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SCF considered the potent c-KIT legend growth factor and
known as mast cell growth factor or steel factor, its gene encodes a 45 kDa
glycoprotein which is a noncovalent homodimer. It has been shown that its
overexpression is associated with development and progression of several types
of human cancers which showed SCF/c-KIT system
role as anticancer therapy (Cardoso
et al. 2017)

In the present study we have
correlated SCF expression in PC, chronic prostatitis and BPH with
clinic-pathological and follow up criteria and we found that SCF expression in
PC was associated with poor clinic-pathological criteria as higher grade and
advanced stage.

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That was similar to Siddique et
al. 2013 has found that SCF secreted by tumor cells in PC
proportionate positively with the progression of its stage and grade.

As we proved that high SCF
expression was correlated with poor outcomes as advanced D’Amico risk group,
recurrence of the tumor after successful therapy, disease free survival and
overall survival rates. Near to our results (Wang
et al. 2014) reported that higher expression of SCF is associated
with poor prognosis of patients with HCC and showed shorter time to recurrence,
a similar results by (Wang et al. 2017
) increased expression of SCF in hepatocellular carcinoma (HCC) patients is
highly associated with metastasis and poor prognosis. Also, (Bellone
et al. 2006) who found that SCF
expression correlated positively with advanced Dukes’ stages in colorectal
adenocarcinoma where they found the trend of SCF  expression progressively increased towards
advanced stages. Gao et al. 2015 found the same results in pancreatic
ductual adenocarcinoma, SCF mainly
promoted invasion and proliferation of pancreatic cancer cells. The
hypoxia-induced SCF expression might further accelerate the progression of
pancreatic cancer. Near to our results; (Yasuda
et al. 2006) stated that increased activation
of SCF-KIT pathway enhanced the proliferation and invasiveness in
SCF-KIT-positive cancer cell lines. 

Esposito
et al. 2002 found different results from us
as they have concluded that there was no significant relation between SCF
expression and tumor grading, TNM status or stage in pancreatic ductal
adenocarcinoma(Esposito
et al. 2002).

By contrast to our results,
another study has suggest that the c-kit/SCF pathway plays an important role in
the maintenance of normal growth of mammary epithelium and that the process of
malignant transformation is accompanied by their progressive loss (Ulivi
et al. 2004) .

Different results may be due to
different organ or may attributable to different methodologies and
morphologic approaches defining the cellular source of SCF expression or
different method of marker interpretation.

Our results can be explained by that although
SCF has important function in healthy tissues, through activation of c-KIT
pathway, but SCF overexpression leads to over-activation of SCF/c-Kit pathway in
tumors and in pre-cancerous lesions that leads to increased cancer 

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