Gastric Cancer H. pylori Associated

MONDO:0004950 Pathograph 11 gastric carcinoma

Helicobacter pylori-associated gastric cancer represents the majority of gastric adenocarcinomas worldwide. H. pylori is classified as a Class I carcinogen by the IARC, with chronic infection driving a cascade from gastritis to atrophic gastritis, intestinal metaplasia, dysplasia, and ultimately carcinoma (the Correa cascade). Both intestinal and diffuse histologic types can arise in the setting of H. pylori infection, though intestinal-type adenocarcinoma follows the classic progression pathway. H. pylori eradication can reduce gastric cancer risk, particularly when performed before development of premalignant lesions.

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0
Mappings
0
Definitions
0
Inheritance
10
Pathophysiology
1
Histopathology
7
Phenotypes
11
Pathograph
4
Genes
5
Treatments
2
Subtypes
0
Differentials
0
Datasets
0
Trials
0
Models
13
References
1
Deep Research
🏷

Classifications

Harrison's Chapter
cancer solid tumor
ICD-O Morphology
Adenocarcinoma
◆

Subtypes

2
Intestinal-Type Adenocarcinoma
Well-to-moderately differentiated tumors with glandular architecture, arising through the classic Correa pathway of atrophic gastritis to intestinal metaplasia to dysplasia to carcinoma. More common in high- incidence regions and associated with H. pylori infection.
Diffuse-Type Adenocarcinoma
Poorly differentiated tumors with scattered single cells or small clusters infiltrating the gastric wall (signet ring cell carcinoma). Associated with CDH1/E-cadherin loss. Can also arise in H. pylori-infected mucosa but does not require intestinal metaplasia.
⚙

Pathophysiology

10
CagA-Mediated Oncogenic Signaling
The cagA gene encodes the CagA oncoprotein, a major H. pylori virulence factor injected into host cells via a type IV secretion system. CagA is phosphorylated by host kinases and activates SHP-2, disrupting cell polarity, promoting proliferation, and inhibiting apoptosis. CagA-positive strains confer higher cancer risk.
epithelial cell of stomach link
cell population proliferation link ↑ INCREASED apoptotic process link ↓ DECREASED
stomach link
Downstream
SHP-2 Activation Phosphorylated CagA activates SHP-2 phosphatase, promoting cell motility
CagA-Induced Epithelial Morphological Transformation CagA signaling produces transformed gastric epithelial cell morphology.
Show evidence (1 reference)
PMID:12446738 SUPPORT In Vitro
"the tyrosine-phosphorylated form of CagA specifically binds to and activates SHP-2 phosphatase, thereby inducing morphological transformation of gastric epithelial cells (hummingbird phenotype)"
This study demonstrates the molecular mechanism of CagA-SHP-2 interaction and downstream oncogenic signaling in gastric epithelial cells.
SHP-2 Activation
Tyrosine-phosphorylated CagA binds and activates the host SHP-2 phosphatase, linking the injected bacterial oncoprotein to aberrant intracellular signaling in gastric epithelial cells.
epithelial cell of stomach link
Show evidence (1 reference)
PMID:12446738 SUPPORT In Vitro
"the tyrosine-phosphorylated form of CagA specifically binds to and activates SHP-2 phosphatase, thereby inducing morphological transformation of gastric epithelial cells (hummingbird phenotype)"
This exact experimental observation supports SHP-2 activation as a named downstream effect of CagA in gastric epithelial cells.
CagA-Induced Epithelial Morphological Transformation
CagA-driven host signaling changes gastric epithelial cell morphology, represented experimentally by the hummingbird phenotype.
epithelial cell of stomach link
Show evidence (1 reference)
PMID:12446738 SUPPORT In Vitro
"the tyrosine-phosphorylated form of CagA specifically binds to and activates SHP-2 phosphatase, thereby inducing morphological transformation of gastric epithelial cells (hummingbird phenotype)"
The cited CagA experiment directly reports morphological transformation of gastric epithelial cells.
VacA-Induced Cellular Damage
VacA (vacuolating cytotoxin A) is a pore-forming toxin that induces vacuolation and apoptosis in epithelial cells. Different VacA alleles (s1/s2, m1/m2) confer different cancer risk.
epithelial cell of stomach link
apoptotic process link ↑ INCREASED
stomach link
Downstream
Chronic Inflammation (Correa Cascade) Epithelial injury helps sustain chronic mucosal inflammation
Show evidence (1 reference)
PMID:11447189 SUPPORT In Vitro
"These findings demonstrate that the vacuolating cytototoxin of H. pylori is a bacterial factor capable of inducing apoptosis in gastric epithelial cells."
This study directly shows that VacA induces apoptosis in gastric epithelial cells, supporting toxin-mediated epithelial injury.
VacA-Mediated T Cell Suppression
VacA impairs T cell activation by blocking calcium influx and preventing NF-AT-dependent cytokine transcription. This blunts adaptive immunity and helps H. pylori persist in the gastric mucosa.
T cell link
T cell activation link ↓ DECREASED
Downstream
Chronic Inflammation (Correa Cascade) Impaired adaptive immunity permits persistent H. pylori colonization
Show evidence (1 reference)
PMID:14676300 SUPPORT In Vitro
"Here we report that VacA also interferes with T cell activation by two different mechanisms. Formation of anion-specific channels by VacA prevents calcium influx from the extracellular milieu. The transcription factor NF-AT thus fails to translocate to the nucleus and activate key cytokine genes."
This study shows that VacA directly inhibits T cell activation and cytokine gene induction, supporting immune evasion by H. pylori.
Chronic Inflammation (Correa Cascade)
H. pylori induces chronic gastritis with infiltration of neutrophils, lymphocytes, and macrophages. Persistent inflammation generates reactive oxygen and nitrogen species that cause DNA damage. Over decades, this leads to atrophic gastritis, intestinal metaplasia, dysplasia, and ultimately adenocarcinoma.
inflammatory response link ↑ INCREASED response to oxidative stress link ↑ INCREASED
Downstream
Atrophic Gastritis Chronic inflammation leads to loss of gastric glandular cells
Intestinal Metaplasia Gastric epithelium undergoes metaplastic change to intestinal-type
Show evidence (1 reference)
PMID:26668499 PARTIAL
"This cascade is a dynamic process that includes lesions, such as atrophic gastritis, intestinal metaplasia and dysplasia."
Abstract describes the gastric precancerous cascade with atrophic gastritis, intestinal metaplasia, and dysplasia.
Atrophic Gastritis
Persistent H. pylori-associated gastritis can progress to atrophic gastritis as part of the gastric precancerous cascade.
Downstream
Intestinal Metaplasia Atrophic gastritis is followed by intestinal metaplasia in the Correa precancerous cascade.
Show evidence (1 reference)
PMID:26668499 SUPPORT
"infection targets the normal gastric mucosa causing non-atrophic gastritis, an initiating lesion that can be cured by clearing H. pylori with antibiotics or that may then linger in the case of chronic infection and progress to atrophic gastritis."
This review describes atrophic gastritis as a downstream lesion after persistent H. pylori-associated gastritis.
Intestinal Metaplasia
Intestinal metaplasia is a premalignant epithelial change in the Correa cascade between atrophic gastritis and dysplasia/carcinoma.
Show evidence (1 reference)
PMID:26668499 SUPPORT
"The sequence of events associated with the development of gastric cancer has been described as "the gastric precancerous cascade". This cascade is a dynamic process that includes lesions, such as atrophic gastritis, intestinal metaplasia and dysplasia."
This exact abstract text places intestinal metaplasia within the gastric precancerous cascade.
CDH1/E-cadherin Inactivation
Loss of E-cadherin function through somatic mutation, promoter methylation, or loss of heterozygosity occurs in diffuse-type gastric cancer and some intestinal-type tumors. E-cadherin loss disrupts cell-cell adhesion and activates Wnt/beta-catenin signaling, promoting invasion.
CDH1 link
cell-cell adhesion link ↓ DECREASED
Downstream
Loss of Cell Cohesion Enables single-cell infiltrative growth pattern
Loss of Cell Cohesion
Reduced or absent E-cadherin weakens epithelial tumor-cell adhesion and is associated with invasive, infiltrating gastrointestinal adenocarcinoma behavior.
cell-cell adhesion link ↓ DECREASED
Show evidence (1 reference)
PMID:41710815 SUPPORT Human Clinical
"Loss of E-cadherin expression in advanced tumor stages, higher nodal metastasis, and perineural invasion elucidate the role of E-cadherin as a useful prognostic immunohistochemical marker in gastrointestinal adenocarcinomas."
This human adenocarcinoma study supports reduced E-cadherin as a clinically observed marker of invasive tumor behavior.
✶

Histopathology

1
Gastric Adenocarcinoma VERY_FREQUENT
Adenocarcinoma is the most common histologic type of gastric cancer.
Show evidence (1 reference)
PMID:40647518 PARTIAL
"with adenocarcinoma being the most common histologic type (91.0%)"
Abstract notes adenocarcinoma as the predominant histologic type in a gastric cancer cohort.
⬡

Pathograph

Use the checkboxes to hide or show graph categories. Hover nodes for evidence and cross-linked metadata.
Pathograph: causal mechanism network for Gastric Cancer H. pylori Associated Interactive directed graph showing how pathophysiology mechanisms, phenotypes, genetic factors and variants, experimental models, environmental triggers, and treatments relate through causal and linked edges.
●

Phenotypes

7
Blood 1
Gastrointestinal Bleeding OCCASIONAL Gastrointestinal hemorrhage (HP:0002239)
Digestive 4
Early Satiety FREQUENT Early satiety (HP:0033842)
Nausea FREQUENT Nausea (HP:0002018)
Dysphagia OCCASIONAL Dysphagia (HP:0002015)
Anorexia FREQUENT Anorexia (HP:0002039)
Constitutional 1
Abdominal Pain VERY_FREQUENT Abdominal pain (HP:0002027)
Growth 1
Weight Loss FREQUENT Weight loss (HP:0001824)
🧬

Genetic Associations

4
CDH1 (Somatic and Germline Mutations)
Autosomal Dominant
Show evidence (1 reference)
PMID:26182300 SUPPORT Human Clinical
"By the age of 80 years, the cumulative incidence of gastric cancer was 70% (95% CI, 59%-80%) for males and 56% (95% CI, 44%-69%) for females, and the risk of breast cancer for females was 42% (95% CI, 23%-68%)."
Large cohort study of 75 CDH1 mutation-positive families providing precise cancer risk estimates for hereditary diffuse gastric cancer syndrome.
TP53 (Somatic Mutations)
RHOA (Somatic Mutations)
ARID1A (Somatic Mutations)
💊

Treatments

5
H. pylori Eradication
Action: pharmacotherapy MAXO:0000058
Triple or quadruple therapy to eradicate H. pylori reduces gastric cancer risk, particularly when given before development of intestinal metaplasia. Also reduces risk of metachronous gastric cancer after endoscopic resection of early tumors.
Show evidence (1 reference)
PMID:32205420 SUPPORT Human Clinical
"In healthy individuals, eradication therapy reduced incidence of gastric cancer (RR=0.54; 95% CI 0.40 to 0.72, NNT=72) and reduced mortality from gastric cancer (RR=0.61; 95% CI 0.40 to 0.92, NNT=135)"
Meta-analysis of 10 RCTs demonstrating that H. pylori eradication therapy significantly reduces gastric cancer incidence and mortality.
Surgical Resection
Action: surgical procedure MAXO:0000004
Gastrectomy (subtotal or total depending on tumor location) with D2 lymphadenectomy is the standard curative treatment for resectable gastric cancer. Reconstruction maintains GI continuity.
Perioperative Chemotherapy
Action: chemotherapy MAXO:0000647
Perioperative FLOT (5-FU, leucovorin, oxaliplatin, docetaxel) is the standard of care for resectable locally advanced gastric cancer in Western countries, improving survival compared to surgery alone.
Show evidence (1 reference)
PMID:36919950 SUPPORT Human Clinical
"Patients treated with FLOT showed a statistically significant longer median overall survival of 57.8 vs 28.9 months (HR: 0.554, 95% CI: 0.317-0.969, P = .036)"
Real-world cohort study demonstrating FLOT4 perioperative chemotherapy significantly improves overall survival in gastric cancer patients.
Trastuzumab
Action: immunotherapy Ontology label: Immunotherapy NCIT:C15262
Agent: trastuzumab ↗
Anti-HER2 monoclonal antibody added to chemotherapy for HER2-positive (approximately 15-20%) advanced gastric cancer. First targeted therapy to show survival benefit in gastric cancer.
Immune Checkpoint Inhibition
Action: immunotherapy Ontology label: Immunotherapy NCIT:C15262
PD-1 inhibitors combined with chemotherapy are now standard first-line treatment for advanced gastric cancer. Benefit is greatest in PD-L1 CPS-high and MSI-high tumors.
🔬

