Catalogo Articoli (Spogli Riviste)

OPAC HELP

Titolo:
Complexity of lung cancer modifiers: Mapping of thirty genes and twenty-five interactions in half of the mouse genome
Autore:
Tripodis, N; Hart, AAM; Fijneman, RJA; Demant, P;
Indirizzi:
Netherlands Canc Inst, Div Mol Genet, NL-1066 CX Amsterdam, Netherlands Netherlands Canc Inst Amsterdam Netherlands NL-1066 CX rdam, Netherlands Vrije Univ Amsterdam, Fac Med, Dept Cell Biol & Immunol, Amsterdam, Netherlands Vrije Univ Amsterdam Amsterdam Netherlands unol, Amsterdam, Netherlands
Titolo Testata:
JOURNAL OF THE NATIONAL CANCER INSTITUTE
fascicolo: 19, volume: 93, anno: 2001,
pagine: 1484 - 1491
Fonte:
ISI
Lingua:
ENG
Soggetto:
RECOMBINANT CONGENIC STRAINS; INDUCED PULMONARY ADENOMAS; QUANTITATIVE TRAIT LOCI; TUMOR SUSCEPTIBILITY; RESISTANCE LOCUS; MICE; GENETICS; TIME;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
30
Recensione:
Indirizzi per estratti:
Indirizzo: Demant, P Netherlands Canc Inst, Div Mol Genet, H5,Plesmanlaan 121, NL-1066 CX Amsterdam, Netherlands Netherlands Canc Inst H5,Plesmanlaan 121 Amsterdam Netherlands NL-1066 CX
Citazione:
N. Tripodis et al., "Complexity of lung cancer modifiers: Mapping of thirty genes and twenty-five interactions in half of the mouse genome", J NAT CANC, 93(19), 2001, pp. 1484-1491

Abstract

Background: Numerous low-penetrance genes control susceptibility to cancerin experimental animals, but the overall genetic information on this groupof genes (i.e., number of loci and their mutual interactions) is missing. We performed a systematic search, scanning roughly half of the mouse genomefor lung cancer susceptibility (Slue) genes affecting tumor size or numberby using mouse recombinant congenic (RC) strains. In each RC strain (OcB),approximately 12.5% of the genome is derived from the lung cancer-resistant strain B10.O20, whereas the rest is derived from the lung cancer-susceptible strain O20. Methods: A total of 730 F-2 hybrids from five (OcB x O20) crosses were tested. Pregnant mice were treated on day 18 of gestation with a single dose of N-ethyl-N-nitrosourea. When offspring were 16 weeks old, whole lungs were removed and sectioned semiserially, and the size of all lung tumors (n = 2658) was determined. Analysis of variance was used for detection of linkage, and models (including main effect and two-way interactions) were tested with a statistical program. Results: We detected a total of 30 Sluc loci (16 new plus 14 previously reported) and 25 two-way interactions. Some of these interactions are counteracting (e.g., Sluc17 and Sluc20), resulting in the partial or total masking of the individual independent effect (main effect) of each involved locus. Seven loci (Sluc1, Slue-5, Sluc12, Sluc16, Sluc18, Sluc20, and Sluc26) and two interactions (Sluc5 x Sluc12 and Sluc5 x Sluc26) were detected in more than one RC strain. Conclusions: The extrapolation of our results to the whole genome suggests approximately60 Sluc loci (90% confidence intervals = 42 to 78). Despite the genetic complexity of lung cancer, use of appropriate map-ping strategies can identify a large number of responsible loci and can reveal their interactions. This study provides an insight into the genetic control of lung tumorigenesis and may serve as a paradigm for investigating the genetics of other cancer types.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 10/04/20 alle ore 15:46:08