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            Prostate
cancer is relatively critical and major disease among men especially those above
40 years old which is death-causing disease (Claudio, 2016). In
2004, an estimated 230110 men were diagnosed with prostate cancer and 29900 of
them were died from this cancer in United States. There are some symptoms for
the patients who suffered from prostate cancer such as frequent urination,
blood in urine or semen, burning sensation during ejaculation and urination and
etc.

In fact, several pre-determinant
factors could be led to prostate cancer initiation such as genetic preferences,
inflammation and increased the rate of cell proliferation
(Ramalingam, Ramamurthy and Njar, 2017). Prostate cancer always associated with
dysregulation of PI3K/AKT/mTOR pathway caused by genetic, functional, post-translational
and epigenetic modifications (Claudio, 2016). All those pathways are crucial to
be activated which can reduce apoptotic rate, malignant transformation, tumour
progression and metastasis (Claudio, 2016) and establishment of chemo and
radio-resistance.

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            The
processes that cause the epithelium of normal prostate initiate the cascading,
which induce the lesions to form. This directly gives a primary prostate cancer
or proliferative inflammatory atrophy (PIA) or stimulates an intermediate stage
known as prostatic intraepithelial neoplasia (PIN)
(Ramalingam,
Ramamurthy and Njar, 2017). As a result, basal cell layers lost the capacity of
proliferation and elevated the activity of luminal secretory cells. There is
scientific proof via molecular and pathological analysis with prostate cancer
of human and animal model which indicated that infectious agents, estrogenic
hormone, age, race, genetic factor and other environmental issues can lead to
deterioration in the prostate epithelium and provoke inflammation which might
be attributed to chronic and recurrent condition of prostate cancer.

To treat prostate cancer, androgen
deprivation therapy (ADT) through chronic administration of
gonadotropin-releasing hormone, anti-androgenic drugs or their combination is
standard choice of treatment. But, most of the prostate cancer patients relapse
and worsen their situation as developing castration resistant prostate cancer
(CRPC) within two years. This is because of the amplification or mutation in
androgen receptors which lead to happening of hormones such as progesterone and
estrogens activation. Besides, a sequential of molecular changes in the pathway
can form androgen-independence prostate cancer and induce cancer progression.

Lastly, prostate cancer is supposed that
initiation and progressive growth of the cancerous cells contributed by cascade
of genetic mutations coupled with epigenetic factors. Androgen receptor, either
hormone dependent or hormone independent is playing vital role in controlling
the prostate cancer, which have to be further investigated to reduce the
mortality rate. 

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