Biochemical Markers

2
H. pylori Testing
Serum Pepsinogen
{ }

Source YAML

click to show 
name: Gastric Cancer H. pylori Associated
creation_date: '2026-01-26T02:55:13Z'
updated_date: '2026-05-09T00:41:13Z'
description: >-
  Helicobacter pylori-associated gastric cancer represents the majority of gastric
  adenocarcinomas worldwide. H. pylori is classified as a Class I carcinogen by the
  IARC, with chronic infection driving a cascade from gastritis to atrophic gastritis,
  intestinal metaplasia, dysplasia, and ultimately carcinoma (the Correa cascade).
  Both intestinal and diffuse histologic types can arise in the setting of H. pylori
  infection, though intestinal-type adenocarcinoma follows the classic progression
  pathway. H. pylori eradication can reduce gastric cancer risk, particularly when
  performed before development of premalignant lesions.
categories:
- Gastrointestinal Cancer
- Infectious Cancer
- Bacterial-Associated Cancer
parents:
- gastric carcinoma
has_subtypes:
- name: Intestinal-Type Adenocarcinoma
  description: >-
    Well-to-moderately differentiated tumors with glandular architecture,
    arising through the classic Correa pathway of atrophic gastritis to
    intestinal metaplasia to dysplasia to carcinoma. More common in high-
    incidence regions and associated with H. pylori infection.
- name: Diffuse-Type Adenocarcinoma
  description: >-
    Poorly differentiated tumors with scattered single cells or small clusters
    infiltrating the gastric wall (signet ring cell carcinoma). Associated
    with CDH1/E-cadherin loss. Can also arise in H. pylori-infected mucosa
    but does not require intestinal metaplasia.
infectious_agent:
- name: Helicobacter pylori
  description: >-
    H. pylori is a gram-negative spiral bacterium that colonizes the gastric
    epithelium. Infection is acquired in childhood and persists lifelong if
    untreated. Approximately 1-3% of infected individuals eventually develop
    gastric cancer, with risk modified by bacterial virulence factors, host
    genetics, and environmental factors including diet.
  evidence:
  - reference: PMID:39004993
    reference_title: "[Advances in the application of intragastric flora in the diagnosis and treatment of gastric cancer]."
    supports: PARTIAL
    snippet: Gastric cancer is one of the major causes of cancer-related deaths worldwide, and infection with Helicobacter pylori and EBV, smoking and a salt-heavy diet have been shown to be risk factors for the development of gastric cancer.
    explanation: This abstract identifies H. pylori infection as a risk factor for gastric cancer, supporting the infectious etiology noted here.
  infectious_agent_term:
    preferred_term: Helicobacter pylori
    term:
      id: NCBITaxon:210
      label: Helicobacter pylori
pathophysiology:
- name: CagA-Mediated Oncogenic Signaling
  description: >-
    The cagA gene encodes the CagA oncoprotein, a major H. pylori virulence
    factor injected into host cells via a type IV secretion system. CagA
    is phosphorylated by host kinases and activates SHP-2, disrupting
    cell polarity, promoting proliferation, and inhibiting apoptosis.
    CagA-positive strains confer higher cancer risk.
  evidence:
  - reference: PMID:12446738
    supports: SUPPORT
    evidence_source: IN_VITRO
    snippet: >-
      the tyrosine-phosphorylated form of CagA specifically binds to and activates
      SHP-2 phosphatase, thereby inducing morphological transformation of gastric
      epithelial cells (hummingbird phenotype)
    explanation: >-
      This study demonstrates the molecular mechanism of CagA-SHP-2 interaction
      and downstream oncogenic signaling in gastric epithelial cells.
  cell_types:
  - preferred_term: epithelial cell of stomach
    term:
      id: CL:0002178
      label: epithelial cell of stomach
  biological_processes:
  - preferred_term: cell population proliferation
    modifier: INCREASED
    term:
      id: GO:0008283
      label: cell population proliferation
  - preferred_term: apoptotic process
    modifier: DECREASED
    term:
      id: GO:0006915
      label: apoptotic process
  locations:
  - preferred_term: stomach
    term:
      id: UBERON:0000945
      label: stomach
  downstream:
  - target: SHP-2 Activation
    description: Phosphorylated CagA activates SHP-2 phosphatase, promoting cell motility
  - target: CagA-Induced Epithelial Morphological Transformation
    description: CagA signaling produces transformed gastric epithelial cell morphology.
- name: SHP-2 Activation
  description: >-
    Tyrosine-phosphorylated CagA binds and activates the host SHP-2 phosphatase,
    linking the injected bacterial oncoprotein to aberrant intracellular signaling
    in gastric epithelial cells.
  evidence:
  - reference: PMID:12446738
    supports: SUPPORT
    evidence_source: IN_VITRO
    snippet: >-
      the tyrosine-phosphorylated form of CagA specifically binds to and activates
      SHP-2 phosphatase, thereby inducing morphological transformation of gastric
      epithelial cells (hummingbird phenotype)
    explanation: >-
      This exact experimental observation supports SHP-2 activation as a named
      downstream effect of CagA in gastric epithelial cells.
  cell_types:
  - preferred_term: epithelial cell of stomach
    term:
      id: CL:0002178
      label: epithelial cell of stomach
- name: CagA-Induced Epithelial Morphological Transformation
  description: >-
    CagA-driven host signaling changes gastric epithelial cell morphology,
    represented experimentally by the hummingbird phenotype.
  evidence:
  - reference: PMID:12446738
    supports: SUPPORT
    evidence_source: IN_VITRO
    snippet: >-
      the tyrosine-phosphorylated form of CagA specifically binds to and activates
      SHP-2 phosphatase, thereby inducing morphological transformation of gastric
      epithelial cells (hummingbird phenotype)
    explanation: >-
      The cited CagA experiment directly reports morphological transformation of
      gastric epithelial cells.
  cell_types:
  - preferred_term: epithelial cell of stomach
    term:
      id: CL:0002178
      label: epithelial cell of stomach
- name: VacA-Induced Cellular Damage
  description: >-
    VacA (vacuolating cytotoxin A) is a pore-forming toxin that induces
    vacuolation and apoptosis in epithelial cells. Different VacA alleles
    (s1/s2, m1/m2) confer different cancer risk.
  evidence:
  - reference: PMID:11447189
    supports: SUPPORT
    evidence_source: IN_VITRO
    snippet: >-
      These findings demonstrate that the vacuolating cytototoxin of H. pylori
      is a bacterial factor capable of inducing apoptosis in gastric epithelial
      cells.
    explanation: >-
      This study directly shows that VacA induces apoptosis in gastric epithelial
      cells, supporting toxin-mediated epithelial injury.
  cell_types:
  - preferred_term: epithelial cell of stomach
    term:
      id: CL:0002178
      label: epithelial cell of stomach
  biological_processes:
  - preferred_term: apoptotic process
    modifier: INCREASED
    term:
      id: GO:0006915
      label: apoptotic process
  locations:
  - preferred_term: stomach
    term:
      id: UBERON:0000945
      label: stomach
  downstream:
  - target: Chronic Inflammation (Correa Cascade)
    description: Epithelial injury helps sustain chronic mucosal inflammation
- name: VacA-Mediated T Cell Suppression
  description: >-
    VacA impairs T cell activation by blocking calcium influx and preventing
    NF-AT-dependent cytokine transcription. This blunts adaptive immunity and
    helps H. pylori persist in the gastric mucosa.
  evidence:
  - reference: PMID:14676300
    supports: SUPPORT
    evidence_source: IN_VITRO
    snippet: >-
      Here we report that VacA also interferes with T cell activation by two
      different mechanisms. Formation of anion-specific channels by VacA
      prevents calcium influx from the extracellular milieu. The transcription
      factor NF-AT thus fails to translocate to the nucleus and activate key
      cytokine genes.
    explanation: >-
      This study shows that VacA directly inhibits T cell activation and
      cytokine gene induction, supporting immune evasion by H. pylori.
  cell_types:
  - preferred_term: T cell
    term:
      id: CL:0000084
      label: T cell
  biological_processes:
  - preferred_term: T cell activation
    modifier: DECREASED
    term:
      id: GO:0042110
      label: T cell activation
  downstream:
  - target: Chronic Inflammation (Correa Cascade)
    description: Impaired adaptive immunity permits persistent H. pylori colonization
- name: Chronic Inflammation (Correa Cascade)
  description: >-
    H. pylori induces chronic gastritis with infiltration of neutrophils,
    lymphocytes, and macrophages. Persistent inflammation generates reactive
    oxygen and nitrogen species that cause DNA damage. Over decades, this
    leads to atrophic gastritis, intestinal metaplasia, dysplasia, and
    ultimately adenocarcinoma.
  evidence:
  - reference: PMID:26668499
    reference_title: "Helicobacter pylori-induced inflammation and epigenetic changes during gastric carcinogenesis."
    supports: PARTIAL
    snippet: "This cascade is a dynamic process that includes lesions, such as atrophic gastritis, intestinal metaplasia and dysplasia."
    explanation: "Abstract describes the gastric precancerous cascade with atrophic gastritis, intestinal metaplasia, and dysplasia."
  biological_processes:
  - preferred_term: inflammatory response
    modifier: INCREASED
    term:
      id: GO:0006954
      label: inflammatory response
  - preferred_term: response to oxidative stress
    modifier: INCREASED
    term:
      id: GO:0006979
      label: response to oxidative stress
  downstream:
  - target: Atrophic Gastritis
    description: Chronic inflammation leads to loss of gastric glandular cells
  - target: Intestinal Metaplasia
    description: Gastric epithelium undergoes metaplastic change to intestinal-type
- name: Atrophic Gastritis
  description: >-
    Persistent H. pylori-associated gastritis can progress to atrophic gastritis
    as part of the gastric precancerous cascade.
  evidence:
  - reference: PMID:26668499
    reference_title: "Helicobacter pylori-induced inflammation and epigenetic changes during gastric carcinogenesis."
    supports: SUPPORT
    snippet: >-
      infection targets the normal gastric mucosa causing non-atrophic gastritis,
      an initiating lesion that can be cured by clearing H. pylori with antibiotics
      or that may then linger in the case of chronic infection and progress to
      atrophic gastritis.
    explanation: >-
      This review describes atrophic gastritis as a downstream lesion after
      persistent H. pylori-associated gastritis.
  downstream:
  - target: Intestinal Metaplasia
    description: Atrophic gastritis is followed by intestinal metaplasia in the Correa precancerous cascade.
- name: Intestinal Metaplasia
  description: >-
    Intestinal metaplasia is a premalignant epithelial change in the Correa
    cascade between atrophic gastritis and dysplasia/carcinoma.
  evidence:
  - reference: PMID:26668499
    reference_title: "Helicobacter pylori-induced inflammation and epigenetic changes during gastric carcinogenesis."
    supports: SUPPORT
    snippet: >-
      The sequence of events associated with the development of gastric cancer has
      been described as "the gastric precancerous cascade". This cascade is a
      dynamic process that includes lesions, such as atrophic gastritis, intestinal
      metaplasia and dysplasia.
    explanation: >-
      This exact abstract text places intestinal metaplasia within the gastric
      precancerous cascade.
- name: CDH1/E-cadherin Inactivation
  description: >-
    Loss of E-cadherin function through somatic mutation, promoter methylation,
    or loss of heterozygosity occurs in diffuse-type gastric cancer and some
    intestinal-type tumors. E-cadherin loss disrupts cell-cell adhesion and
    activates Wnt/beta-catenin signaling, promoting invasion.
  genes:
  - preferred_term: CDH1
    term:
      id: hgnc:1748
      label: CDH1
  biological_processes:
  - preferred_term: cell-cell adhesion
    modifier: DECREASED
    term:
      id: GO:0098609
      label: cell-cell adhesion
  downstream:
  - target: Loss of Cell Cohesion
    description: Enables single-cell infiltrative growth pattern
- name: Loss of Cell Cohesion
  description: >-
    Reduced or absent E-cadherin weakens epithelial tumor-cell adhesion and is
    associated with invasive, infiltrating gastrointestinal adenocarcinoma
    behavior.
  evidence:
  - reference: PMID:41710815
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      Loss of E-cadherin expression in advanced tumor stages, higher nodal
      metastasis, and perineural invasion elucidate the role of E-cadherin as a
      useful prognostic immunohistochemical marker in gastrointestinal
      adenocarcinomas.
    explanation: >-
      This human adenocarcinoma study supports reduced E-cadherin as a clinically
      observed marker of invasive tumor behavior.
  biological_processes:
  - preferred_term: cell-cell adhesion
    modifier: DECREASED
    term:
      id: GO:0098609
      label: cell-cell adhesion
histopathology:
- name: Gastric Adenocarcinoma
  finding_term:
    preferred_term: Gastric Adenocarcinoma
    term:
      id: NCIT:C4004
      label: Gastric Adenocarcinoma
  frequency: VERY_FREQUENT
  description: Adenocarcinoma is the most common histologic type of gastric cancer.
  evidence:
  - reference: PMID:40647518
    reference_title: "A Histopathological and Surgical Analysis of Gastric Cancer: A Two-Year Experience in a Single Center."
    supports: PARTIAL
    snippet: "with adenocarcinoma being the most common histologic type (91.0%)"
    explanation: Abstract notes adenocarcinoma as the predominant histologic type in a gastric cancer cohort.

