Possible to know if prostate C cells are hormone friendly or fesistant

[Karmaji]

I wonder if Biopsy can identify if C cells are Hormone resistant...or hormone friendly

It seems it is possible for female breast C cells

[Tall_Allen]

All acinar adenocarcinoma prostate cancer cells depend on the androgen receptor (AR) for growth. As part of the inevitable genomic transitions that occur over time, external androgens become less necessary to stimulate the AR. The best way to determine if castration resistance is occurring is to monitor PSA and radiological progression under conditions of androgen deprivation.

[Karmaji in reply to Tall_Allen]

So all c cells are hormone dependent to start with till they learn to find food somewhere else...

[Tall_Allen in reply to Karmaji]

It's more complicated than that. All acinar adenocarcinoma prostate cancer have androgen receptors.

[Karmaji in reply to Tall_Allen]

What is radiological progression...

[Tall_Allen in reply to Karmaji]

Progression seen on a radiological scan - bone scan, CT, MRI, PET scan, etc.

[LearnAll in reply to Tall_Allen]

Tall....what is the reason that some men's prostate cancer become androgen resistant in 2 years whereas other men's androgen resistant take 10 or more years ?I

[Tall_Allen in reply to LearnAll]

I have no idea. Everyone's cancer is different. With over 200 genes implicated plus epigenetic factors, no one can predict for the individual.

[tom67inMA in reply to Tall_Allen]

In another post not too long ago, I believe you said something to the effect that "castrate resistant" really meant extremely sensitive to testosterone. So, even sub castrate T levels become enough to activate the cancer cells. Am I understanding that correctly?

[Tall_Allen in reply to tom67inMA]

That is one of the causes of castration resistance - the AR gets "upgraded"

[Hidden]

Yes, very complicated. Here is a hypothesis developed twenty-five plus years ago by Dr. Robert Amato and his team:

“As a working hypothesis, we suspect that the transformation from an androgen-dependent to an androgen-independent phenotype is mediated by the expansion of an androgen-independent clone already present at the time of androgen deprivation. If this model is correct, then it would be desirable to bring treatment to bear on the androgen-independent component when the corresponding tumor burden is minimal. Thus, we view the androgen-independent component as analogous to “microscopic residual” or “micro-metastatic” disease for which adjuvant chemotherapy has shown to be effective in other contexts."

Gourd Dancer

[DarkEnergy in reply to Hidden]

Hi Gourd Dancer,

This relates to my recent post about adding chemo to ADT and Zytiga, even when PSA is "undetectable".

[Hidden in reply to DarkEnergy]

Dark, just remember that this was his working hypothesis. It may or may not be accurate and is in the proving stage. For me it worked, but others will say, “Antidotal.” However, I think that it worthy of discussion with your Medical Oncologist; particularly that part about micro-metastasis. My experience causes me to embrace the hypothesis; while others, will refute. Robert Amato’s published works are worth reading.

GD