Chromosome Studies in the Ehrlich Ascites Tumor of the Mouse Grown in Vitro

Nielsén, Karin

doi:10.1111/j.1601-5223.1967.tb02142.x

Cited by 22 publications

(8 citation statements)

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“…The chromosomes of various ELD strains have been studied on many occasions by members of the Cancer Chromosome Laboratory at Lund ( LEVAN 1954;TJIO and LEVAN 1954;HANSEN-MELANDER 1958;ISING 1958;LEVAN 1959;MELANDER 1963;NIELSEN 1967NIELSEN ,1969NIELSEN ,1971NIELSEN , I972,1973NIELSEN ,1974aNIELSEN , b, 1975NIELSEN , 1976a. With conventional staining techniques it was possible only to distinguish the above-mentioned markers from the large mass of telocentric chromosomes of different length.…”

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Chromosomal evolution in the Ehrlich-Lettré complex of hyperdiploid mouse ascites tumors: Results from seven laboratory strains

Nielsén

2009

Hereditas

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NIELS~N, K. 1976. Chromosomal evolution in the Ehrlich-Lettre complex of hyperdiploid mouse ascites tumors: Results from seven laboratory strains. -Heredim 84: 77-108. Lund, Sweden,The chromosomes of 7 strains of the hyperdiploid Ehrlich-Lettre mouse ascites tumor (ELD) were analyzed by conventional stainings and by Gand C-bandings. A tendency to slow decrease in chromosome number during a 20-year period was revealed in the 7 strains and in the ELD complex in general. A G-band idiogram of the normal mouse chromosomes was elaborated with numbering of regions and bands. By G-band analysis the following average composition of the ELD karyotypes was indicated: unchanged mouse chromosomes (30",), marA, marB, minutes ( I I " o ) , marl -marl2, telocentric markers ( IOU<), anonymous telocentric markers, often strongly rearranged (50%). Great differences were revealed among normal chromosomes and markers in their capacity to persist in the tumor stemline as structurally stable units. The presence of some unchanged chromosomes in most cells of all 7 strains indicated that they involved selective advantage. Evidently chromosomal evolution has operated by preferably maintaining certain elements unchanged and by submitting other elements to heavy rearrangement. The C-band analysis showed that, in addition to the centromeric C-heterochromatin present in all chromosomes, some had interstitial C-bands, as marA in all strains, mar5 and mar7 in specific single strains, and others in numbers varying among the strains.

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Chromosomal evolution in the Ehrlich-Lettré complex of hyperdiploid mouse ascites tumors: Results from seven laboratory strains

Nielsén

2009

Hereditas

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“…Two different alleles are observed in 8 of them, implying that those cell lines would be originated from outbred strains. Three alleles detected at D5Mit357 in Ehrlich ascites (JCRB9090) could be caused by genome instability of tumor cells because this cell line is reported to be aneuploid (Nielsén 1967). …”

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Incorrect strain information for mouse cell lines: sequential influence of misidentification on sublines

Uchio‐Yamada

Kasai

Ozawa

et al. 2016

In Vitro Cell.Dev.Biol.-Animal

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Misidentification or cross-contamination of cell lines can cause serious issues. Human cell lines have been authenticated by short tandem repeat profiling; however, mouse cell lines have not been adequately assessed. In this study, mouse cell lines registered with the JCRB cell bank were examined by simple sequence length polymorphism (SSLP) analysis to identify their strains. Based on comparisons with 7 major inbred strains, our results revealed their strains in 80 of 90 cell lines. However, 12 of the 80 cell lines (15%) were found to differ from registered information. Of them, 4 cell lines originated from the same mouse, which had been generated through mating between two different inbred strains. The genotype of the mouse sample had not been examined after the backcross, leading to strain misidentification in those cell lines. Although 8 other cell lines had been established as sublines of a BALB/c cell line, their SSLP profiles are similar to a Swiss cell line. This affects differences in genotypes between inbred and outbred strains. Because the use of inbred samples and interbreeding between strains are not involved in human materials, our results suggest that the cause and influence of misidentification in mouse cell lines are different from those in human.Electronic supplementary materialThe online version of this article (doi:10.1007/s11626-016-0104-3) contains supplementary material, which is available to authorized users.

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“…TJIO and LEVAN (1954), S C H~N E I C H (1962,1968). and NIELSEN (1967). The stemline number is still high and distinguishes the Go subline from several other ELAT sublines in which.…”

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A genome mutation in three related sublines of the Ehrlich-Lettré mouse ascites tumor1,2

Granzow

Nielsén

2008

Hereditas

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Granzow, C. and Nielsén, K, 1984. A genome mutation in three related sublines of the Ehrlich‐Lettré mouse ascites tumor. —Hereditas 100:93–110. Lund, Sweden. ISSN 0018–0661. Received May 30, 1983 Whilst the Gø subline of the Ehrlich‐Lettré mouse ascites tumor (ELAT) corresponds phenotypically and cytogenetically to H. Lettrés original tumor subline, the three colchicine resistant, glycogen‐storing ELAT sublines, CR, G+, and HD33, differ from it by: (1) A reduction in stemline numbers from 46 to 40 or 41, (2) the existence of only three minute marker chromosomes, (3) the presence of a specific marker chromosome, marAB, and (4) the activity of essentially only one very large NOR, located on marAB. The reduction in stemline numbers is not paralleled by a decrease of the average cellular DNA content, which seems to be influenced more by cell kinetic factors than by the levels of the stemline number. Only minor but constant karyotypical differences exist between the CR and the closely related G + and HD33 sublines. G‐band patterns indicate the origin of marAB from a centric fusion between marA and the q arm of marB present in Gø ascites cells. The genome mutation of the CR subline is probably due to the action of N‐methylcolchicamide (H LETTRÉ and W. KRAMER, Naturwissenschaften 39, 117, 1952). The artificial presence of such mutant cells with altered phenotype in other ELAT sublines may cause misleading experimental results and should he carefully excluded.

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Chromosome Studies in the Ehrlich Ascites Tumor of the Mouse Grown in Vitro

Abstract: KARIN NIEISI?NThe origin of this tuiiior in Dr. LANI~SCIIU'I'Z' cxperiiiiciits :ind its itfentificatioii a\ ;I hyperdiploid strain 0 1 the I Show more

Cited by 22 publications

References 7 publications

Chromosomal evolution in the Ehrlich-Lettré complex of hyperdiploid mouse ascites tumors: Results from seven laboratory strains

Chromosomal evolution in the Ehrlich-Lettré complex of hyperdiploid mouse ascites tumors: Results from seven laboratory strains

Incorrect strain information for mouse cell lines: sequential influence of misidentification on sublines

A genome mutation in three related sublines of the Ehrlich-Lettré mouse ascites tumor1,2

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