Alcohol consumption and risk of stomach cancer: A meta-analysis

Deng, Wenting; Jin, Lan; Zhuo, Haoran; Vasiliou, Vasilis; Zhang, Yawei

doi:10.1016/j.cbi.2021.109365

Cited by 48 publications

(27 citation statements)

References 97 publications

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“…99) Furthermore, a higher daily intake of alcohol was suggested to be associated with a higher risk of gastric cancer. 100) Experimental mouse gastric carcinogenesis studies using pepsinogen as a marker PAPGs were also observed in an MNU-induced experimental model of gastric carcinogenesis induced various mouse strains including BALB/c, C3H, C57BL/6N, CBA, CD-1, DBA/2, and db/db diabetic mice. 101)-107) Trp53 and ras gene mutations were rarely observed in mouse gastric tumors induced by MNU.…”

Section: Additional Studies On Rat Gastric Carcinogenesismentioning

confidence: 99%

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Human gastric cancer risk screening: From rat pepsinogen studies to the ABC method

Furihata

2021

Proceedings of the Japan Academy. Ser. B: Physical and Biologic

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We examined the development of gastric cancer risk screening, from rat pepsinogen studies in an experimental rat gastric carcinogenesis model induced with N-methyl-NB-nitro-N-nitrosoguanidine (MNNG) and human pepsinogen studies in the 1970s and 1980s to the recent "ABC method" for human gastric cancer risk screening. First, decreased expression or absence of a major pepsinogen isozyme, PG1, was observed in the rat gastric mucosa from the early stages of gastric carcinogenesis to adenocarcinomas following treatment with MNNG. In the 1980s, decreases in PGI in the human gastric mucosa and serum were identified as markers of atrophic gastritis. In the 1990s, other researchers revealed that chronic infection with Helicobacter pylori (Hp) causes atrophic gastritis and later gastric cancer. In the 2000s, a gastric cancer risk screening method combining assays to detect serum anti-Hp IgG antibody and serum PGI and PGII levels, the "ABC method", was established. Eradication of Hp and endoscopic follow-up examination after the ABC method are recommended to prevent gastric cancer.

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Section: Additional Studies On Rat Gastric Carcinogenesismentioning

confidence: 99%

“… 99 ) Furthermore, a higher daily intake of alcohol was suggested to be associated with a higher risk of gastric cancer. 100 )…”

Section: Additional Studies On Rat Gastric Carcinogenesismentioning

confidence: 99%

Human gastric cancer risk screening: From rat pepsinogen studies to the ABC method

Furihata

2021

Proceedings of the Japan Academy. Ser. B: Physical and Biologic

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“…This part of gastric cancer is called hereditary diffuse gastric cancer (HDGC) ( Blair et al, 2020 ). In addition, smoking ( Shikata et al, 2008 ) and alcohol consumption ( Deng et al, 2021 ), eating habits ( Takezaki et al, 1999 ; Kobayashi et al, 2002 ), chronic atrophic gastritis, and EBV or Helicobacter pylori infection ( Arif and Syed, 2007 ; Holleczek et al, 2020 ) have been considered the most important risk factors for gastric cancer ( FORMAN, 1991 ).…”

Section: Introductionmentioning

confidence: 99%

Overview on the Role of E-Cadherin in Gastric Cancer: Dysregulation and Clinical Implications

Zhao

Chen

et al. 2021

Front. Mol. Biosci.

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Gastric cancer is the fifth most common cancer and the third most common cause of cancer death all over the world. E-cadherin encoded by human CDH1 gene plays important roles in tumorigenesis as well as in tumor progression, invasion and metastasis. Full-length E-cadhrin tethered on the cell membrane mainly mediates adherens junctions between cells and is involved in maintaining the normal structure of epithelial tissues. After proteolysis, the extracellular fragment of the full-length E-cadhein is released into the extracellular environment and the blood, which is called soluble E-cadherin (sE-cadherin). sE-cadherin promots invasion and metastasis as a paracrine/autocrine signaling molecule in the progression of various types of cancer including gastric cancer. This review mainly summarizes the dysregulation of E-cadherin and the regulatory roles in the progression, invasion, metastasis, and drug-resistance, as well as its clinical applications in diagnosis, prognosis, and therapeutics of gastric cancer.

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“…According to the latest global cancer data released in 2020, GC ranks 6th in incidence and 4th in mortality among all malignancies 1 . Risk factors for GC include chronic Helicobacter pylori infection, alcohol consumption, 2,3 tobacco smoking 4,5 and consumption of foods preserved by salting, 6,7 among others. Chronic H pylori infection is considered the principal cause of non‐cardia GC 1 ; approximately 90% of new cases of non‐cardia GC are associated with H pylori infection 8,9 .…”

Section: Introductionmentioning

confidence: 99%

Bone marrow‐derived mesenchymal stem cells promote Helicobacter pylori‐associated gastric cancer progression by secreting thrombospondin‐2

Shi

Meng

et al. 2021

Cell Proliferation

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Objectives Bone marrow‐derived cells (BMDCs), especially mesenchymal stem cells (MSCs), may be involved in the development of Helicobacter pylori‐associated gastric cancer (GC) in mice, but the specific mechanism remains unclear, and evidence from human studies is lacking. Materials and Methods To verify the role of BM‐MSCs in H pylori‐associated GC, green fluorescent protein (GFP)‐labelled BM‐MSCs were transplanted into the subserosal layers of the stomach in a mouse model of chronic H pylori infection. Three months post‐transplantation, the mice were sacrificed, and the gastric tissues were subjected to histopathological and immunofluorescence analyses. In addition, we performed fluorescence in situ hybridization (FISH) and immunofluorescence analyses of gastric tissue from a female patient with H pylori infection and a history of acute myeloid leukaemia who received a BM transplant from a male donor. Results In mice with chronic H pylori infection, GFP‐labelled BM‐MSCs migrated from the serous layer to the mucosal layer and promoted GC progression. The BM‐MSCs differentiated into pan‐cytokeratin‐positive epithelial cells and α‐smooth muscle actin‐positive cancer‐associated fibroblasts (CAFs) by secreting the protein thrombospondin‐2. FISH analysis of gastric tissue from the female patient revealed Y‐chromosome‐positive cells. Immunofluorescence analyses further confirmed that Y‐chromosome‐positive cells showed positive BM‐MSCs marker. These results suggested that allogeneic BMDCs, including BM‐MSCs, can migrate to the stomach under chronic H pylori infection. Conclusions Taken together, these findings imply that BM‐MSCs participate in the development of chronic H pylori‐associated GC by differentiating into both gastric epithelial cells and CAFs.

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Alcohol consumption and risk of stomach cancer: A meta-analysis

Cited by 48 publications

References 97 publications

Human gastric cancer risk screening: From rat pepsinogen studies to the ABC method

Human gastric cancer risk screening: From rat pepsinogen studies to the ABC method

Overview on the Role of E-Cadherin in Gastric Cancer: Dysregulation and Clinical Implications

Bone marrow‐derived mesenchymal stem cells promote Helicobacter pylori‐associated gastric cancer progression by secreting thrombospondin‐2

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