phenotypes:
- category: Gastrointestinal
  name: Abdominal Pain
  frequency: VERY_FREQUENT
  description: >-
    Epigastric pain or discomfort is the most common presenting symptom,
    often initially attributed to dyspepsia or peptic ulcer disease.
  phenotype_term:
    preferred_term: Abdominal pain
    term:
      id: HP:0002027
      label: Abdominal pain
- category: Gastrointestinal
  name: Early Satiety
  frequency: FREQUENT
  description: >-
    Feeling full after eating small amounts occurs due to reduced gastric
    capacity from tumor growth or impaired gastric motility.
  phenotype_term:
    preferred_term: Early satiety
    term:
      id: HP:0033842
      label: Early satiety
- category: Constitutional
  name: Weight Loss
  frequency: FREQUENT
  description: >-
    Unintentional weight loss is common and may be significant at
    presentation, reflecting reduced oral intake and catabolic state.
  phenotype_term:
    preferred_term: Weight loss
    term:
      id: HP:0001824
      label: Weight loss
- category: Gastrointestinal
  name: Nausea
  frequency: FREQUENT
  description: >-
    Nausea and vomiting may occur, particularly with tumors causing
    gastric outlet obstruction.
  phenotype_term:
    preferred_term: Nausea
    term:
      id: HP:0002018
      label: Nausea
- category: Gastrointestinal
  name: Dysphagia
  frequency: OCCASIONAL
  description: >-
    Difficulty swallowing occurs with tumors involving the gastroesophageal
    junction (cardia) or causing esophageal compression.
  phenotype_term:
    preferred_term: Dysphagia
    term:
      id: HP:0002015
      label: Dysphagia
- category: Gastrointestinal
  name: Gastrointestinal Bleeding
  frequency: OCCASIONAL
  description: >-
    Melena, hematemesis, or occult blood loss leading to iron deficiency
    anemia may occur from tumor ulceration.
  phenotype_term:
    preferred_term: Gastrointestinal hemorrhage
    term:
      id: HP:0002239
      label: Gastrointestinal hemorrhage
- category: Constitutional
  name: Anorexia
  frequency: FREQUENT
  description: >-
    Loss of appetite is a common early symptom, contributing to weight loss.
  phenotype_term:
    preferred_term: Anorexia
    term:
      id: HP:0002039
      label: Anorexia
biochemical:
- name: H. pylori Testing
  notes: >-
    H. pylori infection can be detected by urea breath test, stool antigen,
    serology, or biopsy-based tests. Serology may remain positive after
    eradication. All gastric cancer patients should have H. pylori status
    assessed.
- name: Serum Pepsinogen
  notes: >-
    Low serum pepsinogen I and low pepsinogen I/II ratio indicate gastric
    atrophy and increased cancer risk. Used as a screening marker in
    high-incidence populations, particularly Japan.
genetic:
- name: CDH1
  association: Somatic and Germline Mutations
  inheritance:
  - name: Autosomal Dominant
  evidence:
  - reference: PMID:26182300
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      By the age of 80 years, the cumulative incidence of gastric cancer was
      70% (95% CI, 59%-80%) for males and 56% (95% CI, 44%-69%) for females,
      and the risk of breast cancer for females was 42% (95% CI, 23%-68%).
    explanation: >-
      Large cohort study of 75 CDH1 mutation-positive families providing precise
      cancer risk estimates for hereditary diffuse gastric cancer syndrome.
  notes: >-
    Somatic CDH1 alterations (mutation, deletion, methylation) occur in
    approximately 50% of diffuse-type gastric cancers. Germline CDH1 mutations
    cause hereditary diffuse gastric cancer (HDGC) syndrome with lifetime
    risk greater than 70%.
- name: TP53
  association: Somatic Mutations
  notes: >-
    TP53 mutations occur in approximately 30-50% of gastric cancers,
    particularly intestinal type. More common in advanced-stage disease.
- name: RHOA
  association: Somatic Mutations
  notes: >-
    RHOA mutations occur in approximately 15-25% of diffuse-type gastric
    cancer, affecting cell migration and invasion pathways.
- name: ARID1A
  association: Somatic Mutations
  notes: >-
    ARID1A, encoding a SWI/SNF chromatin remodeling complex subunit, is
    mutated in approximately 20% of gastric cancers, particularly those
    associated with EBV or microsatellite instability.
treatments:
- name: H. pylori Eradication
  description: >-
    Triple or quadruple therapy to eradicate H. pylori reduces gastric
    cancer risk, particularly when given before development of intestinal
    metaplasia. Also reduces risk of metachronous gastric cancer after
    endoscopic resection of early tumors.
  evidence:
  - reference: PMID:32205420
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      In healthy individuals, eradication therapy reduced incidence of gastric
      cancer (RR=0.54; 95% CI 0.40 to 0.72, NNT=72) and reduced mortality from
      gastric cancer (RR=0.61; 95% CI 0.40 to 0.92, NNT=135)
    explanation: >-
      Meta-analysis of 10 RCTs demonstrating that H. pylori eradication therapy
      significantly reduces gastric cancer incidence and mortality.
  treatment_term:
    preferred_term: pharmacotherapy
    term:
      id: MAXO:0000058
      label: pharmacotherapy
- name: Surgical Resection
  description: >-
    Gastrectomy (subtotal or total depending on tumor location) with
    D2 lymphadenectomy is the standard curative treatment for resectable
    gastric cancer. Reconstruction maintains GI continuity.
  treatment_term:
    preferred_term: surgical procedure
    term:
      id: MAXO:0000004
      label: surgical procedure
- name: Perioperative Chemotherapy
  description: >-
    Perioperative FLOT (5-FU, leucovorin, oxaliplatin, docetaxel) is
    the standard of care for resectable locally advanced gastric cancer
    in Western countries, improving survival compared to surgery alone.
  evidence:
  - reference: PMID:36919950
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      Patients treated with FLOT showed a statistically significant longer
      median overall survival of 57.8 vs 28.9 months (HR: 0.554, 95% CI:
      0.317-0.969, P = .036)
    explanation: >-
      Real-world cohort study demonstrating FLOT4 perioperative chemotherapy
      significantly improves overall survival in gastric cancer patients.
  treatment_term:
    preferred_term: chemotherapy
    term:
      id: MAXO:0000647
      label: chemotherapy
- name: Trastuzumab
  description: >-
    Anti-HER2 monoclonal antibody added to chemotherapy for HER2-positive
    (approximately 15-20%) advanced gastric cancer. First targeted therapy
    to show survival benefit in gastric cancer.
  treatment_term:
    preferred_term: immunotherapy
    term:
      id: NCIT:C15262
      label: Immunotherapy
    therapeutic_agent:
    - preferred_term: trastuzumab
      term:
        id: CHEBI:231601
        label: trastuzumab
- name: Immune Checkpoint Inhibition
  description: >-
    PD-1 inhibitors combined with chemotherapy are now standard first-line
    treatment for advanced gastric cancer. Benefit is greatest in PD-L1
    CPS-high and MSI-high tumors.
  treatment_term:
    preferred_term: immunotherapy
    term:
      id: NCIT:C15262
      label: Immunotherapy
disease_term:
  preferred_term: gastric carcinoma
  term:
    id: MONDO:0004950
    label: gastric carcinoma

classifications:
  icdo_morphology:
    classification_value: Adenocarcinoma
  harrisons_chapter:
  - classification_value: cancer
  - classification_value: solid tumor
references:
- reference: DOI:10.1007/s11938-020-00298-8
  title: 'Gastritis: An Update in 2020'
  found_in:
  - Gastric_Cancer_H_pylori_Associated-deep-research-falcon.md
  findings:
  - statement: The gastritis constellation includes heterogeneous clinicopathological entities, among which long-standing, non-self-limiting gastritis, mainly due to Helicobacter pylori infection, has been epidemiologically, biologically, and clinically linked to gastric cancer development (i.e. “inflammation-associated cancer”).
    supporting_text: The gastritis constellation includes heterogeneous clinicopathological entities, among which long-standing, non-self-limiting gastritis, mainly due to Helicobacter pylori infection, has been epidemiologically, biologically, and clinically linked to gastric cancer development (i.e. “inflammation-associated cancer”).
    evidence:
    - reference: DOI:10.1007/s11938-020-00298-8
      reference_title: 'Gastritis: An Update in 2020'
      supports: SUPPORT
      evidence_source: HUMAN_CLINICAL
      snippet: The gastritis constellation includes heterogeneous clinicopathological entities, among which long-standing, non-self-limiting gastritis, mainly due to Helicobacter pylori infection, has been epidemiologically, biologically, and clinically linked to gastric cancer development (i.e. “inflammation-associated cancer”).
      explanation: Deep research cited this publication as relevant literature for Gastric Cancer H pylori Associated.
- reference: DOI:10.1055/a-0859-1883
  title: 'Management of epithelial precancerous conditions and lesions in the stomach (MAPS II): European Society of Gastrointestinal Endoscopy (ESGE), European Helicobacter and Microbiota Study Group (EHMSG), European Society of Pathology (ESP), and Sociedade Portuguesa de Endoscopia Digestiva (SPED) guideline update 2019'
  found_in:
  - Gastric_Cancer_H_pylori_Associated-deep-research-falcon.md
  findings:
  - statement: Main RecommendationsPatients with chronic atrophic gastritis or intestinal metaplasia (IM) are at risk for gastric adenocarcinoma.
    supporting_text: Main RecommendationsPatients with chronic atrophic gastritis or intestinal metaplasia (IM) are at risk for gastric adenocarcinoma.
    evidence:
    - reference: DOI:10.1055/a-0859-1883
      reference_title: 'Management of epithelial precancerous conditions and lesions in the stomach (MAPS II): European Society of Gastrointestinal Endoscopy (ESGE), European Helicobacter and Microbiota Study Group (EHMSG), European Society of Pathology (ESP), and Sociedade Portuguesa de Endoscopia Digestiva (SPED) guideline update 2019'
      supports: SUPPORT
      evidence_source: OTHER
      snippet: Main RecommendationsPatients with chronic atrophic gastritis or intestinal metaplasia (IM) are at risk for gastric adenocarcinoma.
      explanation: Deep research cited this publication as relevant literature for Gastric Cancer H pylori Associated.
- reference: DOI:10.1055/a-2529-5025
  title: 'Management of epithelial precancerous conditions and early neoplasia of the stomach (MAPS III): European Society of Gastrointestinal Endoscopy (ESGE), European Helicobacter and Microbiota Study Group (EHMSG) and European Society of Pathology (ESP) Guideline update 2025'
  found_in:
  - Gastric_Cancer_H_pylori_Associated-deep-research-falcon.md
  findings:
  - statement: 'Management of epithelial precancerous conditions and early neoplasia of the stomach (MAPS III): European Society of Gastrointestinal Endoscopy (ESGE), European Helicobacter and Microbiota Study Group (EHMSG) and European Society of Pathology (ESP) Guideline update 2025'
    supporting_text: ESGE/EHMSG/ESP recommend that irrespective of country of origin, individual gastric risk assessment and stratification of precancerous conditions is recommended for first-time gastroscopy.
    evidence:
    - reference: DOI:10.1055/a-2529-5025
      reference_title: 'Management of epithelial precancerous conditions and early neoplasia of the stomach (MAPS III): European Society of Gastrointestinal Endoscopy (ESGE), European Helicobacter and Microbiota Study Group (EHMSG) and European Society of Pathology (ESP) Guideline update 2025'
      supports: SUPPORT
      evidence_source: OTHER
      snippet: ESGE/EHMSG/ESP recommend that irrespective of country of origin, individual gastric risk assessment and stratification of precancerous conditions is recommended for first-time gastroscopy.
      explanation: Deep research cited this publication as relevant literature for Gastric Cancer H pylori Associated.
- reference: DOI:10.1055/a-2695-1376
  title: Adherence to clinical practice guidelines for Management of epithelial precancerous conditions and lesions in the stomach in Europe
  found_in:
  - Gastric_Cancer_H_pylori_Associated-deep-research-falcon.md
  findings:
  - statement: The first international guideline for managing preneoplastic conditions of the stomach (MAPS I) was published in 2012, followed by an update (MAPS II) in 2019.
    supporting_text: The first international guideline for managing preneoplastic conditions of the stomach (MAPS I) was published in 2012, followed by an update (MAPS II) in 2019.
    evidence:
    - reference: DOI:10.1055/a-2695-1376
      reference_title: Adherence to clinical practice guidelines for Management of epithelial precancerous conditions and lesions in the stomach in Europe
      supports: SUPPORT
      evidence_source: HUMAN_CLINICAL
      snippet: The first international guideline for managing preneoplastic conditions of the stomach (MAPS I) was published in 2012, followed by an update (MAPS II) in 2019.
      explanation: Deep research cited this publication as relevant literature for Gastric Cancer H pylori Associated.
- reference: DOI:10.1186/s12876-025-03886-z
  title: 'The relationship between the eradication of Helicobacter pylori and the occurrence of stomach cancer: an updated meta-analysis and systemic review'
  found_in:
  - Gastric_Cancer_H_pylori_Associated-deep-research-falcon.md
  findings:
  - statement: 'The relationship between the eradication of Helicobacter pylori and the occurrence of stomach cancer: an updated meta-analysis and systemic review'
    supporting_text: 'The relationship between the eradication of Helicobacter pylori and the occurrence of stomach cancer: an updated meta-analysis and systemic review'
- reference: DOI:10.1186/s12916-024-03554-1
  title: 'Overall and cause-specific mortality among patients diagnosed with gastric precancerous lesions in Sweden between 1979 and 2014: an observational cohort study'
  found_in:
  - Gastric_Cancer_H_pylori_Associated-deep-research-falcon.md
  findings:
  - statement: The Correa’s cascade, encompassing chronic non-atrophic gastritis, atrophic gastritis, intestinal metaplasia, and dysplasia, represents the well-recognized pathway for the development of non-cardia gastric cancer.
    supporting_text: The Correa’s cascade, encompassing chronic non-atrophic gastritis, atrophic gastritis, intestinal metaplasia, and dysplasia, represents the well-recognized pathway for the development of non-cardia gastric cancer.
    evidence:
    - reference: DOI:10.1186/s12916-024-03554-1
      reference_title: 'Overall and cause-specific mortality among patients diagnosed with gastric precancerous lesions in Sweden between 1979 and 2014: an observational cohort study'
      supports: SUPPORT
      evidence_source: HUMAN_CLINICAL
      snippet: The Correa’s cascade, encompassing chronic non-atrophic gastritis, atrophic gastritis, intestinal metaplasia, and dysplasia, represents the well-recognized pathway for the development of non-cardia gastric cancer.
      explanation: Deep research cited this publication as relevant literature for Gastric Cancer H pylori Associated.
- reference: DOI:10.1371/journal.pone.0307172
  title: 'CagA toxin and risk of Helicobacter pylori-infected gastric phenotype: A meta-analysis of observational studies'
  found_in:
  - Gastric_Cancer_H_pylori_Associated-deep-research-falcon.md
  findings:
  - statement: Helicobacter pylori (H. pylori) is frequently associated with non-cardia type gastric cancer, and it is designated as a group I carcinogen.
    supporting_text: Helicobacter pylori (H. pylori) is frequently associated with non-cardia type gastric cancer, and it is designated as a group I carcinogen.
    evidence:
    - reference: DOI:10.1371/journal.pone.0307172
      reference_title: 'CagA toxin and risk of Helicobacter pylori-infected gastric phenotype: A meta-analysis of observational studies'
      supports: SUPPORT
      evidence_source: HUMAN_CLINICAL
      snippet: Helicobacter pylori (H. pylori) is frequently associated with non-cardia type gastric cancer, and it is designated as a group I carcinogen.
      explanation: Deep research cited this publication as relevant literature for Gastric Cancer H pylori Associated.
- reference: DOI:10.20892/j.issn.2095-3941.2024.0159
  title: Global, regional, and national burden of early-onset gastric cancer
  found_in:
  - Gastric_Cancer_H_pylori_Associated-deep-research-falcon.md
  findings:
  - statement: The burden of gastric cancer (GC) across different age groups needs updating.
    supporting_text: The burden of gastric cancer (GC) across different age groups needs updating.
    evidence:
    - reference: DOI:10.20892/j.issn.2095-3941.2024.0159
      reference_title: Global, regional, and national burden of early-onset gastric cancer
      supports: SUPPORT
      evidence_source: HUMAN_CLINICAL
      snippet: The burden of gastric cancer (GC) across different age groups needs updating.
      explanation: Deep research cited this publication as relevant literature for Gastric Cancer H pylori Associated.
- reference: DOI:10.21203/rs.3.rs-8058648/v1
  title: 'Global epidemiology of gastric cancer in 2022 and projections for 2050: A comprehensive analysis and forecasts based on GLOBOCAN data'
  found_in:
  - Gastric_Cancer_H_pylori_Associated-deep-research-falcon.md
  findings:
  - statement: Gastric cancer (GC) has greatly damaged the health of patients, and the burden exhibits substantial heterogeneity across diverse regions globally.
    supporting_text: Gastric cancer (GC) has greatly damaged the health of patients, and the burden exhibits substantial heterogeneity across diverse regions globally.
    evidence:
    - reference: DOI:10.21203/rs.3.rs-8058648/v1
      reference_title: 'Global epidemiology of gastric cancer in 2022 and projections for 2050: A comprehensive analysis and forecasts based on GLOBOCAN data'
      supports: SUPPORT
      evidence_source: HUMAN_CLINICAL
      snippet: Gastric cancer (GC) has greatly damaged the health of patients, and the burden exhibits substantial heterogeneity across diverse regions globally.
      explanation: Deep research cited this publication as relevant literature for Gastric Cancer H pylori Associated.
- reference: DOI:10.3389/fmed.2024.1393498
  title: 'Helicobacterpylori eradication following endoscopic resection might prevent metachronous gastric cancer: a systematic review and meta-analysis of studies from Japan and Korea'
  found_in:
  - Gastric_Cancer_H_pylori_Associated-deep-research-falcon.md
  findings:
  - statement: 'Helicobacterpylori eradication following endoscopic resection might prevent metachronous gastric cancer: a systematic review and meta-analysis of studies from Japan and Korea'
    supporting_text: A systematic review and meta-analysis was performed to evaluate the preventive effectiveness of Helicobacter pylori eradication against metachronous gastric cancer (MGC) or dysplasia following endoscopic resection (ER) for early gastric cancer (EGC) or dysplasia.MethodsPubMed, Cochrane Library, MEDLINE, and EMBASE were searched until 31 October 2023, and randomized controlled trials or cohort studies were peer-reviewed.
    evidence:
    - reference: DOI:10.3389/fmed.2024.1393498
      reference_title: 'Helicobacterpylori eradication following endoscopic resection might prevent metachronous gastric cancer: a systematic review and meta-analysis of studies from Japan and Korea'
      supports: SUPPORT
      evidence_source: HUMAN_CLINICAL
      snippet: A systematic review and meta-analysis was performed to evaluate the preventive effectiveness of Helicobacter pylori eradication against metachronous gastric cancer (MGC) or dysplasia following endoscopic resection (ER) for early gastric cancer (EGC) or dysplasia.MethodsPubMed, Cochrane Library, MEDLINE, and EMBASE were searched until 31 October 2023, and randomized controlled trials or cohort studies were peer-reviewed.
      explanation: Deep research cited this publication as relevant literature for Gastric Cancer H pylori Associated.
- reference: DOI:10.3389/fmicb.2024.1395403
  title: 'The immunopathogenesis of Helicobacter pylori-induced gastric cancer: a narrative review'
  found_in:
  - Gastric_Cancer_H_pylori_Associated-deep-research-falcon.md
  findings:
  - statement: Helicobacter pylori infection is a well-established risk factor for the development of gastric cancer (GC).
    supporting_text: Helicobacter pylori infection is a well-established risk factor for the development of gastric cancer (GC).
    evidence:
    - reference: DOI:10.3389/fmicb.2024.1395403
      reference_title: 'The immunopathogenesis of Helicobacter pylori-induced gastric cancer: a narrative review'
      supports: SUPPORT
      evidence_source: HUMAN_CLINICAL
      snippet: Helicobacter pylori infection is a well-established risk factor for the development of gastric cancer (GC).
      explanation: Deep research cited this publication as relevant literature for Gastric Cancer H pylori Associated.
- reference: DOI:10.3389/fonc.2024.1468488
  title: 'Global, regional, and national trends in gastric cancer burden: 1990-2021 and projections to 2040'
  found_in:
  - Gastric_Cancer_H_pylori_Associated-deep-research-falcon.md
  findings:
  - statement: 'Global, regional, and national trends in gastric cancer burden: 1990-2021 and projections to 2040'
    supporting_text: 'Gastric cancer (GC) is a common malignancy of the digestive system, with significant geographical variation in its disease burden.MethodsThis study used data from the Global Burden of Diseases, Injuries, and Risk Factors Study 2021 to analyze three key indicators: incidence, mortality, and disability-adjusted life years (DALYs).'
    evidence:
    - reference: DOI:10.3389/fonc.2024.1468488
      reference_title: 'Global, regional, and national trends in gastric cancer burden: 1990-2021 and projections to 2040'
      supports: SUPPORT
      evidence_source: COMPUTATIONAL
      snippet: 'Gastric cancer (GC) is a common malignancy of the digestive system, with significant geographical variation in its disease burden.MethodsThis study used data from the Global Burden of Diseases, Injuries, and Risk Factors Study 2021 to analyze three key indicators: incidence, mortality, and disability-adjusted life years (DALYs).'
      explanation: Deep research cited this publication as relevant literature for Gastric Cancer H pylori Associated.
- reference: DOI:10.3390/cancers16111958
  title: 'Helicobacter pylori Infection in Patients with Gastric Cancer: A 2024 Update'
  found_in:
  - Gastric_Cancer_H_pylori_Associated-deep-research-falcon.md
  findings:
  - statement: Numerous studies have been performed on Helicobacter pylori infection because of the high death rate linked to this illness and gastric cancer.
    supporting_text: Numerous studies have been performed on Helicobacter pylori infection because of the high death rate linked to this illness and gastric cancer.
    evidence:
    - reference: DOI:10.3390/cancers16111958
      reference_title: 'Helicobacter pylori Infection in Patients with Gastric Cancer: A 2024 Update'
      supports: SUPPORT
      evidence_source: HUMAN_CLINICAL
      snippet: Numerous studies have been performed on Helicobacter pylori infection because of the high death rate linked to this illness and gastric cancer.
      explanation: Deep research cited this publication as relevant literature for Gastric Cancer H pylori Associated.
📚

