“Malgun” (clear) Cell Change of Gastric Epithelium in Chronic Helicobacter pylori Gastritis

Lee, Hunkyung; Jang, Jaejung; Kim, Yunjung; Ahn, Sang-Ho; Gong, Mikyung; Choi, Eun Sun; Lee, Inchul

doi:10.1016/s0344-0338(00)80026-6

Cited by 5 publications

(10 citation statements)

References 35 publications

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“…10 Malgun cells were readily recognized in the proliferative and surface zones based on the following characteristics: 1) nuclear enlargement, 2) euchromatin pattern, 3) conspicuous nucleoli, and 4) expanded cytoplasm with decreased stainability on H&E staining. 12 They were distinguished from endocrine cells by the characteristic cytological change and the location; endocrine cells were located in the deep glandular zone mostly. If necessary, a triple silver impregnation (modified Warthin-Starry staining) was done according to Genta and colleagues 19 to get a sharper contrast.…”

Section: Study Population and Histopathological Analysismentioning

confidence: 99%

“…The mitotic activity indicated that they were not just degenerating but metabolically active cells; occasionally atypical mitotic figures were noted. 12…”

Section: Histopathological Characterizationmentioning

confidence: 99%

“…10 In association with acute foveolitis, nonendocrine epithelial cells with clear, enlarged nuclei and cytoplasm are frequently scattered. 12 They are present as single cells and/or in small clusters. They are mitotically active, and atypical mitotic figures may also be found.…”

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confidence: 99%

“…[13][14][15][16] In Korea, in which the prevalence rate of H. pylori infection and gastric cancer incidence remain very high, 17,18 acute foveolitis and the malgun cell change are frequently found in gastric biopsies. 10,12 In this study, we analyzed the pathobiological nature of malgun cells using the terminal dUTP nick-end labeling (TUNEL) method and immunohistochemical staining for DNA repair-related proteins. We found that they were consistently positive for the TUNEL staining and had up-regulated DNA repair proteins.…”

mentioning

confidence: 99%

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Malgun (Clear) Cell Change in Helicobacter pylori Gastritis Reflects Epithelial Genomic Damage and Repair

Jang

Lee

Jung

et al. 2003

The American Journal of Pathology

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Cancers may develop in the background of genomic instability with accumulated mutations. Helicobacter pylori gastritis is characterized by acute foveolitis of the proliferative zone, which is found in any stage of the gastritis as long as the infection persists. Because acute foveolitis targets specifically the proliferative zone of pits, the proliferating epithelial cells are under severe and persistent mutagenic pressure. In H. pylori gastritis, a characteristic morphological change of epithelial cells, the malgun (clear) cell change is frequently present in association with acute foveolitis. Malgun cells have enlarged euchromatic nuclei and abundant cytoplasm. The expression of proliferating cell nuclear antigen and cytokeratin 8 are typically up-regulated in them indicating that they are mitotically and metabolically active. Here, we report evidence for DNA damage and repair in malgun cells. Significant double-strand DNA breaks were shown by the consistent terminal dUTP nick-end labeling in the nuclei of malgun cells. Proteins related to DNA damage and repair, such as Ku, poly(ADP-ribosyl) polymerase, OGG1, and MSH2 were selectively up-regulated in malgun cells. Inducible nitric oxide synthase was also up-regulated. There were occasional bcl2- and p53-expressing cells suggesting that further steps of carcinogenesis took place at the single cell level. Our results suggest that the malgun cell change represents a characteristic morphological sign of cellular genomic damage and repair, and may be implicated in an early stage of carcinogenesis. It is suggested that acute foveolitis of the proliferative zone is a major pathogenetic step of gastric carcinogenesis in H. pylori gastritis.

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Section: Study Population and Histopathological Analysismentioning

confidence: 99%

“…The mitotic activity indicated that they were not just degenerating but metabolically active cells; occasionally atypical mitotic figures were noted. 12…”

Section: Histopathological Characterizationmentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

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Malgun (Clear) Cell Change in Helicobacter pylori Gastritis Reflects Epithelial Genomic Damage and Repair

Jang

Lee

Jung

et al. 2003

The American Journal of Pathology

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“…To date, limited investigation has focused on genetic damage associated with infection in these animals, but available data are still incomplete. Enhanced DNA fragmentation was observed in gastric cells of infected mice (19), in which dsDNA breaks were also detected by TUNEL assay (20,21). Mutagenicity in reporter genes recovered from gastric DNA of male and female Big Blue transgenic mice 6 mo after infection with H. pylori or Helicobacter felis has also been reported (22).…”

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confidence: 91%

Mutagenic potency ofHelicobacter pyloriin the gastric mucosa of mice is determined by sex and duration of infection

Sheh

Lee

Masumura

et al. 2010

Proc. Natl. Acad. Sci. U.S.A.

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Helicobacter pylori is a human carcinogen, but the mechanisms evoked in carcinogenesis during this chronic inflammatory disease remain incompletely characterized. We determined whether chronic H. pylori infection induced mutations in the gastric mucosa of male and female gpt delta C57BL/6 mice infected for 6 or 12 mo. Point mutations were increased in females infected for 12 mo. The mutation frequency in this group was 1.6-fold higher than in uninfected mice of both sexes (P < 0.05). A:T-to-G:C transitions and G:C-to-T:A transversions were 3.8 and 2.0 times, respectively, more frequent in this group than in controls. Both mutations are consistent with DNA damage induced by oxidative stress. No increase in the frequency of deletions was observed. Females had more severe gastric lesions than males at 6 mo postinfection (MPI; P < 0.05), but this difference was absent at 12 MPI. In all mice, infection significantly increased expression of IFNγ, IL-17, TNFα, and iNOS at 6 and 12 mo, as well as H. pylori-specific IgG1 levels at 12 MPI (P < 0.05) and IgG2c levels at 6 and 12 MPI (P < 0.01 and P < 0.001). At 12 MPI, IgG2c levels in infected females were higher than at 6 MPI (P < 0.05) and also than those in infected males at 12 MPI (P < 0.05). Intensity of responses was mediated by sex and duration of infection. Lower H. pylori colonization indicated a more robust host response in females than in males. Earlier onset of severe gastric lesions and proinflammatory, Th1-biased responses in female C57BL/6 mice may have promoted mutagenesis by exposing the stomach to prolonged oxidative stress.gpt delta mouse | Helicobacter | inflammation | mutagenesis | sexual dimorphism

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Ethnic difference ofHelicobacter pylorigastritis: Korean and Japanese gastritis is characterized by male- and antrum-predominant acute foveolitis in comparison with American gastritis

Lee¹

2005

WJG

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“Malgun” (clear) Cell Change of Gastric Epithelium in Chronic Helicobacter pylori Gastritis

Cited by 5 publications

References 35 publications

Malgun (Clear) Cell Change in Helicobacter pylori Gastritis Reflects Epithelial Genomic Damage and Repair

Malgun (Clear) Cell Change in Helicobacter pylori Gastritis Reflects Epithelial Genomic Damage and Repair

Mutagenic potency ofHelicobacter pyloriin the gastric mucosa of mice is determined by sex and duration of infection

Ethnic difference ofHelicobacter pylorigastritis: Korean and Japanese gastritis is characterized by male- and antrum-predominant acute foveolitis in comparison with American gastritis

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