Poorly differentiated prostate cancer produce less PSA per tumor volume than well differentiated PCa. Localized treatment failure is common because of the uncertainty that exists at diagnosis. A biopsy result is representative of the sample but not necessarily of the cancer present in the prostate gland. Occult prostate cancer can progress from a larger majority of androgen dependent cancer cells to one of androgen independent cells.
When the ratio of androgen independent cells to the androgen dependent cells in the tumor load increases, the cancer becomes resistant and is able to progress using various growth sources other than androgen. PSA level is not representative depending of the degree of dedifferentiation present in the tumor volume. Other markers, like PAP, AlkP, CGA and NSE are available to support PSA monitoring.
How to explain what happen to men who are diagnosed with very advanced disease before the disease is detected? Their response to androgen deprivation is usually poor or not existent. In other words, in such cases through a process of dedifferentiation the cancer, before being detected or any treatment applied(including androgen deprivation), has mutated causing chromosomal gains or depletions that makes it very difficult to treat with our current forms of treatment. Hence, until the present, the high disease mortality in these men. New hormonal treatments have shown that what was considered androgen independence can be still treated with some survival benefits.
The rare variant forms of prostate cancer constitute a very small component of PCa diagnosed these days. The most common variant forms: Signet ring cell, Mucinous, Ductal or Intraductal, Squamous cell and Neuroendocrine. These constitute 1.6% of all the PCa diagnosed while plain old adenocarcinoma of the prostate makes the great majority of cases. Yes, these variants are rare and have a higher mortality rate than the common form of the disease.
D M Marcus et al. A Comprehensive Review of Incidence and Survival in Patients With Rare Histological Variants of Prostate Cancer in the United States From 1973 to 2008
Prostate Cancer Prostatic Dis. 2012;15(3):283-288.
The views or opinions expressed here are my own and are not endorsed nor supported by any agency or institution. Ask your physician for medical advice.
DX at age 58 in 1992. RP; Orchiectomy; GS (4 + 2); bilateral seminal vesicle invasion; tumor attached to rectal wall; Stage T4; Last PSA Dec, 2012: <0.1 www.pcainaz.org