The increasing quantity of cells at G2/M phase was related to induction of the CDK inhibitors; p21 and p27 through the silence of cyclin E/CDK2 which is the G1/S-promoting kinases that lead to arrest G1 arrest. degree of drug resistance which limits its clinical efficacy (Khelwatty et al., 2017). Some studies showed that there are several mutations that occurred in many downstream effector molecules of the EGFR signaling pathway indicating that additional markers are needed to predict the response to anti-EGFR therapy (Chen et al., 2015). Amphiregulin is one of the ligands of the EGF family that mediates the biological functions through binding to EGFR in both epithelial and mesenchymal cells (Yarden et al., 2001). Thus, Amphiregulin participates in malignancy cell proliferation, migration, invasion, and angiogenesis in human carcinomas (Ma et al., 2001), so Amphiregulin was incriminated as a predictive biomarker of anti-EGFR therapy for most EGFR-driven carcinomas (Zarkavelis et al., 2017). Phosphatase and tensin homologue (and expression expression in mCRC patients to correlate their levels of expression with clinicopathological criteria of the tumor and with the outcome of cetuximab sensitivity treatment. Materials and Methods This is a prospective study including all DDR-TRK-1 patients with left side CRC who were operated at General Surgery Department and treated in Medical Oncology and Clinical Departments, Zagazig University or college hospitals during the period from December 2016 to December 2018. Patients who were clinically suspected to have CRC underwent full clinical examination, radiological evaluation in the form of pelvic abdominal computed tomography, and colonoscopy biopsies were taken and histopathological confirmation in Pathology Department, Faculty of Medicine, Zagazig University or college. All patients had received the specific post-operative protocol. The inclusion criteria were age 18 years old, pathological diagnosed CRC, left-sided wild RAS type with a metastatic disease either denovo or after adjuvant MYH11 therapy. they started the systemic treatment with a cetuximab-based protocol. Only 23 patients were eligible. The samples were prepared, diagnosed, graded, and staged according to the eighth edition of the American Joint Committee on Malignancy staging system (AJCC-8) classification and the World Health Business (WHO) classification (Amin et al., 2017, DDR-TRK-1 Ueno et al., 2012). Clinical and pathological criteria have been recognized by review of the patients files. Patients were followed for 2 years from the date of metastatic disease diagnosis. was found in the cytoplasm and the membrane of tumor cells, the expression of was in the cytoplasm and nucleus of tumor cells, and the expression of Amphiregulin, PTEN,and were assessed by DDR-TRK-1 calculation of the phi coefficient considering (+) sign as an indication for the direct relationship and considering the (-) sign as an indication for the inverse relationship. Overall Survival (OS) rate was considered as the time from CRC diagnosis to the time of patients death or the time of most recent follow-up time (censored). Progression-Free Survival (DFS) rate was considered as the time from starting CRC treatment to the date of its progression or to date of patients most recent follow-up time during which the patients were progression-free. Stratification and categorization of OS and DDR-TRK-1 PFS rates were assessed in relation to andP21expression and were estimated by using the method of Kaplan-Meier plot, and were compared by using the two-sided exact log-rank test. A p-value 0.05 was DDR-TRK-1 considered significant. Statistics of the current study were done by using SPSS 22.0 for windows (SPSS Inc., USA) and MedCalc windows (MedCalc Software bvba 13, Belgium). Results Expression and End result of Included Patients with Metastatic Colorectal Malignancy.

The increasing quantity of cells at G2/M phase was related to induction of the CDK inhibitors; p21 and p27 through the silence of cyclin E/CDK2 which is the G1/S-promoting kinases that lead to arrest G1 arrest