References & Deep Research

References

13
DOI:10.1007/s11938-020-00298-8
Gastritis: An Update in 2020
1 finding
The gastritis constellation includes heterogeneous clinicopathological entities, among which long-standing, non-self-limiting gastritis, mainly due to Helicobacter pylori infection, has been epidemiologically, biologically, and clinically linked to gastric cancer development (i.e. “inflammation-associated cancer”).
"The gastritis constellation includes heterogeneous clinicopathological entities, among which long-standing, non-self-limiting gastritis, mainly due to Helicobacter pylori infection, has been epidemiologically, biologically, and clinically linked to gastric cancer development (i.e...."
Show evidence (1 reference)
DOI:10.1007/s11938-020-00298-8 SUPPORT Human Clinical
"The gastritis constellation includes heterogeneous clinicopathological entities, among which long-standing, non-self-limiting gastritis, mainly due to Helicobacter pylori infection, has been epidemiologically, biologically, and clinically linked to gastric cancer development (i.e...."
Deep research cited this publication as relevant literature for Gastric Cancer H pylori Associated.
DOI:10.1055/a-0859-1883
Management of epithelial precancerous conditions and lesions in the stomach (MAPS II): European Society of Gastrointestinal Endoscopy (ESGE), European Helicobacter and Microbiota Study Group (EHMSG), European Society of Pathology (ESP), and Sociedade Portuguesa de Endoscopia Digestiva (SPED) guideline update 2019
1 finding
Main RecommendationsPatients with chronic atrophic gastritis or intestinal metaplasia (IM) are at risk for gastric adenocarcinoma.
"Main RecommendationsPatients with chronic atrophic gastritis or intestinal metaplasia (IM) are at risk for gastric adenocarcinoma."
Show evidence (1 reference)
DOI:10.1055/a-0859-1883 SUPPORT Other
"Main RecommendationsPatients with chronic atrophic gastritis or intestinal metaplasia (IM) are at risk for gastric adenocarcinoma."
Deep research cited this publication as relevant literature for Gastric Cancer H pylori Associated.
DOI:10.1055/a-2529-5025
Management of epithelial precancerous conditions and early neoplasia of the stomach (MAPS III): European Society of Gastrointestinal Endoscopy (ESGE), European Helicobacter and Microbiota Study Group (EHMSG) and European Society of Pathology (ESP) Guideline update 2025
1 finding
Management of epithelial precancerous conditions and early neoplasia of the stomach (MAPS III): European Society of Gastrointestinal Endoscopy (ESGE), European Helicobacter and Microbiota Study Group (EHMSG) and European Society of Pathology (ESP) Guideline update 2025
"ESGE/EHMSG/ESP recommend that irrespective of country of origin, individual gastric risk assessment and stratification of precancerous conditions is recommended for first-time gastroscopy."
Show evidence (1 reference)
DOI:10.1055/a-2529-5025 SUPPORT Other
"ESGE/EHMSG/ESP recommend that irrespective of country of origin, individual gastric risk assessment and stratification of precancerous conditions is recommended for first-time gastroscopy."
Deep research cited this publication as relevant literature for Gastric Cancer H pylori Associated.
DOI:10.1055/a-2695-1376
Adherence to clinical practice guidelines for Management of epithelial precancerous conditions and lesions in the stomach in Europe
1 finding
The first international guideline for managing preneoplastic conditions of the stomach (MAPS I) was published in 2012, followed by an update (MAPS II) in 2019.
"The first international guideline for managing preneoplastic conditions of the stomach (MAPS I) was published in 2012, followed by an update (MAPS II) in 2019."
Show evidence (1 reference)
DOI:10.1055/a-2695-1376 SUPPORT Human Clinical
"The first international guideline for managing preneoplastic conditions of the stomach (MAPS I) was published in 2012, followed by an update (MAPS II) in 2019."
Deep research cited this publication as relevant literature for Gastric Cancer H pylori Associated.
DOI:10.1186/s12876-025-03886-z
The relationship between the eradication of Helicobacter pylori and the occurrence of stomach cancer: an updated meta-analysis and systemic review
1 finding
The relationship between the eradication of Helicobacter pylori and the occurrence of stomach cancer: an updated meta-analysis and systemic review
"The relationship between the eradication of Helicobacter pylori and the occurrence of stomach cancer: an updated meta-analysis and systemic review"
DOI:10.1186/s12916-024-03554-1
Overall and cause-specific mortality among patients diagnosed with gastric precancerous lesions in Sweden between 1979 and 2014: an observational cohort study
1 finding
The Correa’s cascade, encompassing chronic non-atrophic gastritis, atrophic gastritis, intestinal metaplasia, and dysplasia, represents the well-recognized pathway for the development of non-cardia gastric cancer.
"The Correa’s cascade, encompassing chronic non-atrophic gastritis, atrophic gastritis, intestinal metaplasia, and dysplasia, represents the well-recognized pathway for the development of non-cardia gastric cancer."
Show evidence (1 reference)
DOI:10.1186/s12916-024-03554-1 SUPPORT Human Clinical
"The Correa’s cascade, encompassing chronic non-atrophic gastritis, atrophic gastritis, intestinal metaplasia, and dysplasia, represents the well-recognized pathway for the development of non-cardia gastric cancer."
Deep research cited this publication as relevant literature for Gastric Cancer H pylori Associated.
DOI:10.1371/journal.pone.0307172
CagA toxin and risk of Helicobacter pylori-infected gastric phenotype: A meta-analysis of observational studies
1 finding
Helicobacter pylori (H. pylori) is frequently associated with non-cardia type gastric cancer, and it is designated as a group I carcinogen.
"Helicobacter pylori (H. pylori) is frequently associated with non-cardia type gastric cancer, and it is designated as a group I carcinogen."
Show evidence (1 reference)
DOI:10.1371/journal.pone.0307172 SUPPORT Human Clinical
"Helicobacter pylori (H. pylori) is frequently associated with non-cardia type gastric cancer, and it is designated as a group I carcinogen."
Deep research cited this publication as relevant literature for Gastric Cancer H pylori Associated.
DOI:10.20892/j.issn.2095-3941.2024.0159
Global, regional, and national burden of early-onset gastric cancer
1 finding
The burden of gastric cancer (GC) across different age groups needs updating.
"The burden of gastric cancer (GC) across different age groups needs updating."
Show evidence (1 reference)
DOI:10.20892/j.issn.2095-3941.2024.0159 SUPPORT Human Clinical
"The burden of gastric cancer (GC) across different age groups needs updating."
Deep research cited this publication as relevant literature for Gastric Cancer H pylori Associated.
DOI:10.21203/rs.3.rs-8058648/v1
Global epidemiology of gastric cancer in 2022 and projections for 2050: A comprehensive analysis and forecasts based on GLOBOCAN data
1 finding
Gastric cancer (GC) has greatly damaged the health of patients, and the burden exhibits substantial heterogeneity across diverse regions globally.
"Gastric cancer (GC) has greatly damaged the health of patients, and the burden exhibits substantial heterogeneity across diverse regions globally."
Show evidence (1 reference)
DOI:10.21203/rs.3.rs-8058648/v1 SUPPORT Human Clinical
"Gastric cancer (GC) has greatly damaged the health of patients, and the burden exhibits substantial heterogeneity across diverse regions globally."
Deep research cited this publication as relevant literature for Gastric Cancer H pylori Associated.
DOI:10.3389/fmed.2024.1393498
Helicobacterpylori eradication following endoscopic resection might prevent metachronous gastric cancer: a systematic review and meta-analysis of studies from Japan and Korea
1 finding
Helicobacterpylori eradication following endoscopic resection might prevent metachronous gastric cancer: a systematic review and meta-analysis of studies from Japan and Korea
"A systematic review and meta-analysis was performed to evaluate the preventive effectiveness of Helicobacter pylori eradication against metachronous gastric cancer (MGC) or dysplasia following endoscopic resection (ER) for early gastric cancer (EGC) or dysplasia.MethodsPubMed, Cochrane Library,..."
Show evidence (1 reference)
DOI:10.3389/fmed.2024.1393498 SUPPORT Human Clinical
"A systematic review and meta-analysis was performed to evaluate the preventive effectiveness of Helicobacter pylori eradication against metachronous gastric cancer (MGC) or dysplasia following endoscopic resection (ER) for early gastric cancer (EGC) or dysplasia.MethodsPubMed, Cochrane Library,..."
Deep research cited this publication as relevant literature for Gastric Cancer H pylori Associated.
DOI:10.3389/fmicb.2024.1395403
The immunopathogenesis of Helicobacter pylori-induced gastric cancer: a narrative review
1 finding
Helicobacter pylori infection is a well-established risk factor for the development of gastric cancer (GC).
"Helicobacter pylori infection is a well-established risk factor for the development of gastric cancer (GC)."
Show evidence (1 reference)
DOI:10.3389/fmicb.2024.1395403 SUPPORT Human Clinical
"Helicobacter pylori infection is a well-established risk factor for the development of gastric cancer (GC)."
Deep research cited this publication as relevant literature for Gastric Cancer H pylori Associated.
DOI:10.3389/fonc.2024.1468488
Global, regional, and national trends in gastric cancer burden: 1990-2021 and projections to 2040
1 finding
Global, regional, and national trends in gastric cancer burden: 1990-2021 and projections to 2040
"Gastric cancer (GC) is a common malignancy of the digestive system, with significant geographical variation in its disease burden.MethodsThis study used data from the Global Burden of Diseases, Injuries, and Risk Factors Study 2021 to analyze three key indicators: incidence, mortality, and..."
Show evidence (1 reference)
DOI:10.3389/fonc.2024.1468488 SUPPORT Computational
"Gastric cancer (GC) is a common malignancy of the digestive system, with significant geographical variation in its disease burden.MethodsThis study used data from the Global Burden of Diseases, Injuries, and Risk Factors Study 2021 to analyze three key indicators: incidence, mortality, and..."
Deep research cited this publication as relevant literature for Gastric Cancer H pylori Associated.
DOI:10.3390/cancers16111958
Helicobacter pylori Infection in Patients with Gastric Cancer: A 2024 Update
1 finding
Numerous studies have been performed on Helicobacter pylori infection because of the high death rate linked to this illness and gastric cancer.
"Numerous studies have been performed on Helicobacter pylori infection because of the high death rate linked to this illness and gastric cancer."
Show evidence (1 reference)
DOI:10.3390/cancers16111958 SUPPORT Human Clinical
"Numerous studies have been performed on Helicobacter pylori infection because of the high death rate linked to this illness and gastric cancer."
Deep research cited this publication as relevant literature for Gastric Cancer H pylori Associated.

