@denis76 I would first preface by saying that what might appear to be logical, might not be scientific. Any hypotheses not vetted (& controlled), might introduce unintended variables or confounders that make the results unpredictable. As a retired computer scientist, I’m cautious about defining scenarios that appear to be comparable (or at least similar), but may or may not be.

What we do know is that while testosterone may be the dominant factor early and through the prostate cancer diagnosis, there is evidence that it may not be such a primary factor later in the diagnosis (i.e., the non-survivors), when just like other cancers (brain, lung, lymphoma, etc.), glutamine (& possibly other factors) fuels cancer growth, metastasis, and disease progression.
—> that would be a partial answer to your question of “What fuels cancer after resistance develops?”
—> it’s also known that prostate cancers absorb amino acids at a much more rapid pace than do normal prostate cells. That is another possible fuel source.

This is a very complex mechanism and I would hesitate to synthesize it down to a (seemingly) simple scenario,