Matches in SemOpenAlex for { <https://semopenalex.org/work/W2034343047> ?p ?o ?g. }
Showing items 1 to 86 of
86
with 100 items per page.
- W2034343047 abstract "2-Amino-3-methylimidazo[4,5-f]quinoline (IQ) is a very potent mutagen that is carcinogenic in rodents and nonhuman primates. IQ-induced CDF1 mouse lung and liver tumors were examined for activated Ki-ras and Ha-ras genes, respectively. Polymerase chain reaction (PCR)-amplified target DNAs were analyzed for mutations of codons 12, 13, and 61 by single-strand conformation polymorphism (SSCP) and direct sequencing methods. All mutations were localized to codon 61 of the ras genes. Forty-nine of 54 lung tumors induced by IQ possessed activating Ki-ras mutations, as did 20 of 26 lung tumors from the vehicle-treated animals; 80% and 75% of these mutations, respectively, were A-->T transversions of the second nucleotide redundant. One lung adenoma from the IQ-treated group contained a tandem duplication of the sequence corresponding to codons 50-57 of the Ki-ras gene (unpublished observations). In addition, seven of 34 IQ-induced liver tumors harbored activating Ha-ras mutations: five were C-->A (G-->T) transversions at the first nucleotide, and two were A-->T transversions at the second nucleotide of codon 61. None of the 15 liver tumors collected from the vehicle-treated mice possessed Ha-ras mutations in codon 12, 13, or 61. These data indicate that IQ induces Ha-ras gene activation in CDF1 mouse liver tumors. The mechanisms of lung tumor induction by IQ, however, is obscured by the high frequency of Ki-ras A-->T mutations observed in both the IQ-induced and spontaneous lung tumors. The different ras mutational spectra in lung and liver tumors may suggest either that two different pathways of IQ metabolism exist in these organs or that IQ contributes to CDF1 lung tumorigenesis by a mechanism other than its direct interaction with the Ki-ras gene." @default.
- W2034343047 created "2016-06-24" @default.
- W2034343047 creator A5002800938 @default.
- W2034343047 creator A5019022652 @default.
- W2034343047 creator A5050018727 @default.
- W2034343047 creator A5061594020 @default.
- W2034343047 date "1993-01-01" @default.
- W2034343047 modified "2023-09-27" @default.
- W2034343047 title "ras mutations in 2-amino-3-methylimidazo-[4,5-f]quinoline—induced tumors in the CDF1 mouse" @default.
- W2034343047 cites W149149583 @default.
- W2034343047 cites W1560539518 @default.
- W2034343047 cites W1967608710 @default.
- W2034343047 cites W1977262016 @default.
- W2034343047 cites W1984466882 @default.
- W2034343047 cites W1988897136 @default.
- W2034343047 cites W1996027687 @default.
- W2034343047 cites W1996238010 @default.
- W2034343047 cites W2002120723 @default.
- W2034343047 cites W2009748752 @default.
- W2034343047 cites W2009773967 @default.
- W2034343047 cites W2013873616 @default.
- W2034343047 cites W2017106093 @default.
- W2034343047 cites W2022710599 @default.
- W2034343047 cites W2026301882 @default.
- W2034343047 cites W2033371627 @default.
- W2034343047 cites W2033741635 @default.
- W2034343047 cites W2048649566 @default.
- W2034343047 cites W2051181008 @default.
- W2034343047 cites W2056920355 @default.
- W2034343047 cites W2062861859 @default.
- W2034343047 cites W2068568989 @default.
- W2034343047 cites W2081341484 @default.
- W2034343047 cites W2118094114 @default.
- W2034343047 cites W2234525015 @default.
- W2034343047 cites W2414043456 @default.
- W2034343047 doi "https://doi.org/10.1002/mc.2940080311" @default.
- W2034343047 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/8216739" @default.
- W2034343047 hasPublicationYear "1993" @default.
- W2034343047 type Work @default.
- W2034343047 sameAs 2034343047 @default.
- W2034343047 citedByCount "11" @default.
- W2034343047 crossrefType "journal-article" @default.
- W2034343047 hasAuthorship W2034343047A5002800938 @default.
- W2034343047 hasAuthorship W2034343047A5019022652 @default.
- W2034343047 hasAuthorship W2034343047A5050018727 @default.
- W2034343047 hasAuthorship W2034343047A5061594020 @default.
- W2034343047 hasConcept C104317684 @default.
- W2034343047 hasConcept C114246631 @default.
- W2034343047 hasConcept C129219603 @default.
- W2034343047 hasConcept C153911025 @default.
- W2034343047 hasConcept C2776639595 @default.
- W2034343047 hasConcept C36823959 @default.
- W2034343047 hasConcept C501734568 @default.
- W2034343047 hasConcept C502942594 @default.
- W2034343047 hasConcept C54355233 @default.
- W2034343047 hasConcept C555283112 @default.
- W2034343047 hasConcept C86803240 @default.
- W2034343047 hasConceptScore W2034343047C104317684 @default.
- W2034343047 hasConceptScore W2034343047C114246631 @default.
- W2034343047 hasConceptScore W2034343047C129219603 @default.
- W2034343047 hasConceptScore W2034343047C153911025 @default.
- W2034343047 hasConceptScore W2034343047C2776639595 @default.
- W2034343047 hasConceptScore W2034343047C36823959 @default.
- W2034343047 hasConceptScore W2034343047C501734568 @default.
- W2034343047 hasConceptScore W2034343047C502942594 @default.
- W2034343047 hasConceptScore W2034343047C54355233 @default.
- W2034343047 hasConceptScore W2034343047C555283112 @default.
- W2034343047 hasConceptScore W2034343047C86803240 @default.
- W2034343047 hasLocation W20343430471 @default.
- W2034343047 hasLocation W20343430472 @default.
- W2034343047 hasOpenAccess W2034343047 @default.
- W2034343047 hasPrimaryLocation W20343430471 @default.
- W2034343047 hasRelatedWork W136468098 @default.
- W2034343047 hasRelatedWork W2047185566 @default.
- W2034343047 hasRelatedWork W2075089097 @default.
- W2034343047 hasRelatedWork W2088111429 @default.
- W2034343047 hasRelatedWork W2258430434 @default.
- W2034343047 hasRelatedWork W2349638566 @default.
- W2034343047 hasRelatedWork W2350102540 @default.
- W2034343047 hasRelatedWork W2351845239 @default.
- W2034343047 hasRelatedWork W2419448289 @default.
- W2034343047 hasRelatedWork W2469776549 @default.
- W2034343047 isParatext "false" @default.
- W2034343047 isRetracted "false" @default.
- W2034343047 magId "2034343047" @default.
- W2034343047 workType "article" @default.