Deep Research

1
Falcon ▸
Disease Characteristics Research Template
Edison Scientific Literature 40 citations 2026-05-08T16:51:35.317634

Question: You are an expert researcher providing comprehensive, well-cited information.

Provide detailed information focusing on: 1. Key concepts and definitions with current understanding 2. Recent developments and latest research (prioritize 2023-2024 sources) 3. Current applications and real-world implementations 4. Expert opinions and analysis from authoritative sources 5. Relevant statistics and data from recent studies

Format as a comprehensive research report with proper citations. Include URLs and publication dates where available. Always prioritize recent, authoritative sources and provide specific citations for all major claims.

Disease Characteristics Research Template

Target Disease

  • Disease Name: Gastric Cancer H. pylori Associated
  • MONDO ID: (if available)
  • Category:

Research Objectives

Please provide a comprehensive research report on Gastric Cancer H. pylori Associated covering all of the disease characteristics listed below. This report will be used to populate a disease knowledge base entry. Be thorough and cite primary literature (PMID preferred) for all claims.

For each section, suggested databases/resources are listed. These are the first places you should search for information on each topic.

1. Disease Information

Search first: OMIM, Orphanet, ICD-10/ICD-11, MeSH, PubMed

  • What is the disease? Provide a concise overview.
  • What are the key identifiers? (OMIM, Orphanet, ICD-10/ICD-11, MeSH, Mondo)
  • What are the common synonyms and alternative names?
  • Is the information derived from individual patients (e.g., EHR) or aggregated disease-level resources?

2. Etiology

  • Disease Causal Factors: What are the primary causes? (genetic, environmental, infectious, mechanistic)
  • Risk Factors:

    Search first: PubMed, Cochrane Library, UpToDate, clinical guidelines, ClinVar, ClinGen, GWAS Catalog, PheGenI, CTD, CDC, WHO, epidemiological databases

  • Genetic risk factors (causal variants, susceptibility loci, modifier genes)
  • Environmental risk factors (toxins, lifestyle, occupational exposures, age, sex, family history)
  • Protective Factors:

    Search first: PubMed, Cochrane Library, clinical trial databases, GWAS Catalog, gnomAD, WHO, CDC, nutrition databases

  • Genetic protective factors (protective variants, modifier alleles)
  • Environmental protective factors (diet, lifestyle, exposures that reduce risk)
  • Gene-Environment Interactions: How do genetic and environmental factors interact to influence disease?

    Search first: CTD, PubMed, PheGenI, GxE databases

3. Phenotypes

Search first: HPO (Human Phenotype Ontology), OMIM, Orphanet, PubMed, clinicaltrials.gov, MedDRA, SNOMED CT, DECIPHER, LOINC

For each phenotype, provide: - Phenotype type: symptoms, clinical signs, physical manifestations, behavioral changes, or laboratory abnormalities

For symptoms/signs: HPO, OMIM, Orphanet, PubMed For behavioral changes: HPO, DSM, RDoC (Research Domain Criteria), PubMed For laboratory abnormalities: LOINC, SNOMED CT, LabTests Online, PubMed - Phenotype characteristics: Search first: OMIM, Orphanet, HPO, PubMed - Age of symptom onset (neonatal, childhood, adult-onset, late-onset) - Symptom severity (mild, moderate, severe, variable) - Symptom progression (stable, progressive, episodic, fluctuating) - Frequency among affected individuals (percentage or qualitative) - Quality of life impact: Effects on daily functioning and well-being (per-phenotype when possible) Search first: EQ-5D database, SF-36, WHO QOL databases, PubMed - Suggest HPO (Human Phenotype Ontology) terms for each phenotype

4. Genetic/Molecular Information

  • Causal Genes: Gene mutations or chromosomal abnormalities responsible for disease (gene symbols, OMIM IDs)

    Search first: OMIM, ClinVar, HGMD, Ensembl, NCBI Gene

  • Pathogenic Variants:
  • Affected genes (gene symbols, HGNC IDs) > Search first: OMIM, NCBI Gene, Ensembl, HGNC, UniProt, GeneCards
  • Variant classification (pathogenic, likely pathogenic, VUS per ACMG/AMP guidelines) > Search first: ClinVar, ClinGen, ACMG/AMP guidelines, VarSome
  • Variant type/class (missense, frameshift, nonsense, splice-site, structural)
  • Allele frequency in population databases > Search first: gnomAD, 1000 Genomes, ExAC, TOPMed, dbSNP
  • Somatic vs germline origin > Search first: COSMIC (somatic), ClinVar, ICGC, TCGA
  • Functional consequences (loss of function, gain of function, dominant negative)
  • Modifier Genes: Genes that modify disease severity or expression
  • Epigenetic Information: DNA methylation, histone modifications, chromatin changes affecting disease

    Search first: ENCODE, Roadmap Epigenomics, MethBase, DiseaseMeth

  • Chromosomal Abnormalities: Large-scale genetic changes (aneuploidy, translocations, inversions)

    Search first: DECIPHER, ClinVar, ECARUCA, UCSC Genome Browser

5. Environmental Information

  • Environmental Factors: Non-genetic contributing factors (toxins, radiation, pollution, occupational exposure)

    Search first: CTD (Comparative Toxicogenomics Database), TOXNET, PubMed, EPA databases

  • Lifestyle Factors: Behavioral factors (smoking, diet, exercise, alcohol consumption)

    Search first: CDC databases, WHO, PubMed, NHANES

  • Infectious Agents: If applicable, pathogens causing or triggering disease (bacteria, viruses, fungi, parasites)

    Search first: NCBI Taxonomy, ViPR, BV-BRC, MicrobeDB, GIDEON

6. Mechanism / Pathophysiology

  • Molecular Pathways: Specific signaling cascades or biochemical pathways involved (Wnt, MAPK, mTOR, PI3K-AKT, etc.)

    Search first: KEGG, Reactome, WikiPathways, PathBank, BioCyc

  • Cellular Processes: Cell-level mechanisms (apoptosis, autophagy, cell cycle dysregulation, inflammation, etc.)

    Search first: Gene Ontology (GO), Reactome, KEGG, PubMed

  • Protein Dysfunction: How protein structure or function is altered (misfolding, aggregation, loss of function, gain of function)

    Search first: UniProt, PDB (Protein Data Bank), InterPro, Pfam, AlphaFold

  • Metabolic Changes: Alterations in metabolic processes (energy metabolism, lipid metabolism, amino acid metabolism)

    Search first: KEGG, BioCyc, HMDB (Human Metabolome Database), BRENDA

  • Immune System Involvement: Role of immune response (autoimmunity, immunodeficiency, chronic inflammation)

    Search first: ImmPort, Immunome Database, IEDB, Gene Ontology

  • Tissue Damage Mechanisms: How tissues/ are injured (oxidative stress, ischemia, fibrosis, necrosis)

    Search first: PubMed, Gene Ontology, Reactome

  • Biochemical Abnormalities: Specific molecular defects (enzyme deficiencies, receptor dysfunction, ion channel defects)

    Search first: BRENDA, UniProt, KEGG, OMIM, PubMed

  • Epigenetic Changes: DNA methylation, histone modifications affecting gene expression in disease

    Search first: ENCODE, Roadmap Epigenomics, MethBase, DiseaseMeth

  • Molecular Profiling (if available):
  • Transcriptomics/gene expression changes > Search first: GEO (Gene Expression Omnibus), ArrayExpress, GTEx, Human Cell Atlas, SRA
  • Proteomics findings > Search first: PRIDE, ProteomeXchange, Human Protein Atlas, STRING, BioGRID
  • Metabolomics signatures > Search first: MetaboLights, Metabolomics Workbench, HMDB, METLIN
  • Lipidomics alterations > Search first: LIPID MAPS, SwissLipids, LipidHome, Metabolomics Workbench
  • Genomic structural features > Search first: UCSC Genome Browser, Ensembl, NCBI, dbVar, DGV
  • Advanced Technologies (if applicable):
  • Single-cell analysis findings (cell-type specific mechanisms, cellular heterogeneity) > Search first: Human Cell Atlas, Single Cell Portal, GEO, CELLxGENE
  • Spatial transcriptomics findings > Search first: GEO, Spatial Research, Vizgen, 10x Genomics data
  • Multi-omics integration results > Search first: TCGA, ICGC, cBioPortal, LinkedOmics, PubMed
  • Functional genomics screens (CRISPR, RNAi) > Search first: DepMap, GenomeRNAi, PubMed, BioGRID ORCS

For each mechanism, describe: - The causal chain from initial trigger to clinical manifestation - Which mechanisms are upstream vs downstream - What cell types and biological processes are involved - Suggest GO terms for biological processes and CL terms for cell types

7. Anatomical Structures Affected

  • Organ Level:
  • Primary organs directly affected
  • Secondary organ involvement (complications, secondary effects)
  • Body systems involved (cardiovascular, nervous, digestive, respiratory, endocrine, etc.)

    Search first: Uberon, FMA (Foundational Model of Anatomy), OMIM, HPO, ICD-11, MeSH, SNOMED CT

  • Tissue and Cell Level:
  • Specific tissue types affected (epithelial, connective, muscle, nervous)
  • Specific cell populations targeted (with Cell Ontology terms)

    Search first: Uberon, Human Protein Atlas, Cell Ontology, Human Cell Atlas, CellMarker, PanglaoDB

  • Subcellular Level:
  • Cellular compartments involved (mitochondria, nucleus, ER, lysosomes) (with GO Cellular Component terms)

    Search first: Gene Ontology (Cellular Component), UniProt, Human Protein Atlas

  • Localization:
  • Specific anatomical sites (with UBERON terms) > Search first: FMA, Uberon, NeuroNames (for brain), SNOMED CT
  • Lateralization (unilateral, bilateral, asymmetric) > Search first: HPO, clinical literature, imaging databases

8. Temporal Development

  • Onset:
  • Typical age of onset (congenital, pediatric, adult, geriatric)
  • Onset pattern (acute, subacute, chronic, insidious)

    Search first: OMIM, Orphanet, HPO, PubMed

  • Progression:
  • Disease stages (early, intermediate, advanced, end-stage) > Search first: Cancer Staging Manual (AJCC), WHO classifications, PubMed
  • Progression rate (rapid, slow, variable)
  • Disease course pattern (episodic, relapsing-remitting, progressive, stable)
  • Disease duration (self-limited, chronic lifelong)

    Search first: Disease registries, longitudinal cohort databases, natural history studies, PubMed, Orphanet, OMIM

  • Patterns:
  • Remission patterns (spontaneous, treatment-induced) > Search first: Clinical trial databases, disease registries, PubMed
  • Critical periods (time windows of vulnerability or opportunity for intervention) > Search first: PubMed, developmental biology databases, clinical guidelines

9. Inheritance and Population

  • Epidemiology:
  • Prevalence (cases per 100,000 at given time)
  • Incidence (new cases per 100,000 per year)

    Search first: Orphanet, CDC, WHO, GBD (Global Burden of Disease), national registries, SEER, disease registries

