There to treat a smaller volume, thus lower

There are two treatment options for
stages 1 and 2: radical prostatectomy or radical radiotherapy. But there is no
consensus as to which to prefer or greater option. The 10-year survival rate
following treatment is usually in the 80-90 per cent range. If the patient is
in old age, there may not be necessary to therapeutically treat the tumor, as the
patient is more likely to die before the related diseases happen after
diagnosis. Radiotherapy is usually employed instead of surgery in stage 3 and
some cases of stage 4 cancer. Since many patients have urinary symptoms,
hormonal manipulation to reduce the level of testosterone may be used to reduce
the tumor size before radiotherapy. The reduction of the cancer cell size will
also allow the oncologist to treat a smaller volume, thus lower the potential
side impacts of radiotherapy. (“Cancer
Malaysia, Kevin H., 2012”)

Advanced cancer that has spread
outside the prostate and its surrounding structures is treated by either
surgical or medical castration. The first would be the removal of both the
testes by surgery. Medical castration is preferable as it uses hormones and is
reversible. The hormones are implanted under the skin once a month or every
three months, depending on the preparation. The advantage of medical castration
over surgical castration is the side-effects of castration, such as impotence
and hot flushes, are temporary. (“Cancer
Malaysia, Kevin H., 2012”)

Treatment should be started earlier
without waiting for symptoms to occur. This has been shown to prolong survival.
Treatment is usually successful in the short term. Either method achieves a
median survival of 30 months and 80% symptom relief. Radiotherapy is used to
combat pain from bone metastases. Other methods include taking anti-androgens
or estrogens. The doctor may recommend the patient to continue the medical
castration for a prolonged period (e.g. three years), even after radiotherapy,
as clinical trials have shown this to be of some interference of carcinogenesis.
For those cancers that are hormone refractory, systemic chemotherapy may be
considered. A patient diagnosed with prostate cancer should be managed in a
multidisciplinary control with the supervision of an oncologist and the
urologist. In this manner the patient would be able to make anmature and wise decision.
If chemotherapy is prescribed, it should be given by an oncologist.(“Cancer
Malaysia, Kevin H., 2012”)

Usage of Natural Compounds in Treatment of Prostate Cancer

Natural products that have
anticancer properties can be discovered in diverse species of vegetables,
fruits, herbs, and fermented plant products and extracts. The anticancer
activity of these plants can be associated to their functions on cells as antioxidants,
free-radical eliminators, and inhibitors of DNA mutating enzymes. With all these
combined, these characters are expected to be shielding against somatic
mutations and adverse epigenetic DNA alteration (Reddy, et al., 2003). These are the most possible
candidates discovered for chemical remediation because related negative side
effects, if any at all, are reported to be reduced to the lowest.
Epidemiological studies show that natural products defend against a wide range of
malignancies such as lung, colorectal, stomach and esophageal cancers and to a
lesser extent prostate cancer. Prostate cancer has a long latency before
clinical symptoms emerge and a very elevated prevalence rate in most
economically developed countries such as European nation and North America
which cause this cancer could be a preferred target for chemotherapeutic agent(Horie, 2012; Sarkar
& Li, 2002)(Cimino et al., 2012; Horie,

Researchers have shown that
anticancerproperties of various natural compounds, such as soy isoflavones
(mostly genestein), elegiac acid and ellagitannins from pomegranate extract,
green tea polyphenols, curcumin, lycopene, vitamins D and L-selenomethionine,
both in vitro and in vivo. These agents target one or more signaling pathways
that are deregulated in prostate cancer, such as AR, nuclear factor ?B (NF-?B),
Wnt, Akt, Notch and Hedgehog (Hh) signaling (Sarkar & Li, 2002).

