| pubmed-article:7523879 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:7523879 | lifeskim:mentions | umls-concept:C0003392 | lld:lifeskim |
| pubmed-article:7523879 | lifeskim:mentions | umls-concept:C0027923 | lld:lifeskim |
| pubmed-article:7523879 | lifeskim:mentions | umls-concept:C0205147 | lld:lifeskim |
| pubmed-article:7523879 | lifeskim:mentions | umls-concept:C0205145 | lld:lifeskim |
| pubmed-article:7523879 | lifeskim:mentions | umls-concept:C0017337 | lld:lifeskim |
| pubmed-article:7523879 | lifeskim:mentions | umls-concept:C0026882 | lld:lifeskim |
| pubmed-article:7523879 | lifeskim:mentions | umls-concept:C0022885 | lld:lifeskim |
| pubmed-article:7523879 | lifeskim:mentions | umls-concept:C0392366 | lld:lifeskim |
| pubmed-article:7523879 | lifeskim:mentions | umls-concept:C0162735 | lld:lifeskim |
| pubmed-article:7523879 | lifeskim:mentions | umls-concept:C0376249 | lld:lifeskim |
| pubmed-article:7523879 | lifeskim:mentions | umls-concept:C0205263 | lld:lifeskim |
| pubmed-article:7523879 | lifeskim:mentions | umls-concept:C1704666 | lld:lifeskim |
| pubmed-article:7523879 | lifeskim:mentions | umls-concept:C1517892 | lld:lifeskim |
| pubmed-article:7523879 | lifeskim:mentions | umls-concept:C1883709 | lld:lifeskim |
| pubmed-article:7523879 | lifeskim:mentions | umls-concept:C0208973 | lld:lifeskim |
| pubmed-article:7523879 | lifeskim:mentions | umls-concept:C0020775 | lld:lifeskim |
| pubmed-article:7523879 | pubmed:issue | 1 | lld:pubmed |
| pubmed-article:7523879 | pubmed:dateCreated | 1994-10-31 | lld:pubmed |
| pubmed-article:7523879 | pubmed:abstractText | The mutagenicity of the antitumor agent ICR-170 (2-methoxy-6-chloro-9-[(ethyl-2-chloroethyl)amino propylamino] acridine dihydrochloride) in the adenine-3 (ad-3) region was studied with a two-component heterokaryon (H-12) of Neurospora crassa. The objective was to characterize the genetic damage produced by this acridine nitrogen mustard derivative to determine in a lower eukaryotic organism the basis for its potent activity against ascites tumors in mice. As in higher eukaryotes, specific-locus mutations in the ad-3 region of strain H-12 result from gene/point mutations, multiple-locus mutations, and multilocus deletion mutations at the closely linked ad-3A and ad-3B loci. Six different treatments of conidial suspensions of H-12 with ICR-170 were used to obtain dose-response curves for inactivation of conidia as well as the overall induction of ad-3 forward mutations using a direct method based on pigment accumulation rather than a requirement for adenine. These experiments demonstrated that: (1) the slope of the dose-response curve for ICR-170-induced specific-locus mutations in the ad-3 region was 1.97 +/- 0.02, and (2) ICR-170 is a potent mutagen (maximum forward-mutation frequency between 1000 and 10,000 ad-3 mutations per 10(6) survivors) for the induction of specific-locus mutations in the ad-3 region. Both biochemical and classical genetic tests were used to characterize the ICR-170-induced ad-3 mutations from each of the six treatments to distinguish the different genotypic classes and subclasses. The overall data base demonstrates that ICR-170-induced ad-3 mutations result exclusively from gene/point mutations at the ad-3A and ad-3B loci and not multilocus deletion mutations. In addition, the frequency of multiple-locus ad-3 mutations resulting from gene/point mutations at the ad-3A and ad-3B loci with a separate site of recessive lethal damage elsewhere in the genome increases as a function of dose. However, an exceptionally high frequency of multiple-locus ad-3 mutations consisting of gene/point mutations at the ad-3A and ad-3B loci with a separate site of closely linked recessive lethal damage was found at all doses. Comparison of the dose-response curves for the major classes and subclasses of ICR-170-induced ad-3 mutations demonstrates that the gene/point ad-3 mutations and multiple-locus ad-3 mutations with a separate site of recessive lethal damage elsewhere in the genome have different induction kinetics.(ABSTRACT TRUNCATED AT 400 WORDS) | lld:pubmed |
| pubmed-article:7523879 | pubmed:language | eng | lld:pubmed |
| pubmed-article:7523879 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:7523879 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:7523879 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:7523879 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:7523879 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:7523879 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:7523879 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:7523879 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:7523879 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:7523879 | pubmed:month | Oct | lld:pubmed |
| pubmed-article:7523879 | pubmed:issn | 0027-5107 | lld:pubmed |
| pubmed-article:7523879 | pubmed:author | pubmed-author:MallingH VHV | lld:pubmed |
| pubmed-article:7523879 | pubmed:author | pubmed-author:de SerresF... | lld:pubmed |
| pubmed-article:7523879 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:7523879 | pubmed:day | 1 | lld:pubmed |
| pubmed-article:7523879 | pubmed:volume | 310 | lld:pubmed |
| pubmed-article:7523879 | pubmed:geneSymbol | ad-3 | lld:pubmed |
| pubmed-article:7523879 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:7523879 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:7523879 | pubmed:pagination | 15-36 | lld:pubmed |
| pubmed-article:7523879 | pubmed:dateRevised | 2006-11-15 | lld:pubmed |
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| pubmed-article:7523879 | pubmed:meshHeading | pubmed-meshheading:7523879-... | lld:pubmed |
| pubmed-article:7523879 | pubmed:year | 1994 | lld:pubmed |
| pubmed-article:7523879 | pubmed:articleTitle | Forward-mutation tests on the antitumor agent ICR-170 in Neurospora crassa demonstrate that it induces gene/point mutations in the ad-3 region and an exceptionally high frequency of multiple-locus ad-3 mutations with closely linked sites of recessive lethal damage. | lld:pubmed |
| pubmed-article:7523879 | pubmed:affiliation | Center for Life Sciences and Toxicology, Research Triangle Institute, Research Triangle Park, NC 27709-2194. | lld:pubmed |
| pubmed-article:7523879 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:7523879 | pubmed:publicationType | Research Support, U.S. Gov't, Non-P.H.S. | lld:pubmed |