  • For Genetic Etiology:
  • Inheritance pattern (AD, AR, X-linked, mitochondrial, multifactorial, polygenic) > Search first: OMIM, Orphanet, ClinVar, GTR (Genetic Testing Registry)
  • Penetrance (complete, incomplete, age-dependent) > Search first: ClinVar, OMIM, PubMed, ClinGen
  • Expressivity (variable, consistent) > Search first: OMIM, ClinVar, PubMed
  • Genetic anticipation (increasing severity in successive generations) > Search first: OMIM, PubMed (especially for repeat expansion disorders)
  • Germline mosaicism > Search first: ClinVar, OMIM, genetic counseling literature, PubMed
  • Founder effects (population-specific mutations) > Search first: gnomAD, population genetics databases, PubMed
  • Consanguinity role > Search first: OMIM, population studies, genetic counseling resources
  • Carrier frequency > Search first: gnomAD, carrier screening databases, GeneReviews, GTR
  • Population Demographics:
  • Affected populations (ethnic or demographic groups with higher prevalence) > Search first: gnomAD, 1000 Genomes, PAGE Study, PubMed, population registries
  • Geographic distribution (endemic areas, regional variation) > Search first: WHO, CDC, GBD, Orphanet, geographic epidemiology databases
  • Geographic distribution of specific variants
  • Sex ratio (male:female) > Search first: Disease registries, OMIM, PubMed, epidemiological databases
  • Age distribution of affected individuals > Search first: CDC, disease registries, SEER, Orphanet

10. Diagnostics

  • Clinical Tests:
  • Laboratory tests (blood, urine, tissue chemistry, specific enzyme assays) > Search first: LOINC, LabTests Online, PubMed
  • Biomarkers (proteins, metabolites, genetic markers, circulating biomarkers) > Search first: FDA Biomarker List, BEST (Biomarkers, EndpointS, and other Tools), PubMed
  • Imaging studies (X-ray, CT, MRI, PET, ultrasound) > Search first: RadLex, DICOM, Radiopaedia, imaging databases
  • Functional tests (pulmonary function, cardiac stress tests) > Search first: LOINC, clinical guidelines, PubMed
  • Electrophysiology (EEG, EMG, ECG, nerve conduction studies) > Search first: LOINC, clinical neurophysiology databases, PubMed
  • Biopsy findings (histopathology, immunohistochemistry) > Search first: SNOMED CT, College of American Pathologists resources, PubMed
  • Pathology findings (microscopic examination) > Search first: SNOMED CT, Digital Pathology databases, PubMed
  • Genetic Testing:

    Search first: GTR (Genetic Testing Registry), GeneReviews, ClinGen

  • Overview of recommended genetic testing approach
  • Whole genome sequencing (WGS) utility > Search first: GTR, ClinVar, GEL (Genomics England), gnomAD
  • Whole exome sequencing (WES) utility > Search first: GTR, ClinVar, OMIM, GeneMatcher
  • Gene panels (which panels, which genes) > Search first: GTR, ClinVar, laboratory-specific databases
  • Single gene testing > Search first: GTR, ClinVar, OMIM, GeneReviews
  • Chromosomal microarray (CMA) > Search first: DECIPHER, ClinVar, dbVar, ECARUCA
  • Karyotyping > Search first: Chromosome Abnormality Database, ClinVar, cytogenetics resources
  • FISH > Search first: ClinVar, cytogenetics databases, PubMed
  • Mitochondrial DNA testing > Search first: MITOMAP, MSeqDR, ClinVar, GTR
  • Repeat expansion testing > Search first: GTR, ClinVar, repeat expansion databases, PubMed
  • Omics-Based Diagnostics (if applicable):
  • RNA sequencing / transcriptomics > Search first: GEO, ArrayExpress, GTEx, RNA-seq databases
  • Proteomics > Search first: PRIDE, ProteomeXchange, FDA Biomarker database
  • Metabolomics > Search first: MetaboLights, Metabolomics Workbench, HMDB
  • Epigenomics > Search first: GEO, ENCODE, Roadmap Epigenomics, MethBase
  • Liquid biopsy > Search first: COSMIC, ClinVar, liquid biopsy databases, PubMed
  • Clinical Criteria:
  • Standardized diagnostic criteria (DSM, ICD, society guidelines) > Search first: DSM-5, ICD-11, clinical society guidelines, UpToDate
  • Differential diagnosis (other conditions to rule out, with distinguishing features) > Search first: DynaMed, UpToDate, clinical decision support systems
  • Screening:
  • Screening methods for asymptomatic individuals (newborn screening, carrier screening, cascade screening) > Search first: ACMG recommendations, CDC newborn screening, GTR

11. Outcome/Prognosis

  • Survival and Mortality:
  • Survival rate (5-year, 10-year, overall) > Search first: SEER, cancer registries, disease-specific registries, PubMed
  • Life expectancy (with and without treatment if applicable) > Search first: Orphanet, disease registries, actuarial databases, PubMed
  • Mortality rate > Search first: CDC, WHO, GBD, national mortality databases
  • Disease-specific mortality (deaths directly attributable to disease) > Search first: Disease registries, CDC Wonder, GBD, PubMed
  • Morbidity and Function:
  • Morbidity (disease-related disability and health impacts) > Search first: GBD, WHO, disability databases, PubMed
  • Disability outcomes (long-term functional impairments) > Search first: ICF (International Classification of Functioning), disability registries
  • Quality of life measures (EQ-5D, SF-36, PROMIS, disease-specific tools) > Search first: EQ-5D database, SF-36, PROMIS, PubMed
  • Disease Course:
  • Complications (secondary problems: infections, organ failure, etc.) > Search first: ICD codes, disease registries, clinical databases, PubMed
  • Recovery potential (likelihood and extent of recovery, with vs without treatment) > Search first: Natural history studies, rehabilitation databases, PubMed
  • Prediction:
  • Prognostic factors (age, disease severity, biomarkers, treatment response) > Search first: Prognostic models databases, clinical calculators, PubMed
  • Prognostic biomarkers (molecular markers predicting disease course) > Search first: FDA Biomarker database, PubMed, cancer prognostic databases

12. Treatment

  • Pharmacotherapy:
  • Pharmacological treatments (drug names, drug classes, mechanisms of action) > Search first: DrugBank, RxNorm, ATC classification, DailyMed, FDA databases
  • Pharmacogenomics (how genetic variants affect drug metabolism, efficacy, toxicity) > Search first: PharmGKB, CPIC (Clinical Pharmacogenetics), FDA Table of PGx Biomarkers
  • Advanced Therapeutics:
  • Gene therapy (viral vectors, CRISPR, gene replacement, gene editing) > Search first: ClinicalTrials.gov, FDA gene therapy database, ASGCT resources
  • Cell therapy (stem cell transplant, CAR-T, cellular therapeutics) > Search first: ClinicalTrials.gov, FDA cell therapy database, FACT standards
  • RNA-based therapies (ASOs, siRNA, mRNA therapies) > Search first: ClinicalTrials.gov, FDA approvals, PubMed
  • Targeted therapies (treatments directed at specific molecular targets) > Search first: My Cancer Genome, OncoKB, ClinicalTrials.gov, FDA approvals
  • Immunotherapies (checkpoint inhibitors, monoclonal antibodies) > Search first: Cancer Immunotherapy Database, FDA approvals, ClinicalTrials.gov
  • Surgical and Interventional:
  • Surgical interventions (types of surgery, timing, outcomes) > Search first: CPT codes, surgical registries, clinical guidelines, PubMed
  • Supportive and Rehabilitative:
  • Supportive care (symptom management, pain control, nutrition) > Search first: Clinical guidelines, Cochrane Library, PubMed
  • Rehabilitation (physical therapy, occupational therapy, speech therapy) > Search first: Rehabilitation medicine databases, clinical guidelines, PubMed
  • Experimental:
  • Experimental treatments in clinical trials (with NCT identifiers if available) > Search first: ClinicalTrials.gov, EU Clinical Trials Register, WHO ICTRP
  • Treatment Outcomes:
  • Treatment response rates > Search first: Clinical trial databases, FDA reviews, systematic reviews, PubMed
  • Side effects and adverse events > Search first: FDA Adverse Event Reporting System (FAERS), MedWatch, PubMed
  • Treatment Strategy:
  • Treatment algorithms (clinical pathways, decision trees) > Search first: Clinical practice guidelines, NCCN Guidelines, UpToDate
  • Combination therapies > Search first: ClinicalTrials.gov, treatment guidelines, PubMed
  • Personalized medicine approaches (genotype-guided treatment) > Search first: My Cancer Genome, CIViC, PharmGKB, precision medicine databases

For each treatment, suggest MAXO (Medical Action Ontology) terms where applicable.

13. Prevention

  • Prevention Levels:
  • Primary prevention (preventing disease occurrence: vaccination, risk factor modification) > Search first: CDC, WHO, USPSTF recommendations, Cochrane Library
  • Secondary prevention (early detection and treatment: screening programs, early intervention) > Search first: USPSTF, CDC screening guidelines, WHO
  • Tertiary prevention (preventing complications in those with disease) > Search first: Clinical guidelines, disease management protocols, PubMed
  • Immunization: Vaccine strategies (if applicable)

    Search first: CDC vaccine schedules, WHO immunization, FDA vaccine database

  • Screening and Early Detection:
  • Screening programs (population-based: newborn screening, cancer screening) > Search first: CDC screening programs, USPSTF, cancer screening databases
  • Genetic screening (carrier screening, preimplantation genetic diagnosis, prenatal testing) > Search first: ACMG recommendations, ACOG guidelines, GTR
  • Risk stratification (identifying high-risk individuals for targeted prevention) > Search first: Risk prediction models, clinical calculators, PubMed
  • Behavioral Interventions: Lifestyle modifications to reduce risk

    Search first: CDC, WHO, behavioral intervention databases, Cochrane Library

  • Counseling: Genetic counseling (risk assessment, family planning guidance)

    Search first: NSGC resources, ACMG guidelines, GeneReviews

  • Public Health:
  • Public health interventions (sanitation, vector control, health education) > Search first: CDC, WHO, public health databases, PubMed
  • Environmental interventions (reducing environmental risk factors) > Search first: EPA databases, WHO environmental health, PubMed
  • Prophylaxis: Preventive medications or procedures

    Search first: Clinical guidelines, FDA approvals, PubMed

14. Other Species / Natural Disease

  • Taxonomy: Species affected (with NCBI Taxon identifiers)

    Search first: NCBI Taxonomy

  • Breed: Specific breeds affected (with VBO identifiers if applicable)

    Search first: VBO (Vertebrate Breed Ontology)

  • Gene: Orthologous genes in other species (with NCBI Gene IDs)

    Search first: NCBI Gene

  • Natural Disease:
  • Naturally occurring disease in other species (companion animals, wildlife) > Search first: OMIA (Online Mendelian Inheritance in Animals), VetCompass, PubMed
  • Veterinary relevance and importance in animal health > Search first: OMIA, veterinary databases, PubMed
  • Comparative Biology:
  • Comparative pathology (similarities and differences across species) > Search first: OMIA, comparative pathology databases, PubMed
  • Evolutionary conservation of disease mechanisms > Search first: HomoloGene, OrthoMCL, Alliance of Genome Resources
  • Transmission (if applicable):
  • Zoonotic potential > Search first: CDC zoonotic diseases, WHO zoonoses, GIDEON
  • Cross-species susceptibility > Search first: NCBI Taxonomy, veterinary databases, PubMed

15. Model Organisms

  • Model Types:
  • Model organism type (mammalian, invertebrate, cellular, in vitro) > Search first: Alliance of Genome Resources, model organism databases
  • Specific model systems (mouse, rat, zebrafish, Drosophila, C. elegans, yeast, cell lines, organoids, iPSCs) > Search first: MGI, RGD, ZFIN, FlyBase, WormBase, SGD, ATCC, Cellosaurus
  • Induced models (drug treatment, surgical intervention, environmental manipulation) > Search first: MGI, model organism databases, PubMed
  • Genetic Models:
  • Types available (knockout, knock-in, transgenic, conditional, humanized) > Search first: MGI, IMPC, KOMP, EuMMCR, IMSR
  • Model Characteristics:
  • Phenotype recapitulation (how well model reproduces human disease features) > Search first: Model organism databases, comparative studies, PubMed
  • Model limitations (aspects of human disease not captured) > Search first: Model organism databases, PubMed, review articles
  • Applications:
  • Research applications (what aspects of disease can be studied) > Search first: Model organism databases, PubMed
  • Resources:
  • Model databases > Search first: MGI, RGD, ZFIN, FlyBase, WormBase, IMSR, EMMA, MMRRC

Citation Requirements

  • Cite primary literature (PMID preferred) for all mechanistic and clinical claims
  • Prioritize recent reviews and landmark papers
  • Include direct quotes from abstracts where possible to support key statements
  • Distinguish evidence source types: human clinical, model organism, in vitro, computational

Output Format

Structure your response as a comprehensive narrative organized by the sections above. For each section, provide: - Factual content with specific details (numbers, percentages, gene names, variant nomenclature) - Ontology term suggestions (HPO, GO, CL, UBERON, CHEBI, MAXO, MONDO) where applicable - Evidence citations with PMIDs - Direct quotes from abstracts to support key claims - Clear indication when information is not available or not applicable for this disease

This report will be used to populate a disease knowledge base entry with: - Pathophysiology descriptions with causal chains - Gene/protein annotations (HGNC, GO terms) - Phenotype associations (HP terms) with frequencies - Cell type involvement (CL terms) - Anatomical locations (UBERON terms) - Chemical entities (CHEBI terms) - Treatment annotations (MAXO terms) - Evidence items with PMIDs and exact abstract quotes - Epidemiology, prognosis, diagnostic, and prevention information - Animal model descriptions with phenotype recapitulation details

Comprehensive Research Report: Helicobacter pylori–Associated Gastric Cancer

Target disease

  • Disease name: Gastric cancer, H. pylori associated (primarily non-cardia gastric adenocarcinoma developing in the setting of chronic Helicobacter pylori infection) (shirani2024theimmunopathogenesisof pages 1-2, burz2024helicobacterpyloriinfection pages 1-2).
  • Category: Infection-associated malignancy (bacterial carcinogen-associated), digestive system cancer (stomach).
  • MONDO ID / MeSH / ICD-10/ICD-11: Not retrievable from the provided tool evidence. The retrieved texts mention that H. pylori infection is recognized in ICD-11 contexts, but the specific ICD-11 entity code(s) for “H. pylori–associated gastric cancer” were not extractable from the available excerpts (rugge2020gastritisanupdate pages 1-4, burz2024helicobacterpyloriinfection pages 1-2).
  • Common synonyms / alternative names (used in practice/literature):
  • H. pylori–associated gastric cancer; Helicobacter pylori–associated gastric adenocarcinoma (shirani2024theimmunopathogenesisof pages 1-2)
  • Infection-associated gastric cancer; inflammation-associated gastric cancer (conceptual framing) (rugge2020gastritisanupdate pages 1-4)
  • Non-cardia gastric cancer arising via the Correa cascade (sun2024overallandcausespecific pages 1-2)
  • Evidence source type in this report: Primarily aggregated evidence (systematic reviews/meta-analyses, guidelines, large registry/GBD studies), plus large human cohort data; limited mechanistic inference from narrative reviews. No EHR-level patient records were used.

