Objective: Gastric-colon cancer is a complex, multi-stage disease involving deregulation of different signaling cascades. This study was conducted to determine the extent of apoptosis, angiogenesis, inflammation, and oxidative stress in patients with gastric-colon cancers. Plasma levels of soluble (s) Fas, bcl-2 as antiapoptotic indices; cathepsin D (CD), calpain I and II as proteolytic, apoptotic indices; nitric oxide (NO), lipid peroxides (LPER) as oxidative stress, angiogenic indices, and tumor necrosis factor (TNF)-α as apoptotic, inflammatory, angiogenic indices were measured in gastric-colon cancer patients. Methods: Thirty gastric-colon cancer patients [colorectal (n=20), gastric (n=10) cancers], 30 with benign gastrointestinal tract (GIT) masses and 30 healthy controls, were recruited. sFas, bcl-2 and TNF-α were measured by immunosorbent assay kits, and CD, calpain I and II, LPER and NO by chemical methods. Results: sFas, bcl-2, CD, calpain I, calpain II, NO, and TNF-α were higher in malignant and benign GIT masses than controls, and in malignant than benign masses. In gastric tumors, calpain I, calpain II, CD, LPER, and NO levels were higher than colorectal. In benign and malignant GIT masses, positive correlations were found between sFas, bcl-2, CD, calpain I, calpain II, LPER, NO and TNF- α. Conclusions: Gastric-colon malignancy patients exhibited decreased apoptosis, as evident by an increase in antiapoptotic indices, i.e. sFas and bcl-2, and increased angiogenic activity, as evident by enhanced proteolytic activity of cathepsin-D and calpain I and II. These parameters were higher in gastric than colorectal cancers reflecting aggressive behavior of the earlier. Thus, decreased apoptosis and enhanced angiogenesis give growth priority in gastric-colon cancers, and the angiogenic factors’ blockage may delay the tumor’s spread.
Research Date
Research Department
Research Journal
Archives of Clinical and Experimental Surgery
Research Member
Research Rank
Q2
Research Vol
1
Research Website
DOI: 10.5455/aces.20120216121853
Research Year
1
Research_Pages
71-84
Research Abstract