Clonal analysis of glandular stomach carcinogenesis in  ↔  chimeric mice treated with N-methyl-N-nitrosourea

Tatematsu, Masae; Fukami, Hiroko; Yamamoto, Masami; Nakanishi, Hayao; Masui, Tsuneo; Kusakabe, Noriaki; Sakakura, Teruyo

doi:10.1016/0304-3835(94)90296-8

Cited by 54 publications

(42 citation statements)

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“…9) For the C3H↔BALB/c chimeras used in this study, combinations in terms of sex chromosomes were XY↔XY, XY↔XX, XX↔XY and XX↔XX (note that the left side of the arrow is for C3H and the right one is for BALB/c). Sex chromosome analysis in chimeric mice has previously been achieved by karyotype preparation 9,22) or mating and evaluation of offspring. 10) However, these methods are time-consuming and do not reveal the karyotype of sex chromosomes in a strain-specific manner.…”

Section: Discussionmentioning

confidence: 99%

“…25) Although PBP74/CSA has been reported to be constitutively expressed, 24,25,27) immunohistochemical detection of CSA may be affected by quantitative or qualitative changes of PBP74/CSA expression. Changes in the level of PBP74/ CSA expression in tumor tissues have not yet been thoroughly examined, though CSA has been used as a stably expressed marker for tumors of the liver, 10) forestomach, 14) glandular stomach, 22) colon, 15) and urinary bladder. 28) To re-confirm the stability of CSA expression in liver tumors, another marker was sought to provide complementary results.…”

Section: Discussionmentioning

confidence: 99%

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Mouse Strain Susceptibility to Diethylnitrosamine Induced Hepatocarcinogenesis Is Cell Autonomous Whereas Sex‐susceptibility Is Due to the Micro‐environment: Analysis with C3H ↔ BALB/c Sexually Chimeric Mice

Tsukamoto

Inada

Fukami

et al. 2000

Japanese Journal of Cancer Research

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In man, liver cancer is on the increase, especially in males. Sex differences also exist in rodent models. To elucidate the mechanisms, chimeric mice were produced by amalgamation of early embryos from high and low hepatocarcinogen-susceptible strains, C3H and BALB/c. Tumor formation was initiated with 10 mg/kg of diethylnitrosamine at the ages of 7 and 14 days and mice were sacrificed at 30 and 45 weeks. The chimeras were classified into XY ↔ ↔ ↔ ↔XY, XY ↔ ↔ ↔ ↔XX, XX ↔ ↔ ↔ ↔XY, and XX ↔ ↔ ↔ ↔XX in terms of sex chromosomes by means of polymerase chain reaction-simple sequence length polymorphism analysis (SSLP) using Y chromosome-specific Sry primers in combination with the D3Mit21 marker. Liver lesions were analyzed histopathologically, by immunostaining using a C3H strain-specific antibody and by DNA in situ hybridization with the Y chromosomespecific digoxigenin-labeled Y353/B probe. Sex and strain genotyping by SSLP analysis matched histological observations, confirming the reliability of our system. The strain differences in liver tumor numbers of each strain type in XY↔ ↔ ↔ ↔XY and XX ↔ ↔ ↔ ↔XX subtypes of C3H↔ ↔ ↔ ↔BALB/c chimeras were retained well (P < < < <0.0001 and P < < < <0.001, respectively), indicating a minimum influence of the C3H or BALB/c surrounding milieu on development of individual lesions. On the other hand, significant promotion of XX cell tumors was evident in phenotypically male sexually chimeric XY ↔ ↔ ↔ ↔XX and XX ↔ ↔ ↔ ↔XY chimeras for both C3H (P < < < <0.02) and BALB/c (P < < < <0.01) lesions compared to the XX ↔ ↔ ↔ ↔XX case. The results suggest the presence of hormonal or micro-environmental factors specific for males, which are not caused cell-autonomously. Basic strain differences, however, are determined by intrinsic genetic factors rather than the strain-dependent micro-environment.Key words: Chimera -Hepatocarcinogenesis -Strain susceptibilityIn man, the occurrence of primary liver cancer has been on the increase for several years, changes in rates being more marked in males than in females. 1) In Japan, 1996 death rates for intrahepatic neoplasia were 37.5 and 14.6/ 100 000 for males and females, respectively, according to the National Health and Welfare Statistics. 2)In rodent models, there also are sex differences in spontaneous and carcinogen-induced hepatocarcinogenesis, males being more susceptible than females.3, 4) One fundamental question is whether the sex differences are cellautonomous or caused by hormonal or micro-environmental factors. To address this issue, Kemp et al. 5) utilized Tfm (testicular feminization) mutant mice and showed that liver tumor promotion by testosterone required a functional androgen receptor in the intact animal. Other researchers reported that castration of males reduced the incidence of carcinomas and adenomatous nodules in 3′ ′ ′ ′-methyl-4-dimethylaminoazobenzene (3′-Me-DAB)-treated 6) and in N,N-diethylnitrosamine (DEN)-treated mice.7) The results with DEN-initiated and 2-acetylaminofluorenetreated rats appear similar. 8) Furth...

