One year after starting finasteride, LS returned, complaining of increased dysuria and urinary hesitancy. DRE revealed a larger prostatic mass than was felt several months before. His PSA was elevated...

One year after starting finasteride, LS returned, complaining of increased dysuria and urinary hesitancy. DRE revealed a larger prostatic mass than was felt several months before. His PSA was elevated several-fold higher than his previous level. What step in the pathogenesis of this new event is NOT likely to have occurred?

A. Tumor growth was suppressed via androgen receptor antagonism by finasteride, as the relatively well-differentiated tumor cells require androgen stimulation for growth.

B. Genetic instability led to the loss of p53 function and normal DNA repair capacity, causing acceleration in the rate of genetic mutation.

C. A subpopulation of androgen-independent tumor cells arose against the selective pressure of finasteride therapy.

D. A new primary prostatic tumor arose due to the selective pressure of finasteride.

E. A subpopulation of highly proliferative tumor cells arose from spontaneous mutation, yielding a high growth fraction and accelerated tumor growth.