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Journal ArticleDOI

Chromosome analysis of trifluorothymidine‐resistant L5178y mouse lymphoma cell colonies

TLDR
Cells from small (sigma) and large (lambda) trifluorothymidine-resistant (TFTr) colonies induced by chemical mutagen treatment of TK+/-L5178Y mouse lymphoma cells were examined for chromosomal abnormalities.
Abstract
Cells from small (sigma) and large (lambda) trifluorothymidine-resistant (TFTr) colonies induced by chemical mutagen treatment of TK+/-L5178Y mouse lymphoma cells were examined for chromosomal abnormalities. Analysis of G-banded metaphase chromosomes from 34 sigma-TFTr colonies revealed that cells from 20 (59%) possessed one or more chromosomal abnormalities. The most frequent (16/20 colonies) abnormality observed in cells from sigma-TFTr colonies involved the addition of extra chromatin to the distal region of one chromosome number 11. In 13 of these 16 colonies, the origin of the chromatin translocated to chromosome number 11 could not be identified; the chromatin was not missing elsewhere in the genome. The remaining three sigma-TFTr colonies with an abnormal chromosome number 11 had apparently whole chromosomes translocated, in tandem, to the distal region of chromosome number 11. Chromosomal abnormalities observed in cells from sigma-TFTr colonies with normal number 11 chromosomes included 2N/4N and 2N/4N/8N mosaicism (two colonies), a Robertsonian translocation involving chromosome 10 and a marker chromosome (one colony), and trisomy 7 (one colony). In most (14/16) sigma-TFTr colonies with structural damage to chromosome number 11, the cells within a colony were heterogeneous in that some possessed chromosomal damage whereas others were apparently normal. Analysis of chromosomes in cells from eight lambda-TFTr colonies revealed one colony in which all cells had a Robertsonian translocation involving chromosomes 1 and 16 plus other structural abnormalities. The chromosomes of cells from the remaining lambda-TFTr colonies were apparently normal.

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Citations
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Journal ArticleDOI

Molecular dissection of mutations at the heterozygous thymidine kinase locus in mouse lymphoma cells.

TL;DR: The variety of mutagenic lesions recorded at the heterozygous Tk locus may be representative of events observed in human malignancy and may include a wider range ofmutagenic events than can be observed at hemizygous test loci.
Journal ArticleDOI

Responses of the L5178Y mouse Lymphoma cell forward mutation assay. V: 27 coded chemicals.

TL;DR: Twenty‐seven chemicals were tested for their mutagenic potential in the L5178Y tk+/tk− mouse lymphoma cell forward mutation assay using procedures based upon those described by McGregor et al. (1987).
Journal ArticleDOI

Fragrance material review on cinnamaldehyde.

TL;DR: A toxicologic and dermatologic review of cinnamaldehyde when used as a fragrance ingredient is presented and its application in cosmetics and fragrances is presented.
Journal ArticleDOI

The L5178Y/tk+/− mouse lymphoma specific gene and chromosomal mutation assay: A phase III report of the U.S. environmental protection agency Gene-Tox program

TL;DR: The L5178Y/tk+/−-3.7.2C mouse lymphoma assay (MLA) as mentioned in this paper detects mutations affecting the heterozygous thymidine kinase (tk) locus is capable of responding to chemicals acting as clastogens as well as point mutagens.
Journal ArticleDOI

Chemical mutagenesis at the thymidine kinase locus in L5178Y mouse lymphoma cells: Results for 31 coded compounds in the national toxicology program

TL;DR: Experimental data from the testing of 31 chemicals for mutagenicity at the TK locus in L5178Y mouse lymphoma cells are presented and evaluated and Discordant evaluations with respect to carcinogenicity were discussed from the standpoint of how the predictive performance of the in vitro mutation assay might be improved.
References
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Journal ArticleDOI

Validation and characterization of the L5178Y/TK+/- mouse lymphoma mutagen assay system.

TL;DR: Characterization of the TK-/- mutants suggests that two mutagenic mechanisms contribute to their final yield, and is consistent with the induction of slow-growing specific locus mutants by a chromosomal mechanism and their subsequent dilution during this long expression time.
Journal ArticleDOI

Chemically-induced unscheduled DNA synthesis in primary rat hepatocyte cultures: A comparison with bacterial mutagenicity using 218 compounds

TL;DR: The results support the complementary and confirmatory nature of these tests for genotoxic chemicals and indicate the usefulness of the hepatocyte UDS system as a component in a battery of short-term predictive tests for mutagens/carcinogens.
Journal ArticleDOI

A mutational assay system using the thymidine kinase locus in mouse lymphoma cells

TL;DR: An estimate can be made of the relative mutagenicities of various treatments of the TK locus and the observed induced mutation rates with the spontaneous TK +/− → TK −/− mutation rate.
Journal ArticleDOI

Cytogenetic analysis of the L5178Y/TK+/− → TK−/− mouse lymphoma mutagenesis assay system

TL;DR: It seems likely that λ and σ mutants result from 2 different mutational mechanisms that may be distinguished on the basis of mutant colony morphology, possibly related to the type of chromosomal damage sustained.
Journal ArticleDOI

Point mutations at the thymidine kinase locus in L5178Y mouse lymphoma cells. II. Test validation and interpretation

TL;DR: Data indicate this mammalian cell assay for gene mutations at the thymidine kinase (TK) locus can be expected to detect a majority of carcinogens as mutagens including some missed by more established point-mutation assays.
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