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Trial Title:
Study on the Probiotics Regulating miRNA in H. Pylori-induced Wnt/β-catenin Gastric Carcinogenesis.
NCT ID:
NCT05544396
Condition:
H. Pylori Infection
Carcinogenesis
Conditions: Official terms:
Carcinogenesis
Conditions: Keywords:
H. Pylori
Wnt/beta-catenin
miRNA
carcinogenesis
Study type:
Interventional
Study phase:
N/A
Overall status:
Recruiting
Study design:
Allocation:
Randomized
Intervention model:
Parallel Assignment
Primary purpose:
Treatment
Masking:
None (Open Label)
Intervention:
Intervention type:
Other
Intervention name:
probiotic
Description:
probiotic group give probiotics (2 packs per day) for 6 months.
Arm group label:
control group
Arm group label:
probiotic group
Summary:
Background. H. pylori has recognized as a type 1 carcinogen for gastric adenocarcinoma.
Although H. pylori eradication promises to reduce the risk of gastric cancer, the
regression rate of intestinal metaplasia (IM) after eradication is unsatisfactory.
Therefore, to find the mechanism of IM persistent and a new strategy to improve IM
regression are critical for reducing gastric cancer development. The canonical
Wnt/beta-catenin signaling pathway upregulating cyclooxygenase-2 (COX-2) transcriptional
activity involves gastric carcinogenesis after H. pylori infection. Investigators have
established an in vitro model that H. pylori induces a cagA-dependent nuclear COX-2
expression in both GES-1 and AGS cells. MicroRNAs (miRNAs) are a class of widespread
non-coding RNAs and have been shown to involve in the gastric carcinogenesis. Among these
gastric cancer-related miRNA candidates, some were reported to interact with
Wnt/β-catenin pathway. Clinically, H. pylori eradication plus celecoxib therapy results
in about one-third cases being IM regression, which correlated to the nuclear β-catenin
and COX-2 expression before treatment. Based on the probiotics ingestion can ameliorate
H. pylori-induced inflammatory pathways, investigators hypothesis that H. pylori
eradication with probiotics supplement may promote IM regression through regulating
certain miRNAs and Wnt/β-catenin signaling. The aims of this 3-year grant will
1. to establish the H. pylori induces the Wnt/beta-catenin and COX-2 signaling pathway
in vitro.
2. to investigate the effects and mechanisms of L. acidophilus and B. latis on H.
pylori-induced Wnt/beta-catenin oncogenesis pathway.
3. to study whether probiotics ingestion promote IM regression or ameliorate IM
progression in H. pylori-infected patients after successful eradication therapy.
Materials and Methods. A H. pylori (HP238) isolate strain, GES-1, and AGS cells will be
used for in vitro study. The protein levels of cell tests will measured by western blot.
The differences of miRNAs expression between monk, cells infected with H. pylori, and
cells pretreated with probiotics than infected by H. pylori will be analyzed by next
generation sequencing method. H. pylori-infected patients with IM will be randomly
allocated to receive probiotics or controls, the 2nd endoscopy will be arranged at the
12th month to evaluate the IM status.
Anticipated results. This study will to establish the H. pylori-induced Wnt/beta-catenin
oncogenesis pathway in vitro. Furthermore, the effect and mechanism of probiotics inhibit
the H. pylori-induced Wnt/beta-catenin signaling will be clarified. Finally,
investigators will provide an evidence for the probiotics ingestion promote the rate of
IM regression in patients after H. pylori eradication.
Detailed description:
What are already know
1. H. pylori-induced Wnt/beta-catenin cascades leads to gastric carcinogenesis.
2. Nuclear beta-catenin and COX-2 expression correlated to the IM regression rate in
human after H. pylori eradication.
3. Administration of selective COX-2 inhibitos, celecoxib, results in partial IM
regression in patients with long-term IM persistence after H. pylori eradication
4. Certain miRNAs involve in gastric oncogenesis by targeting Wnt/beta-catenin
signaling pathway.
What will be add
1. The Wnt/beta-catenin oncogenesis induction is different between primary (GES-1), and
cancer (AGS) gastric cells after H. pylori infection.
2. Probiotics ameliorate or prevent H. pylori-induced gastric Wnt/beta-catenin/COX2
carcinogenesis signaling through regulating miRNAs.
3. Probiotics administration improves regression rate in patients with CAG and IM after
H. pylori successful eradication.
Diagram of clinical trial to evaluate probiotics ingestion improves H. pylori-related
intestinal metaplasia (IM) in patients after eradication therapy
A.The dyspeptic patients receiving PES and biopsies will be continuously enrolled to find
H. pylori infection and IM.
B.Investigators keep to allocate patients into probiotics-treatment and controls (each
group 30 patients).
C.To compare the miRNA(s) serum levels in patients with IM regression and IM persistent
by real-time PCR.
D.To analyze the significance of probiotics ingestion improves IM regression rate in the
RTC.
Criteria for eligibility:
Criteria:
Inclusion Criteria:
- 20 years of age or older
- Have undergone gastroscopy
- First discovered H.pylori infection and intestinal metaplasia
Exclusion Criteria:
- Massive bleeding is life-threatening
- Gastric cancer
- Previous treatment for H.pylori
- Long-term use of non-steroidal anti-inflammatory drugs (eg, aspirin), and hydrogen
ion pump inhibitors.
Gender:
All
Minimum age:
20 Years
Maximum age:
N/A
Healthy volunteers:
No
Locations:
Facility:
Name:
National Cheng Kung University & Hospital
Address:
City:
Tainan
Zip:
704
Country:
Taiwan
Status:
Recruiting
Contact:
Last name:
Yao-jong Yang, PhD
Phone:
+886 928 720 689
Email:
yaojong@mail.ncku.edu.tw
Start date:
March 20, 2024
Completion date:
July 31, 2030
Lead sponsor:
Agency:
National Cheng-Kung University Hospital
Agency class:
Other
Source:
National Cheng-Kung University Hospital
Record processing date:
ClinicalTrials.gov processed this data on November 12, 2024
Source: ClinicalTrials.gov page:
https://clinicaltrials.gov/ct2/show/NCT05544396