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Mouse Strain Susceptibility to Diethylnitrosamine Induced Hepatocarcinogenesis Is Cell Autonomous Whereas Sex‐susceptibility Is Due to the Micro‐environment: Analysis with C3H ↔ BALB/c Sexually Chimeric Mice

Tsukamoto

Inada

Fukami

et al. 2000

Japanese Journal of Cancer Research

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“…Radioactive labeling studies first revealed the dynamics of these granule-free cells in adult animals (Lee and Leblond, 1985). Subsequent analyses of chromosome patterns in XX-XY chimeric mice (Thompson et al, 1990) and of strain-specific antigens in C3H; BALB/c chimeric mice (Tatematsu et al, 1994) indicated that gastric glands are largely monoclonal, although 10-25% of glands remain polyclonal in adults (Nomura et al, 1998). Tracing an Xlinked lacZ transgene after random X-chromosome inactivation in mice showed that glands begin as polyclonal units and rapidly become monoclonal in the first 3 weeks of life, a period that coincides with extensive gland fission (Nomura et al, 1998), whereby individual glands enlarge and subsequently produce two glands.…”

Section: Stomach Differentiation Epithelial (Mucosal) Differentiationmentioning

confidence: 99%

Stomach development, stem cells and disease

2016

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The stomach, an organ derived from foregut endoderm, secretes acid and enzymes and plays a key role in digestion. During development, mesenchymal-epithelial interactions drive stomach specification, patterning, differentiation and growth through selected signaling pathways and transcription factors. After birth, the gastric epithelium is maintained by the activity of stem cells. Developmental signals are aberrantly activated and stem cell functions are disrupted in gastric cancer and other disorders. Therefore, a better understanding of stomach development and stem cells can inform approaches to treating these conditions. This Review highlights the molecular mechanisms of stomach development and discusses recent findings regarding stomach stem cells and organoid cultures, and their roles in investigating disease mechanisms.

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“…Mathematical models predict that when murine antral glands are initially established, they contain approximately three stem cells 6 . These initially polyclonal glands resolve to a primarily monoclonal state over the first six weeks of life 4,6,7,9 , though a few residual polyclonal glands (5-10%) persist in the adult 9 .…”

Section: Introductionmentioning

confidence: 99%

Prospective Identification of a Multilineage Progenitor in Murine Stomach Epithelium

et al. 2007

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Background and Aims-Epithelial stem cells in the stomach are responsible for constant renewal of the epithelium through generation of multiple gastric cell lineages that populate the gastric glands. However, gastric stem or progenitor cells have not been well-characterized due to the lack of specific markers that permit their prospective recognition. We identified an intestinal promoter that is active in a rare subpopulation of gastric epithelial cells and investigated whether these cells possess multilineage potential.

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Clonal analysis of glandular stomach carcinogenesis in ↔ chimeric mice treated with N-methyl-N-nitrosourea

Cited by 54 publications

References 5 publications

Mouse Strain Susceptibility to Diethylnitrosamine Induced Hepatocarcinogenesis Is Cell Autonomous Whereas Sex‐susceptibility Is Due to the Micro‐environment: Analysis with C3H ↔ BALB/c Sexually Chimeric Mice

Mouse Strain Susceptibility to Diethylnitrosamine Induced Hepatocarcinogenesis Is Cell Autonomous Whereas Sex‐susceptibility Is Due to the Micro‐environment: Analysis with C3H ↔ BALB/c Sexually Chimeric Mice

Stomach development, stem cells and disease

Prospective Identification of a Multilineage Progenitor in Murine Stomach Epithelium

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