Editorial: Genomania of p53 Protein in Gastric Cancer

Abstract

The role of oncogenes and tumor suppressor genes in the pathogenesis of gastric cancer has recently received considerable attention. p53 is a tumor suppressor gene that is essential in the cell cycle; it prevents G1/S phase transition, after exposure to ionizing radiation or DNA-damaging chemotherapy. This allows the cell to repair its DNA or, if the damage is irreversible, to elicit apoptotic cell death. p53 mutations are seen in many human tumors including gastric carcinoma. Evidence suggests that mutant p53 is associated with shorter life expectancy in gastric, breast, lung, and colorectal cancer. A number of studies have shown cellular resistance to chemotherapy in the presence of mutant p53. Currently, increasing interest has been devoted to the potential role of mutant p53 as a screening tool.

Non-steroidal anti-inflammatory drug-induced apoptosis in gastric cancer cells is blocked by protein kinase C activation through inhibition of c-myc

“…A high prevalence of p53 mutation has been detected in gastric cancer (Uchino et al, 1993;Triantafillou et al, 1996). In indomethacin-treated AGS cells, we did not observe any change in p53 mRNA and protein expression.…”

Molecular genetic changes in gastric carcinoma

“…e mutations in other canonical oncogenes (KRAS, CTNNB1, and PIK3CA) and tumor suppressor genes (SMAD4, APC) have also seen in GCs. [37] e aberrant expression of TP53 have been found in over half of human cancers including leukemia, breast, colon, and lung carcinoma and alteration in TP53 is the most common event in human cancers. Normally, TP53 plays key role in cell cycle progression preventing G1/S transition after DNA damage occurred and allowing DNA repair/cell apoptosis.…”

“…Normally, TP53 plays key role in cell cycle progression preventing G1/S transition after DNA damage occurred and allowing DNA repair/cell apoptosis. [37] Some studies shown that TP53 abnormalities can occurs in nonneoplastic gastric mucosa with intestinal metaplasia suggesting TP53 mutation as early phenomena in gastric carcinogenesis [38] 2. PTEN: It is aTSG, discovered in 1997.…”

Preliminary exploration of the relationship between apoptosis and gastric carcinoma and its precancerosis

“…Recent studies proved that radiotherapy could cause cell apoptosis, the mechanism of which may involve the partaking of the inhibitory oncogene p53. Triantafillou (7) indicat-ed that DNA damage of gastric mucous cell often occurred in treating gastric cancer with radiotherapy, which would cause high expression of p53 gene and thus induce cell apoptosis of normal cells, lymphocytes and cancer cells. To induce cancer cell apoptosis is also included in the mechanism of some chemotherapeutic agents such as cisplatinum, topo-enzyme ]1 inhibitor and the differentiation inducing agent as retinoic acid.…”