الفهرس 
Introduction and Aim of workOnly 14 pages are availabe for public view
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Abstract
In our study younger patients had a high colorectal cancer rates with more advanced disease as well as a progressive behavior and most of the colon carcinomas were in distal parts in our study, so intensive screening and post- treatment surveillance programs have to be modified in hope that early detection of asymptomatic tumors or recurrences will increase the proportion of patients who are potentially eligible for curative therapy.
Adequate pathologic assessment of the resected lymph nodes is important with a goal of evaluating at least 12 nodes. Adjuvant therapy with FOLFOX or CapeOx , FLOX , 5-FU/LV, or capecitabine is recommended for patients with stage III disease. Adjuvant therapy for patients with high-risk stage II disease is also an option; recommends 5-FU/LV with or without oxaliplatin (FOLFOX or FLOX) or capecitabine with or without oxaliplatin. The post-treatment surveillance program includes serial CEA determinations, and periodic chest, abdominal, and pelvic CT scans; colonoscopic evaluations; and a survivorship plan to manage long-term side effects of treatment, facilitate disease prevention, and promote a healthy lifestyle.
Regarding rectal cancer, patients with very-early stage tumors that are node-negative by endorectal ultrasound or endorectal or pelvic MRI and who meet carefully defined criteria can be
managed with a transanal excision. A transabdominal resection is appropriate for all other rectal lesions. Perioperative chemoRT and chemotherapy are preferred for the majority of patients with suspected or proven T3-4 disease and/or regional node involvement.
The presence of KRAS mutation was significantly associated with poorer prognosis .Although KRAS mutation scan be considered a highly specific negative biomarker for response to anti-EGFR mAbs (specificity of 93%), it is also poorly sensitive (sensitivity of 47%), since WT KRAS does not guarantee benefit from these agents This had led to investigation of additional markers of primary resistance to cetuximab and panitumumab in KRASWT tumors, thus focusing on the analysis of molecules involved in the downstream of EGFR signalling .
It seems clear that BRAF mutations define a genetically distinct subset of CRCs characterized by an extremely poor prognosis. Whether BRAF mutational status should be used as a selection factor for treatment with EGFR targeted agents in patients with WT KRAS tumors is still controversial. The investigation of other biomarkers such as EGFR, expression levels of EGFR ligands , EGFR gene polymorphisms, NRAS or PIK3CA (exon 20) Mutations or loss of PTEN expression also seem relevant to positively identify responders. It is becoming increasingly apparent that disease progression is largely driven by complex pathways and analysis of one single marker is unlikely to predict progression of disease with a high degree of accuracy and reproducibility.
Therefore, concomitant analysis of multiple genetic and epigenetic events involved in the EGFR-initiated oncogenic signalling cascadeis likely to enhance the prediction ability of the biomarkers used individually.
Although there are no drugs available for the specific and direct inhibition of KRAS, a number of agents designed to inhibit the kinase activity of BRAF are either already clinically approved.