The correlation between KRAS mutations and H. pylori in gastric cancer patients

Abstract EN

: Helicobacterpylori (H.

pylori) is the most important ctiologic factor for gastric cancer ,it is onc of the most common human pathogens, which colonizcs in the mucus laycr of the gastric epithelium in more than 50% of the population.

It is the only bactcrium that elassified as a class I carcinogen by the WHO .The clinical outcomcs of H.

pylori infection is détermine by host gcnctic prédisposition, bactcrial virulence factors, and cnvironmental factors.

H.

pylori can inducc chronic inflammation and oxidativc stress that provides a permissive environment to DNA damage, this damage can Icad to genetic instability and cventually, ncoplastic transformation.

KRAS is onc of the most frcquently mutated oncogenes in human cancers, in particular in pancrcatic, colorectal and lung cancers.

How-evcr, oncogcnic mutations of KRAS arc infrequent in gastric cancer.

Point mutations of the KRAS are found prcdominantly in adcnocarcinomas.

Codons 12 and 13 arc the most frcquently dctcctcd mutation “hot spots”, they makc the protein résistant to GTP hydrolysis by GTPases, thereby Icading to constitutive KRAS activity.

The results rcvealcd that no mutations in codons 12 orI3 dctcctcd in ail patient groups, but the scqucncing analysis dctcctcd other mutations in exon 2.

These mutations were found in 7 /20 (35%) patients of HIP-GC group, 5/16(31.25%) patients of HIN-GC group and 4/15(26.7%) patients of the ulccr group.