<i>In vitro</i> cell experiments revealed that the PI3K activity was enhanced and the PI3K/Akt pathway was significantly activated after HP infection in tumor cells, thus promoting the proliferation of tumor cells (p<0.05) in a time-dependent manner.
<i>In vitro</i> cell experiments revealed that the PI3K activity was enhanced and the PI3K/Akt pathway was significantly activated after HP infection in tumor cells, thus promoting the proliferation of tumor cells (p<0.05) in a time-dependent manner.
<i>In vitro</i> cell experiments revealed that the PI3K activity was enhanced and the PI3K/Akt pathway was significantly activated after HP infection in tumor cells, thus promoting the proliferation of tumor cells (p<0.05) in a time-dependent manner.
<i>In vitro</i> cell experiments revealed that the PI3K activity was enhanced and the PI3K/Akt pathway was significantly activated after HP infection in tumor cells, thus promoting the proliferation of tumor cells (p<0.05) in a time-dependent manner.
Hyperplastic polyps and serrated adenomas of the colorectum show mixed gastrointestinal differentiation, expressing both gastric (M1 or MUC5AC) and intestinal (MUC2) mucins.
Hyperplastic polyps (HPs) share some histologic and molecular characteristics with SSA/P, but it is unclear whether SSA/Ps are derived from HPs or whether they develop by a different pathogenetic pathway.
Hyperplastic polyps (HPs) share some histologic and molecular characteristics with SSA/P, but it is unclear whether SSA/Ps are derived from HPs or whether they develop by a different pathogenetic pathway.
HP infection is the most definite insult leading to GC, and a protective function of mucin 1 protein has been suggested by studies on Muc1 knocked-out mice.
MP significantly reduced the invasion of VEGFD-SK cells, tumor volume, lymphatic metastasis rates and lymphatic vessel density compared with control groups (P<0.05), accompanied with down-expression of VEGF-D and MMP-2 and increased apoptosis.
BRAF mutations were found in 11 of 215 (5.1%) colorectal adenocarcinomas, 3 of 108 (2.8%) sporadic adenomas, 1 of 63 (1.6%) adenomas from familial adenomatous polyposis (FAP) patients, and 1 of 3 (33%) hyperplastic polyps.
BRAF, K-ras and BAT26 genes have the potential to be molecular markers for colorectal adenomas and HPs, and can be used as non-invasive screening markers for colorectal polyps.
BRAF mutation was rare in adenomas (1/248 [0.4%]) but common in SSAs (78%), traditional serrated adenomas (66%), mixed polyps (57%), and microvesicular hyperplastic polyps (70%).
BRAF gene mutations in the colorectum have been associated with serrated adenomas and less frequently with hyperplastic polyps, villous adenomas, tubular adenomas, and carcinomas.