الفهرس 
IntroductionOnly 14 pages are availabe for public view
 |  | from | 279 |  |  |
| | | from | 279 | | |
Abstract
Colorectal cancer (CRC) is currently the third most common cancer type worldwide and it is still the second leading cause of cancer-related deaths worldwide despite of recent advances in neo-adjuvant chemotherapeutic regimens. It is considered the most frequent gastrointestinal malignancy. In Egypt, CRC constitutes 4.2% being the 7th in men and the 4th in women.
Autophagy has be recently studied to have a strong role in pathogenesis and progression of tumors including CRC. The relationship between cancer cells and host immunity in the tumor has been the object of growing interest, and cancer cell escape from the immune system response was recently recognized as an independent hallmark of cancer. Autophagy is an evolutionarily conserved and intricately regulated cellular process in which damaged or aggregated proteins, organelles, and pathogen-derived components are engulfed by double-membrane structures, termed autophagosomes, and targeted for lysosomal degradation. Cancer cells are, therefore, exposed to a variety of external and internal stimuli that would intensify their autophagic activity. Although autophagy is a major cell survival pathway, excessive activation leads to massive degradation of cellular components, shifting the balance to self-destruction and autophagic cell death (type II programmed cell death).
Therefore, the aim of this study was to characterize the immunohistochemical (IHC) expression of autophagy proteins (Beclin-1, ATG-5 and LC3 both isoform A and B) and immunity proteins (ISG-15, ICOS and TRIM24) in non-neoplastic colonic tissue, adenoma and CRC