As a follow-up to an earlier post (linked below), this more recent research confirms the heterogeneous and dispersed nature of prostate tissue as cancer develops and may explain the reasons why PCa, especially in an advanced and/or metastatic case, is so difficult to treat.
This excerpt from the MedPage Today article summarizes the issue and the suggestion for using a more complete treatment strategy when surgical removal of the entire prostate is not employed:
A new study published today reveals that the prostate as a whole, including cells that appear normal, is different in men with prostate cancer.
It suggests that tissue cells throughout the whole prostate are primed and ready to develop prostate cancer.
This means that it may be better to treat the whole prostate rather than only the areas in the prostate that have cancer.
The wide-ranging diversity of cellular typology may well explain the similar range of treatment responses seen in advanced PCa. Seems we may need numerous silver bullets to cure PCa for all patients.
The MedPage Today article can be found here:
How prostate cancer may begin, ScienceDaily, September 21, 2022, University of East Anglia.
The architecture of clonal expansions in morphologically normal tissue from cancerous and non-cancerous prostates, Molecular Cancer, Published 22 September 2022.
very interesting findings cujoe. Seems your travels have not impaired your keen explorations of knowledge. Of course! Just one reason why we treasure you.
The implication is that the higher burden of genetic mutations in the PC patients vs those without PC are already developing many different clones (populations of cells) within the prostate gland, even prior to the spread of cancer elsewhere (invasion and metastasis).
It reminds me of how tiny quantum fluctuations (variations) in the early universe shortly after the Big Band was subjected to rapid expansion (inflation) and led to the density variations of matter that gave rise to the distribution of galaxies in the observed universe. The small is printed upon the large. OK, my example like my imagination is over reaching here.
But the implication is that we must consider the mechanisms that produce and accumulate genetic damage and diversity of genetic clones. These are the source of what will enable resistance to treatments via these competing relentless clones.
How can we best protect our genomes in a way that limits and slows genetic damage and instability? Not just after we have cancer, but throughout life? Let us continue to explore that more deeply and more holistically. Paul /MB
Pablo - How about this for and over-reaching imagination:
While I'm sure it is a mnenomic typo, I am intrigued with the notion that "it" all started via a Big BAND vs a Big BANG. I can just picture horn, string, and percussion sections of evolutionary forces all lead by some creative genius like, Count Basie, Benny Goodman, or maybe even, Cab Calloway orchestrating an evolutionary event like this:
When Nalakrats used to say, "Take out the Mothership !!!"... he was right on the money...... An intelligent man, but another deemed dangerous individual... I miss that guy... my thoughts on taking out the mothership is that you change the metastatic milieu... the evolution of the disease changes since the mothership holds the foundation of the disease process and the evolution... I believe that some communication between Pca cells is lost and/or slowed down with the elimination of the mothership... slowing the evolution.
That sounds good. When you present it as you did. I practically lose track of anything contrary that I hold onto.
I don't know and my head might explode if I research and think about it more.
I guess I feel (feel isn't the best science lol, but "feel" wraps up what I have learned and is a lazy way to communicate) that the mutations that have spread are the same ones in the prostate, the tumors outside (bones, etc.) are the same mutations found in the prostate. Seems too that all tumors mutate within themselves. Hence systemic tx.
If PCa is spread by the release or breaking off of cancer clusters as well as individual cells (metastasis), then taking out the mothership removes a lot of potential seeding that could occur, as well as messaging/ evolution..
It is why I watch the development of Metarrestin with great interest (Nalakrats also followed this drug !)
I also watch the development of Osteodex which hopefully will start Phase III trials soon...Osteodex binds onto bone tumors and puts the brakes on MCRPC.... I do wonder how that might work in MHSPC...
Yes, Fish. The primary tumors in the prostate send out signaling molecules to enable wandering PC stem cells to set up permanent bases. Altering micro environments for invasion, immune evasion, vascular support. Mother ship indeed!
Nalakrats spent years on the other forum. He considered it a mission to help others with PCa. He had a post on peripheral neuropathy that was particularly helpful. All of his years of work and his profile were deleted, and not by Nalakrats. Consequently, he will not return.
Not on this forum..... we have no administrator here... I am not aware of any other sites he may be on currently.. please feel free to PM me for a response to your questions...
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Seminal Vesicle Invasion & Senescent tumor cells.
Dose titration for CRPC 