Two triterpenoid compounds in the
G. lucidum extract which yield the greatest suppression of 5-?-reductase
activity were identified to be ganoderic acids DM and TR, both of which
inhibited the enzyme activity with an IC50 of 10 µM. (J. Liu et al., 2012)

Studies have shown that consumption
of the extract from licorice root (Glycyrrhiziaglabra) is associated with
reduced circulating testosterone in humans (Grant & Ramasamy, 2012). A research showed this effect has
revealed that glycyrrhetinic acid (GA), a bioactive metabolite of glycyrrhizic
acid (GL) found in licorice, is responsible for this activity (Hawthorne & Gallagher, 2008). This compound targets two enzymes
correlated in androgen synthesis. GA inhibits the enzyme, 17,20-lyase which is
required for the conversion of 17-hydroxyprogesterone to androstenedione, the
precursor molecule to testosterone. Furthermore, it prevents 17?-hydroxysteroid
dehydrogenase from completing the conversion of androstenedione to testosterone
(Grant & Ramasamy, 2012)(Hawthorne & Gallagher, 2008).

By targeting the biochemical
pathway involved in the production of androgens, these compounds have a greatpossiblity
to prevent some sort of mechanisms of resistance to ADT for prostate cancer.
Since there is a scare amount of androgen maybe remained in a patient
undergoing ADT, methods to further decrease androgen production are essentialmethods
of research.By inhibiting the pathways involved in testosterone synthesis, and
preventing catalysis to the more potent ligand, DHT.(Watson, et al., 2015)

Green tea polyphenols have been
reported to inhibit tumor development in the so-called transgenic
adenocarcinoma of the mouse prostate (TRAMP) model.(Gupta, Hastak, Ahmad, Lewin, &
Mukhtar, 2001; Liao & Hiipakka,
1995). The activity of green tea
polyphenols in the TRAMP model may be related to the known inhibitory effects
of the green tea catechin epigallocatechin-3-gallate (ECGC) on the activity of
the enzyme 5?-reductase, which converts the male sex hormone testosterone to the
active androgen 5?-dihydrotestosterone(Liao & Hiipakka, 1995).

Silibinin derived from Silybin or
extract from the milk thistle plant has been show to inhibit prostate tumor formation
in the TRAMP model,(Raina et al., 2007) but this effect appeared to be
limited to inhibition of the growth of established prostate neoplasms late in
the process of tumor progression.(Singh, Raina, Sharma, & Agarwal,
2008)(Raina et al., 2008) This suggests that the impacts of
silibinin in the TRAMP model are more inclined to a therapeutic nature than

The dietary exposure to soy
isoflavones also can reduce the risk of getting prostate cancer. However, there
are research findings that in the TRAMP model the major soy isoflavonegenistein
at lower, nutritionally relevant, doses stimulated carcinogenesis and greatly enhanced
metastatic capacity.(El Touny & Banerjee, 2007)(El Touny & Banerjee, 2009) Clearly, both the dose and form of
the agent as well as probably the timing of administration are critical
determinants for whether genistein, and by inference soy, have
cancer-preventive effects or enhance prostate cancer development. The
anti-cancer effects of genistein have been attributed to its known inhibitory
effects on tyrosine kinase, topoisomerase II, 5?-reductase, and angiogenesis,
and its activation of several growth factor receptor pathways, but most of
these effects, particularly those on tyrosine kinase activity, occur only at
non-physiologically high concentrations.(Peterson, 1995)(Holzbeierlein, McIntosh, &
Thrasher, 2005)(Linassier, Pierre, Le Pecq, &
Pierre, 1990)(Sarkar & Li, 2002) The other main soy isoflavone,
diadzein, is far less biologically active. Daidzein, but not genistein, is
converted to equol by intestinal microbes in  approximate 30 – 60% of humans, a phenomenon
that appears to be quite stable within a given individual.(Setchell & Clerici, 2010)(Setchell, Brown, & Lydeking-Olsen,
2002) This daidzein metabolite has convincing
estrogenic and anti-androgenic activities, including prostatic effects in rats.(Lund et al., 2004) It is conceivable that the
chemical preventivefunction of soy isoflavones may differ in men who produce
equol and those who do not and that is related to the hormonal properties of
equol,(Setchell & Clerici, 2010).