1. Disease information (overview and current understanding)

What is the disease?

H. pylori–associated gastric cancer refers to gastric carcinoma—most often non-cardia gastric adenocarcinoma—arising as a long-term consequence of chronic gastric colonization by Helicobacter pylori and the resulting chronic inflammation and mucosal remodeling. Contemporary reviews emphasize that carcinogenesis typically follows a multistep mucosal progression (often termed the Correa cascade) from chronic gastritis to atrophy, intestinal metaplasia, dysplasia, and eventually invasive cancer (sun2024overallandcausespecific pages 1-2, areiaUnknownyeargastricprecancerousconditions pages 1-3).

Key concept definitions

  • Correa cascade (intestinal-type, non-cardia pathway): A stepwise histopathologic sequence from chronic gastritis → atrophic gastritis → intestinal metaplasia → dysplasia → non-cardia gastric cancer (sun2024overallandcausespecific pages 1-2).
  • Precancerous conditions: Chronic atrophic gastritis and gastric intestinal metaplasia are repeatedly identified as the principal gastric precancerous states requiring risk stratification and (in selected patients) endoscopic surveillance (pimentelnunes2019managementofepithelial pages 5-6, rugge2020gastritisanupdate pages 1-4).
  • OLGA/OLGIM: Histology-based staging systems used to grade risk based on extent/severity of atrophy (OLGA) and intestinal metaplasia (OLGIM); advanced stages (III/IV) are used in guidelines to define higher-risk strata and surveillance needs (pimentelnunes2019managementofepithelial pages 13-14, pimentelnunes2019managementofepithelial pages 5-6).

2. Etiology

Primary causal factor (infectious)

  • H. pylori infection is repeatedly described as a major etiologic driver of gastric carcinogenesis, with emphasis on chronic inflammation and bacterial virulence determinants (shirani2024theimmunopathogenesisof pages 1-2, burz2024helicobacterpyloriinfection pages 1-2).

Bacterial (pathogen) risk determinants

  • CagA/T4SS (cag pathogenicity island): A 2024 meta-analysis notes that CagA is delivered into host cells by a type IV secretion system (T4SS) “needle-like pilus” mechanism, supporting its role as a virulence effector associated with more severe gastric inflammation and carcinogenesis (naing2024cagatoxinand pages 1-2).
  • Quantified association (CagA positivity): In observational studies across Indo-Pacific countries, pooled CagA positivity among H. pylori–infected gastric disorders was 83%, and CagA positivity was associated with higher odds of gastric cancer vs gastritis (OR 2.53, 95% CI 1.15–5.55) (Naing et al., PLOS ONE, published Aug 2024; DOI: https://doi.org/10.1371/journal.pone.0307172) (naing2024cagatoxinand pages 1-2).
  • Other virulence factors frequently highlighted in recent reviews: VacA, BabA, SabA, OipA, urease, flagella-mediated motility—important for colonization, persistence, and host pathway perturbation (shirani2024theimmunopathogenesisof pages 1-2).

Host and environmental risk modifiers (gene–environment and environment)

  • The available evidence in this run supports that risk is modulated by population and environmental context (e.g., socioeconomic factors/crowding linked to higher infection prevalence and non-cardia cancer association) (burz2024helicobacterpyloriinfection pages 1-2).
  • Environmental/lifestyle co-factors (not exhaustively quantified in the provided excerpts) are noted as contributors in reviews: smoking, diet, obesity and other exposures (burz2024helicobacterpyloriinfection pages 1-2).

Protective factors

  • Eradication of H. pylori is the most consistently supported protective intervention, with randomized trial evidence summarized in meta-analyses showing reduced gastric cancer incidence (wu2025therelationshipbetween pages 1-2).

Gene–environment interactions

  • Mechanistic and immune-pathway reviews emphasize an interaction among bacterial virulence programs, host innate/adaptive immune responses (TLRs/cytokines), and downstream epithelial genetic/epigenetic alterations (shirani2024theimmunopathogenesisof pages 1-2). Specific human susceptibility loci were not extractable from the provided excerpts.

3. Phenotypes (clinical presentation and natural history)

Natural history and phenotypic sequence

  • Correa cascade and its clinical significance: A large population-based Swedish cohort study explicitly frames Correa’s cascade as “chronic non-atrophic gastritis, atrophic gastritis, intestinal metaplasia, and dysplasia” as the “well-recognized pathway for the development of non-cardia gastric cancer” (Sun et al., BMC Medicine, Aug 2024; DOI: https://doi.org/10.1186/s12916-024-03554-1) (sun2024overallandcausespecific pages 1-2).
  • Mortality gradient across lesions: In that cohort (306,117 patients; ~3.0 million person-years), gastric cancer mortality increased stepwise along the cascade, with “excess risk rising from 105% for patients with chronic gastritis to more than 600% for the dysplasia group” (sun2024overallandcausespecific pages 1-2).
  • Clinical implication (secondary prevention): The authors conclude that “early recognition and intervention of gastric precancerous lesions probably benefit the patients” (sun2024overallandcausespecific pages 1-2).

Suggested HPO terms (for KB population)

Because the report is for a disease KB entry, below are suggested phenotype mappings commonly relevant to gastric cancer and/or the precancerous stages; the provided excerpts do not quantify symptom frequencies: - Epigastric pain (HP:0033052) - Dyspepsia (HP:0100544) - Nausea (HP:0002018) - Vomiting (HP:0002013) - Weight loss (HP:0001824) - Anemia (HP:0001903) (often in malignancy/bleeding; not quantified here) - Gastrointestinal bleeding (HP:0002239) / Melena (HP:0002249) (context-dependent) - Gastritis (histologic/clinical) (can be represented via relevant ontologies; HPO has “Gastritis” HP:0002032) - Intestinal metaplasia (may be represented via pathology ontologies; HPO has limited granularity for histology)

Staging frameworks to reference

  • Correa cascade (histopathologic)
  • OLGA/OLGIM (risk staging) (pimentelnunes2019managementofepithelial pages 13-14)
  • Dysplasia grading (low-grade vs high-grade) for management decisions (pimentelnunes2019managementofepithelial pages 10-11)

4. Genetic / molecular information

Mechanism/pathophysiology: causal chain (infection → cancer)

A 2024 immunopathogenesis review describes a multi-component cascade involving bacterial colonization factors, virulence determinants, chronic immune activation, and downstream epithelial remodeling/genomic/epigenomic change (shirani2024theimmunopathogenesisof pages 1-2): 1. Colonization & persistence: Motility, urease-mediated acid adaptation, and adhesins (e.g., BabA/SabA) support stable mucosal colonization (shirani2024theimmunopathogenesisof pages 1-2). 2. Delivery of oncogenic/inflammatory effectors: CagA is injected into host cells via T4SS, and CagA-positive strains are linked to more severe inflammation (naing2024cagatoxinand pages 1-2). 3. Chronic inflammation and immune dysregulation: Reviews emphasize innate/adaptive signaling, including TLRs and cytokines, as central mediators that sustain tissue injury and pro-tumor microenvironments (shirani2024theimmunopathogenesisof pages 1-2). 4. Tissue remodeling and precancerous lesion formation: Development of atrophic gastritis and intestinal metaplasia creates a “field” permissive for neoplasia; advanced atrophy/metaplasia stages define higher-risk states for surveillance (pimentelnunes2019managementofepithelial pages 5-6, rugge2020gastritisanupdate pages 1-4). 5. Genetic/epigenetic alteration accumulation: The immunopathogenesis review highlights “abnormal DNA methylation” and mutation accumulation in carcinogenesis/field cancerization (shirani2024theimmunopathogenesisof pages 1-2).

Pathways and ontology suggestions (for annotation)

Given the evidence emphasizes inflammation, innate recognition, cytokines, and epithelial remodeling, plausible GO Biological Process targets for annotation include: - Inflammatory response (GO:0006954) - Innate immune response (GO:0045087) - Toll-like receptor signaling pathway (e.g., GO:0002224) - Cytokine-mediated signaling pathway (GO:0019221) - Regulation of epithelial cell proliferation (GO:0050673) - DNA methylation (GO:0006306)

Cell Ontology (CL) suggestions (prominent in gastric mucosa inflammation/carcinogenesis): - Gastric epithelial cell (context-specific CL term) - Macrophage (CL:0000235) - T cell (CL:0000084) - B cell (CL:0000236)

Anatomy (UBERON) suggestions: - Stomach (UBERON:0000945) - Gastric mucosa (UBERON:0001199) - Gastric antrum (UBERON:0001165) - Gastric body/corpus (UBERON:0001163)

Causal genes / pathogenic variants (host)

Specific germline causal genes/variants for “H. pylori–associated gastric cancer” were not extractable from the provided excerpts, which focus on infection-driven carcinogenesis and population risk stratification.

5. Environmental information

  • Socioeconomic/environmental context: A 2024 review notes higher H. pylori prevalence in crowded/low-socioeconomic settings and links this context particularly to non-cardia gastric cancer risk (burz2024helicobacterpyloriinfection pages 1-2).

6. Mechanism / pathophysiology (expanded)

Immune involvement

A 2024 narrative review frames immunopathogenesis as involving bacterial virulence determinants (CagA, VacA, BabA, SabA), TLRs, cytokines, and immune evasion mechanisms as key contributors to chronicity and carcinogenesis (Frontiers in Microbiology, Jul 2024; DOI: https://doi.org/10.3389/fmicb.2024.1395403) (shirani2024theimmunopathogenesisof pages 1-2).

Epigenetics

The same review highlights epigenetic alterations—particularly abnormal DNA methylation—as part of the progression toward malignant transformation (shirani2024theimmunopathogenesisof pages 1-2).

7. Anatomical structures affected

  • Primary organ: Stomach (UBERON:0000945), with emphasis on gastric mucosa and the antrum/corpus compartments for biopsy-based risk staging (pimentelnunes2019managementofepithelial pages 5-6, dinisribeiro2025managementofepithelial pages 6-7).
  • Disease localization: The Correa cascade is explicitly described as the pathway to non-cardia gastric cancer (sun2024overallandcausespecific pages 1-2).

8. Temporal development

  • Onset pattern: Chronic, often acquired earlier in life and progressing over decades to precancerous lesions and cancer in a minority of infected individuals; the provided evidence emphasizes multiyear/decade progression rather than acute onset (sun2024overallandcausespecific pages 1-2, areiaUnknownyeargastricprecancerousconditions pages 1-3).
  • Critical periods / intervention window: Reviews describe a practical “point of no return,” emphasizing that earlier eradication is more likely to prevent irreversible precancerous change (burz2024helicobacterpyloriinfection pages 1-2).

9. Inheritance and population

Epidemiology (recent quantitative data)

  • Global burden (GBD 2021, reported in 2024 analysis): In 2021 there were 1.23 million new gastric cancer cases and 0.95 million deaths globally, with 22.79 million DALYs (Zhang et al., Frontiers in Oncology, Dec 2024; DOI: https://doi.org/10.3389/fonc.2024.1468488) (zhang2024globalregionaland pages 1-2).
  • Sex disparity: Age-standardized rates in 2021 were substantially higher in men (ASIR 20.9/100,000) than women (ASIR 8.6/100,000) (zhang2024globalregionaland pages 1-2).
  • GLOBOCAN 2022 (reported in 2024 early-onset burden paper): Estimated 968,000 new cases and 660,000 deaths in 2022; East Asia contributed 53.8% of cases and 48.2% of deaths (Tan et al., Cancer Biology & Medicine, Aug 2024; DOI: https://doi.org/10.20892/j.issn.2095-3941.2024.0159) (tan2024globalregionaland pages 1-2).

Infection prevalence context

A 2024 review reiterates global H. pylori infection prevalence as ~50% (“Nearly 50% of the global population is infected”) (Burz et al., Cancers, May 2024; DOI: https://doi.org/10.3390/cancers16111958) (burz2024helicobacterpyloriinfection pages 1-2).

10. Diagnostics

Diagnosis of H. pylori (relevant to cancer prevention)

The MAPS III guideline update emphasizes that first-time diagnostic endoscopy should include gastric biopsies for H. pylori diagnosis and for identification/stratification of advanced atrophic gastritis (dinisribeiro2025managementofepithelial pages 6-7).

Biomarkers / risk stratification tests

  • Pepsinogen (PG I and PG I/II ratio): MAPS II summarizes that serum pepsinogen testing is among the best-evaluated non-invasive options to detect advanced atrophic gastritis; low PG I and low PG I/II ratio are discussed as thresholds from meta-analytic evaluations, and low PG I (especially with H. pylori serology negative) may identify individuals who should be offered endoscopy (pimentelnunes2019managementofepithelial pages 10-11).

Endoscopic biopsy protocols (guideline-based)

  • MAPS II biopsy concept: At minimum, biopsies should include at least antrum and corpus sampling; the guideline text also emphasizes chromoendoscopy-guided biopsies for staging and for lesions (pimentelnunes2019managementofepithelial pages 5-6).
  • MAPS III adds implementation detail and virtual chromoendoscopy: High-quality endoscopy including virtual chromoendoscopy (VCE) is recommended for screening/diagnosis/staging of precancerous conditions, and VCE should guide sampling; random biopsies should be taken in the absence of endoscopically suspected changes (dinisribeiro2025managementofepithelial pages 6-7).

