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Prostate
Cancer: Neuroendocrine Carcinoma
Febrary 23, 2009
In my clinic, American Diseases of the Prostate, as in any clinic
that sees a large number of prostate cancer patients, I’ve
encountered prostate cancers that deviate from the well-established
behavior of the common adenocarcinoma. One of those unusual forms
of prostate cancer is neuroendocrine carcinoma.
Neuroendocrine cells are found in the normal prostate gland,
where they have been shown to produce a range of hormones including
serotonin, bombesin, and calcitonin. However, we do not know
the role these neuroendocrine cells play in normal prostate biology.
In the standard adenocarcinoma of the prostate gland, neuroendocrine
cells are nearly always found scattered throughout the cancer
mass. In this setting, these neuroendocrine cells do not make
PSA, are not growing and do not have the androgen receptor. In
the test tube, even though the neuroendocrine cells do not grow,
the hormones produced by these cells are capable of fueling the
growth of the adenocarcinoma cells. One report claimed that in
the prostate cancer specimens obtained at surgery, the prostate
cancer cells near the neuroendocrine cells were growing more
rapidly than those distant from these cells. This suggests that
the neuroendocrine cells might fuel prostate cancer progression.
In fact, the larger the proportion of the cancer mass composed
of neuroendocrine cells at diagnosis, the more likely the patient
would do poorly over time.
While serum chromogranin A has generally been found to be the
best marker to detect the development of neuroendocrine cells
in prostate cancer, there is some evidence that it is more than
just a marker. For example, if you add chromogranin A to prostate
cancer in tissue culture, it triggers the formation of proteins
that improve the cancer cell's resistance to treatment.
In prostate cancer research, there are certain classic studies
that define issues with great clarity. In 1991, Kadmon, et al.
showed that an elevated chromogranin A level made evolution of
hormone resistance more likely. Furthermore, once hormonal therapy
started, chromogranin A levels initially increased in many patients,
but would later decline back to normal. When chromogranin A levels
stayed elevated or when it started to increase late in hormonal
therapy, hormone resistance was very likely to follow. This observation
has been repeatedly confirmed.
Up to this point, we have been discussing the impact of neuroendocrine
cells that are not themselves capable of growth and where the
impact appears to be thought an effect on the prostatic adenocarcinoma
cells. In small cell carcinoma of the prostate gland we have
neuroendocrine cells that are able to rapidly grow and spread.
Again, these cells make very little or no PSA and make little
or no androgen receptor. While they can make chromogranin A and
other neuroendocrine markers, in many cases they make no detectable
markers.
To read the remainder of this article on neuroendocrine carcinoma
of the prostate gland as well as other articles on unusual forms
of prostate cancer, visit
our back issues section where you can download
Volume 10 Issue 9 of Prostate Forum. |
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