الفهرس 
Introduction& Aim of the workOnly 14 pages are availabe for public view
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Abstract
Genetics has a major role in controlling colorectal cancer According to a large twin study, 35% of colorectal cancer risk might be due to many genetic factors. Apart from hereditary forms, such as familial adenomatous polyposis and hereditary non-polyposis colon cancer (Lynch syndrome), which are determined by well known Genetic deviations, but account for less than 5% of all colorectal cancer .
CRC develops in a progressive fashion during which normal colon epithelial cells transform to form benign growths such as polyps. These polyps may then progress to benign adenomas, and ultimately to invasive
cancer lesions. The progression of the cancer has also been associated with sequential genetic changes in genes such as K-RAS, APC, and P53
APC gene mutations are one of the first stages in the multistep process of colorectal cancer formation and occur in more than 70% of colorectal adenomas.
The promotion of the adenoma–carcinoma sequence is occurred by activating mutations of the KRAS oncogene and inactivating mutations of the P53 tumour suppressor gene.
MiRNA genes are transcribed by RNA polymerase II in the cell nucleus to produce primary miRNAs (pri-miRNAs), that consist of a 5′-cap, at least one ~70-nucleotide hairpin structure and a 3′-poly (A) tail.
MiRNA expression is frequently disregulated in cancer cells, and specific miRNAs are known to regulate both cell-cycle progression and apoptosis.
Several miRNAs have been identified as mediators and regulators of p53’s tumor suppressing functions.
P53 inhibits epithelial to mesenchymal transition (EMT), stemness, and metabolic adaptations, which are typically found in tumors.In addition, p53 promotes DNA repair, antioxidant defense, and differentiation.
MiR-34a, a highly conserved miRNA has recently emerged as a key tumor suppressor in multiple malignancies through the suppression of multiple targets.
MiR-34a acts as a tumor-suppressor gene by targeting many oncogenes related to proliferation, apoptosis and invasion.
The aim of the present work is to study the role of MicroRNA 34a gene expression In CRC patients.
Regarding Comparison among the three studied groups according to CBC
CRC patients had significantly lower levels of Hb and platelets
(P <0.001) compared with benign and control groups. Benign patients had significantly lower levels of platelets versus control while Hb not differ (P >0.05) between them.
Relation of liver enzymes and renal function tests and CRC patients
There was non-significant statistical difference among the studied groups regarding ALT, AST, Urea and Creatinine.
Relation of CEA and CA19-9 and CRC patients
The present study showed that by Post Hoc Test (Dunn’s multiple comparisons test) , CRC tumor markers including CEA and CA19-9 were significantly higher in CRC patients than benign and control groups (P <0.001) while no significant difference amongst benign and control groups (P>0.05).