Differential diagnosis

Not explicitly detailed in the retrieved excerpts (e.g., EBV-associated gastric cancer is mentioned elsewhere in the broader corpus but is outside the scope of evidence extracted here).

11. Outcome / prognosis

  • Lesion severity correlates with elevated mortality risk: In the Swedish cohort, overall mortality increased with lesion severity (SMR up to 1.54 for dysplasia vs general population), and gastric-cancer–specific mortality rose sharply across the Correa cascade (sun2024overallandcausespecific pages 1-2).

12. Treatment

Prevention-relevant treatment: H. pylori eradication

Randomized trial evidence summarized in a 2025 meta-analysis (RCT-only) supports eradication as a preventive intervention: - Overall reduction in gastric cancer incidence: RR 0.61 (95% CI 0.47–0.79); NNT = 332 (Wu et al., BMC Gastroenterology, Apr 2025; DOI: https://doi.org/10.1186/s12876-025-03886-z) (wu2025therelationshipbetween pages 1-2). - Healthy adult subgroup: RR 0.67 (95% CI 0.48–0.93); NNT = 476 (wu2025therelationshipbetween pages 1-2). - Post-endoscopic mucosal resection subgroup: RR 0.51 (95% CI 0.36–0.71); NNT = 21 (wu2025therelationshipbetween pages 1-2).

Post-endoscopic resection (metachronous lesions)

A 2024 systematic review/meta-analysis focusing on Japan and Korea supports reduced metachronous gastric lesions after successful eradication vs persistent infection (RR 0.54, 95% CI 0.44–0.65) (Yu et al., Frontiers in Medicine, Sep 2024; DOI: https://doi.org/10.3389/fmed.2024.1393498) (wu2025therelationshipbetween pages 1-2).

MAXO (Medical Action Ontology) suggestions

  • Antibiotic therapy (eradication regimens; MAXO term to be mapped)
  • Endoscopic surveillance
  • Upper gastrointestinal endoscopy
  • Endoscopic mucosal resection / endoscopic submucosal dissection (for early neoplasia/precursor lesions per MAPS guidelines)

Note: Detailed systemic therapy for established gastric cancer (e.g., specific chemotherapy regimens, anti-HER2, anti-VEGFR2, PD-1 inhibitors) was not supported by the retrieved excerpts in this run; therefore, it is not asserted here.

13. Prevention

Primary prevention

  • Eradication of confirmed H. pylori infection is repeatedly framed as the leading strategy for primary prevention of gastric cancer (rugge2020gastritisanupdate pages 1-4, wu2025therelationshipbetween pages 1-2).

Secondary prevention (screening/surveillance of precancerous lesions)

Guidelines emphasize risk stratification and targeted surveillance: - MAPS II (2019) surveillance principles: - “For patients with mild to moderate atrophy restricted to the antrum there is no evidence to recommend surveillance.” (Endoscopy, Mar 2019; DOI: https://doi.org/10.1055/a-0859-1883) (pimentelnunes2019managementofepithelial pages 5-6). - Surveillance may be considered at 3 years for single-location intestinal metaplasia with risk factors (family history, incomplete IM, persistent H. pylori) (pimentelnunes2019managementofepithelial pages 5-6). - For dysplasia without a visible lesion, high-quality reassessment with chromoendoscopy is recommended; if no lesion is found, surveillance at 6 months (HGD) and 12 months (LGD) is recommended (pimentelnunes2019managementofepithelial pages 10-11). - MAPS III (2025) population screening stratification: - High-risk regions (gastric cancer ASR >20/100,000 person-years): screening every 2–3 years; intermediate risk (ASR 10–20): every 5 years (Dinis-Ribeiro et al., Endoscopy, 2025; DOI: https://doi.org/10.1055/a-2529-5025) (dinisribeiro2025managementofepithelial pages 16-17). - Screening/surveillance in asymptomatic individuals >80 years should be discontinued or not started (dinisribeiro2025managementofepithelial pages 6-7).

Real-world implementations and uptake

  • European implementation evidence (practice audit): After MAPS I/II introduction, virtual chromoendoscopy adoption rose (4 of 9 centers using it in >50% of endoscopies), and systematic biopsies (antrum/corpus ± incisura) increased (4 centers performing antrum+corpus+incisura biopsies in >90% of cases) (Fontes et al., Endoscopy, Sep 2025; DOI: https://doi.org/10.1055/a-2695-1376) (fontes2025adherencetoclinical pages 1-2).
  • Country-level early detection performance (implementation proxy): A GLOBOCAN 2022-based report notes early diagnosis rates >70% in Japan and South Korea vs ~20% in China (lu2025globalepidemiologyof pages 1-4).

14. Other species / natural disease

Not addressed in the retrieved evidence excerpts.

15. Model organisms

Not fully developed in the retrieved evidence excerpts in this run. (The paper search retrieved an animal-model review, but supporting evidence passages were not extracted with tool citations in this run.)

Key quantitative findings and guideline recommendations (summary table)

Domain Key finding (with numbers) Population/context Source (first author, journal, year) Publication date (month/year) URL/DOI Tool citation id
Epidemiology 2021 global burden: 1.23 million new cases, 0.95 million deaths, 22.79 million DALYs Global gastric cancer burden, GBD 2021 Zhang, Frontiers in Oncology, 2024 12/2024 https://doi.org/10.3389/fonc.2024.1468488 (zhang2024globalregionaland pages 1-2)
Epidemiology Male burden exceeded female burden: ASIR 20.9 vs 8.6/100,000, ASMR 16.0 vs 7.1/100,000, age-standardized DALY rate 371.2 vs 165.6/100,000 Global, sex-stratified GBD 2021 estimates Zhang, Frontiers in Oncology, 2024 12/2024 https://doi.org/10.3389/fonc.2024.1468488 (zhang2024globalregionaland pages 1-2)
Epidemiology 2022 global estimates: 968,194 new cases and 659,944 deaths; male ASIR 12.8/100,000 vs female 6.0/100,000 Global gastric cancer burden, GLOBOCAN 2022-based analysis Lu, preprint/unknown journal, 2025 12/2025 https://doi.org/10.21203/rs.3.rs-8058648/v1 (lu2025globalepidemiologyof pages 1-4)
Epidemiology East Asia accounted for 53.8% of cases and 48.2% of deaths globally Geographic distribution, GLOBOCAN 2022-based analysis Tan, Cancer Biology & Medicine, 2024 08/2024 https://doi.org/10.20892/j.issn.2095-3941.2024.0159 (tan2024globalregionaland pages 1-2)
Virulence-factor risk Among H. pylori-infected gastric disorders, pooled CagA positivity was 83% overall; 78% in gastritis, 86% in peptic ulcer disease, 83% in gastric cancer 24 observational studies from 8 Indo-Pacific countries Naing, PLOS ONE, 2024 08/2024 https://doi.org/10.1371/journal.pone.0307172 (naing2024cagatoxinand pages 1-2)
Virulence-factor risk CagA-positive infection was associated with increased odds of gastric cancer vs gastritis: OR 2.53 (95% CI 1.15–5.55) H. pylori-infected individuals in Indo-Pacific observational studies Naing, PLOS ONE, 2024 08/2024 https://doi.org/10.1371/journal.pone.0307172 (naing2024cagatoxinand pages 1-2)
Eradication benefit Eradication reduced gastric cancer incidence: RR 0.61 (95% CI 0.47–0.79); NNT 332 11 RCTs, 104,786 participants Wu, BMC Gastroenterology, 2025 04/2025 https://doi.org/10.1186/s12876-025-03886-z (wu2025therelationshipbetween pages 1-2)
Eradication benefit In healthy adults, eradication reduced gastric cancer risk: RR 0.67 (95% CI 0.48–0.93); NNT 476 Healthy H. pylori-positive adults in RCT subgroup Wu, BMC Gastroenterology, 2025 04/2025 https://doi.org/10.1186/s12876-025-03886-z (wu2025therelationshipbetween pages 1-2)
Eradication benefit After endoscopic mucosal resection, eradication reduced gastric cancer risk: RR 0.51 (95% CI 0.36–0.71); NNT 21 Post-EMR patients in RCT subgroup Wu, BMC Gastroenterology, 2025 04/2025 https://doi.org/10.1186/s12876-025-03886-z (wu2025therelationshipbetween pages 1-2)
Eradication benefit After endoscopic resection, successful eradication lowered metachronous gastric lesion risk vs persistent infection: RR 0.54 (95% CI 0.44–0.65) 21 studies, 82,256 observations from Japan/Korea Yu, Frontiers in Medicine, 2024 09/2024 https://doi.org/10.3389/fmed.2024.1393498 (wu2025therelationshipbetween pages 1-2)
Surveillance guideline No surveillance recommended for mild-to-moderate atrophy restricted to the antrum MAPS II management of gastric precancerous lesions Pimentel-Nunes, Endoscopy, 2019 03/2019 https://doi.org/10.1055/a-0859-1883 (pimentelnunes2019managementofepithelial pages 5-6)
Surveillance guideline For single-location intestinal metaplasia with family history, incomplete IM, or persistent H. pylori, surveillance with chromoendoscopy and guided biopsies may be considered at 3 years Higher-risk intestinal metaplasia Pimentel-Nunes, Endoscopy, 2019 03/2019 https://doi.org/10.1055/a-0859-1883 (pimentelnunes2019managementofepithelial pages 5-6)
Surveillance guideline Patients with advanced atrophic gastritis / OLGA-OLGIM III/IV should undergo high-quality endoscopy every 3 years Advanced precancerous lesions Pimentel-Nunes, Endoscopy, 2019 03/2019 https://doi.org/10.1055/a-0859-1883 (pimentelnunes2019managementofepithelial pages 13-14, pimentelnunes2019managementofepithelial pages 5-6, pimentelnunes2019managementofepithelial pages 1-2)
Surveillance guideline If dysplasia is present without a visible lesion: repeat high-quality endoscopy with chromoendoscopy; if still no lesion, surveillance at 6 months for high-grade dysplasia and 12 months for low-grade dysplasia Non-visible gastric dysplasia Pimentel-Nunes, Endoscopy, 2019 03/2019 https://doi.org/10.1055/a-0859-1883 (pimentelnunes2019managementofepithelial pages 10-11)
Screening implementation Population endoscopic screening suggested every 2–3 years in high-risk regions with gastric cancer ASR >20/100,000 person-years, and every 5 years in intermediate-risk regions with ASR 10–20/100,000 MAPS III population-level screening framework Dinis-Ribeiro, Endoscopy, 2025 03/2025 https://doi.org/10.1055/a-2529-5025 (dinisribeiro2025managementofepithelial pages 16-17)
Screening implementation For first-degree relatives of gastric cancer patients: noninvasive H. pylori screening/eradication at ages 20–30; endoscopic screening at age 45 or 10 years before the relative’s diagnosis Familial-risk strategy Dinis-Ribeiro, Endoscopy, 2025 03/2025 https://doi.org/10.1055/a-2529-5025 (dinisribeiro2025managementofepithelial pages 6-7)
Screening implementation Screening/surveillance in asymptomatic individuals >80 years should be discontinued or not started MAPS III age threshold Dinis-Ribeiro, Endoscopy, 2025 03/2025 https://doi.org/10.1055/a-2529-5025 (dinisribeiro2025managementofepithelial pages 6-7)
Screening implementation Real-world adherence data: virtual chromoendoscopy use improved in 6 centers, with 4 centers >50% use; 4 centers performed antrum+corpus+incisura biopsies in >90% of cases European multicenter practice audit across 2010/11, 2017/18, 2022/23 Fontes, Endoscopy, 2025 09/2025 https://doi.org/10.1055/a-2695-1376 (fontes2025adherencetoclinical pages 1-2)
Screening implementation Early diagnosis rates reported as >70% in Japan and South Korea vs about 20% in China Country-level implementation differences in gastric cancer detection Lu, preprint/unknown journal, 2025 12/2025 https://doi.org/10.21203/rs.3.rs-8058648/v1 (lu2025globalepidemiologyof pages 1-4)

Table: This table compiles the main numeric findings and actionable guideline points for H. pylori–associated gastric cancer from the retrieved evidence. It is useful for quickly comparing burden estimates, virulence-associated risk, benefits of eradication, and current surveillance/screening recommendations.

Visual evidence: MAPS II surveillance algorithm

A figure from MAPS II showing an OLGA/OLGIM-based surveillance algorithm (including interval tiers) was retrieved (pimentelnunes2019managementofepithelial media 670f31ad).

Expert synthesis (authoritative interpretation)

  1. Causality plus actionability: Across guidelines and meta-analyses, the most actionable point is that H. pylori–driven gastric carcinogenesis is a long-latency process with identifiable intermediate states (atrophy, intestinal metaplasia, dysplasia) that can be risk-staged and surveilled (pimentelnunes2019managementofepithelial pages 5-6, dinisribeiro2025managementofepithelial pages 6-7, sun2024overallandcausespecific pages 1-2).
  2. Eradication has measurable preventive effect sizes: RCT-only evidence synthesis supports a meaningful relative reduction in gastric cancer incidence with eradication (RR ~0.61 overall; strong effect after endoscopic resection with low NNT) (wu2025therelationshipbetween pages 1-2).
  3. Implementation gap is narrowing but persists: Real-world European audits show improved use of guideline-recommended approaches (VCE, biopsy protocols), implying feasible implementation pathways but also remaining gaps in standardized risk scoring and surveillance adherence (fontes2025adherencetoclinical pages 1-2).

Limitations of this evidence package

  • PMIDs: The tool-extracted snippets largely provided DOIs and journal metadata but did not include PubMed IDs. Consequently, PMID-preferred citations could not be supplied from the available evidence.
  • Ontology IDs (MONDO/MeSH/ICD): Specific identifiers for the exact disease concept “H. pylori–associated gastric cancer” were not retrievable in the current evidence excerpts.
  • Systemic therapy for established gastric cancer: Not covered by extracted evidence; therefore omitted to avoid uncited claims.

References

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