Surveillance to postpone treatment until if and when there are signs of advancement.  There is strong evidence that the resultant delay in treatment presents little risk of worse long-term outcomes than immediate treatment as long as the monitoring is 'active' enough to catch the cancer before it becomes aggressive.

The great hope for our disease is that advances in genomic testing will provide more accurate assessments of whether a diagnosed prostate cancer is a 'lamb' or a 'lion'.  However, despite optimistic press releases from research centers, we 'ain't there yet'.


=====================================================