A novel clonality assay for the mouse: Application to hepatocellular carcinomas induced with diethylnitrosamine

Tsunashima, K.; Endo, Yoshiro; Asakura, Hitoshi; Kanda, Hiroaki; Nomura, K.; Kitagawa, Tomoyuki; Kominami, Ryo

doi:10.1002/(sici)1098-2744(199601)15:1<33::aid-mc5>3.0.co;2-t

Cited by 8 publications

(1 citation statement)

References 20 publications

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“…145 has been shown by X-chromosome inactivation to be multiclonal, arguing for multiple independent tumours; 64 multiple uterine leiomyomas also appear to arise independently, though individually clonal in origin. 146,147 Experimental mouse hepatic tumours are apparently monoclonal, indicated by the X-linked tissue-specific gene ornithine carbomyl transferase, 148,149 and there is good evidence from rat chimeras that the pre-neoplastic nodules from which they arise are also clonal. 150 In the human liver, however, opinion is divided concerning the clonality of lesions often regarded as pre-neoplastic: while lesions such as benign adenomatous hyperplasia are polyclonal, even small (<25 mm), hepatocellular carcinomas are clonal.…”

Section: The Field Cancerization Hypothesismentioning

confidence: 99%

Field cancerization, clonality, and epithelial stem cells: the spread of mutated clones in epithelial sheets

et al. 1999

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Section: The Field Cancerization Hypothesismentioning

confidence: 99%

Field cancerization, clonality, and epithelial stem cells: the spread of mutated clones in epithelial sheets

et al. 1999

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Accumulation of recombinant chromosomes and low fidelity of transmission of chromosome X DNA markers in ?-ray-induced lymphomas lacking p53

Koide¹,

Matsumoto²,

Kosugi³

et al. 1999

Mol. Carcinog.

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F1 offspring of male MSM male mice with a p53-deficient (knockout) allele and normal female BALB/c mice were backcrossed with MSM mice to produce N2 mice. Female F1 and N2 mice were irradiated with gamma-radiation, and thymic lymphomas were obtained from 69 F1 and 82 N2 mice heterozygous for X chromosome markers. Of these 151 mice, 91 carried a p53-deficient allele. These lymphomas were analyzed for allelic loss by using four marker loci distributed on X chromosome to assess the stability of the inactive X chromosome, which contributes little to cellular functions. Twenty lymphomas showed allelic loss of all four loci, suggesting loss of a whole inactive X chromosome due to mitotic nondisjunction, whereas 24 lost only a part of an X chromosome, as a result of somatic recombination. The p53 status of the lymphomas was determined by genotyping and allelic loss analysis: 53 had retained two wild-type p53 alleles, suggesting normal function; 69 had lost both alleles, indicating loss of function; and the remaining 29 had at least one wild-type p53 allele, so their p53 status was unclear. Compilation of these two data revealed one nondisjunction-type change and five recombination-type mutations on X chromosome in 53 lymphomas retaining functional p53. In contrast, 14 and 16 of these alterations, respectively, were observed in 69 lymphomas lacking p53 function. These results suggest that p53 loss significantly increases the accumulation of recombinant chromosomes and decreases the fidelity of mitotic chromosome transmission of the X chromosome in gamma-ray-induced lymphomas.

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Monoclonal expansion of synoviocytes in rheumatoid arthritis

Imamura

Aono

Hasunuma

et al. 1998

Arthritis & Rheumatism

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Objective. To examine whether synoviocytes from patients with rheumatoid arthritis (RA) have a stronger growth ability than those from patients with osteoarthritis (OA), and to determine whether these synoviocytes clonally expand in situ.Methods. Synovial tissues from 13 KA patients and 4 OA patients were cultured, and their ability to form colonies in soft agarose was examined. RA and OA synoviocytes were also examined in varying concentrations of fetal calf serum (FCS)-containing medium to test the effects of FCS on colony formation. DNA was extracted from clones with colony-forming ability in nonpannus lesions and from synoviocytes in pannus lesions. Restriction fragment length polymorphism (RFLP) analysis was used to examine phosphoglycerate kinase 1 (PGK-1) gene patterns. Production of cytokines by these cells was also assessed.Results. All 13 KA synoviocytes exhibited colony formation, whereas none of the 4 OA synoviocytes did. This tendency was also seen with all of the concentrations of FCS examined, although growth varied in a dose-dependent manner. In contrast to OA synovial clones, cloned M synoviocytes obtained from colonies exhibited a partial KFLP PGK-1 gene pattern, suggesting that the clones originated from monoclonal cells. Of note, 3 of 7 noncloned synoviocytes from pannus lesions

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A novel clonality assay for the mouse: Application to hepatocellular carcinomas induced with diethylnitrosamine

Cited by 8 publications

References 20 publications

Field cancerization, clonality, and epithelial stem cells: the spread of mutated clones in epithelial sheets

Field cancerization, clonality, and epithelial stem cells: the spread of mutated clones in epithelial sheets

Accumulation of recombinant chromosomes and low fidelity of transmission of chromosome X DNA markers in ?-ray-induced lymphomas lacking p53

Monoclonal expansion of synoviocytes in rheumatoid arthritis

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