الفهرس 
Review of LiteratureOnly 14 pages are availabe for public view
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Abstract
Exposure to cellular stress can trigger the p53 tumor suppressor, a
sequence-specific transcription factor, to induce cell growth arrest or
apoptosis. The choice between these cellular responses is influenced
by many factors, including the type of cell and stress, and the action
of p53 co-activators. P53 stimulates a wide network of signals that act
through two major apoptotic pathways. The extrinsic, death receptor
pathway triggers the activation of a caspase cascade, and the intrinsic,
mitochondrial pathway shifts the balance in the Bcl-2 family towards
the pro-apoptotic members, promoting the formation of the
apoptosome, and consequently caspase-mediated apoptosis. The
impact of these two apoptotic pathways may be enhanced when they
converge through Bid, which is a p53 target. The majority of these
apoptotic effects are mediated through the induction of specific
apoptotic target genes. However, p53 can also promote apoptosis by a
transcription-independent mechanism under certain conditions. Thus,
a multitude of mechanisms are employed by p53 to ensure efficient
induction of apoptosis in a stage-, tissue- and stress-signal-specific
manner. Manipulation of the apoptotic functions of p53 constitutes an
attractive target for cancer therapy.
Aim of the work
The aim of this study is to investigate the level of expression of bcl-2,
p53 Tumor necrotic factor (TNF-α) and Alpha-fetoprotein (AFP) in
liver patients either with Liver cirrhosis (LC) or Hepatocellular
carcinoma (HCC). In addition, the relationship between the
expression of bcl-2, p53, TNF-α and AFP clinical parameters of HCC
patients is studied.