| pubmed-article:11023538 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:11023538 | lifeskim:mentions | umls-concept:C0027651 | lld:lifeskim |
| pubmed-article:11023538 | lifeskim:mentions | umls-concept:C0035647 | lld:lifeskim |
| pubmed-article:11023538 | lifeskim:mentions | umls-concept:C0026882 | lld:lifeskim |
| pubmed-article:11023538 | lifeskim:mentions | umls-concept:C0027270 | lld:lifeskim |
| pubmed-article:11023538 | lifeskim:mentions | umls-concept:C1527249 | lld:lifeskim |
| pubmed-article:11023538 | lifeskim:mentions | umls-concept:C0004083 | lld:lifeskim |
| pubmed-article:11023538 | lifeskim:mentions | umls-concept:C0150312 | lld:lifeskim |
| pubmed-article:11023538 | lifeskim:mentions | umls-concept:C0053241 | lld:lifeskim |
| pubmed-article:11023538 | pubmed:issue | 10 | lld:pubmed |
| pubmed-article:11023538 | pubmed:dateCreated | 2000-11-1 | lld:pubmed |
| pubmed-article:11023538 | pubmed:abstractText | NAD(P)H:quinone oxidoreductase (NQO1) is a polymorphic enzyme involved in the detoxification of potentially mutagenic and carcinogenic quinones. The homozygous C609T NQO1 genotype resulting in loss of reductase activity is found in 2-20% of individuals. In the present study, the NQO1-dependent risk for sporadic colorectal cancer (CRC) was studied in 247 incident CRC cases and 296 hospital-based controls recruited during 1996-1997. Four subgroups of cases were studied: (i) all CRCs; (ii) a molecular CRC subgroup (n = 117, cases with molecular tumor analyses); (iii) within the molecular subgroup those tumors with K-ras mutations in codon 12 (CRC K12); (iv) within the molecular subgroup those tumors with K-ras mutations in codon 13 (CRC K13). The C609T NQO1 genotype was found to be twice as prevalent in all CRC patients (6.8%) compared with controls (3%) and six times more common in the subset CRC K12 (20%). Multivariant analyses in the overall population of 247 cases and 296 controls showed a significant age and gender adjusted risk for CRC associated with the C609T NQO1 genotype (OR 2.9, 95% CI 1.19-6.97; P = 0.01) or with any variant genotype (the low activity allele frequency, i.e. heterozygotes plus homozygotes) (OR 1.41, 95% CI 1.02-1.92; P = 0.03). Within cases of the molecular subgroup (n = 117) the C609T NQO1 genotype was associated with the presence of K-ras codon 12 mutation (OR 6.5 95%, CI 1.39-34.9; P = 0.003). Logistic regression showed an age and gender adjusted risk for K-ras codon 12 mutant CRC associated with the C609T NQO1 genotype (OR 10.5, 95% CI 2.99-36.7; P: = 0.0002) or with any variant NQO1 genotype (OR 2.23, 95% CI 1.23-4.00; P = 0.007) compared with the control group. Genetically determined variations in NQO1 may modify the risk for CRC and these risks may be greatest for tumors containing K-ras codon 12 mutations. CRC with K-ras codon 12 mutations may represent a distinct and etiologically more homogeneous subtype of the disease, which may be associated with toxicants that are metabolized via a NQO1-dependent pathway. | lld:pubmed |
| pubmed-article:11023538 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11023538 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11023538 | pubmed:language | eng | lld:pubmed |
| pubmed-article:11023538 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11023538 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:11023538 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11023538 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:11023538 | pubmed:month | Oct | lld:pubmed |
| pubmed-article:11023538 | pubmed:issn | 0143-3334 | lld:pubmed |
| pubmed-article:11023538 | pubmed:author | pubmed-author:MolinaRR | lld:pubmed |
| pubmed-article:11023538 | pubmed:author | pubmed-author:AscasoCC | lld:pubmed |
| pubmed-article:11023538 | pubmed:author | pubmed-author:BallestaAA | lld:pubmed |
| pubmed-article:11023538 | pubmed:author | pubmed-author:WienckeJ KJK | lld:pubmed |
| pubmed-article:11023538 | pubmed:author | pubmed-author:TriasMM | lld:pubmed |
| pubmed-article:11023538 | pubmed:author | pubmed-author:LafuenteAA | lld:pubmed |
| pubmed-article:11023538 | pubmed:author | pubmed-author:ZhengSS | lld:pubmed |
| pubmed-article:11023538 | pubmed:author | pubmed-author:LafuenteM JMJ | lld:pubmed |
| pubmed-article:11023538 | pubmed:author | pubmed-author:CasteranNN | lld:pubmed |
| pubmed-article:11023538 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:11023538 | pubmed:volume | 21 | lld:pubmed |
| pubmed-article:11023538 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:11023538 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:11023538 | pubmed:pagination | 1813-9 | lld:pubmed |
| pubmed-article:11023538 | pubmed:dateRevised | 2007-11-15 | lld:pubmed |
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| pubmed-article:11023538 | pubmed:meshHeading | pubmed-meshheading:11023538... | lld:pubmed |
| pubmed-article:11023538 | pubmed:year | 2000 | lld:pubmed |
| pubmed-article:11023538 | pubmed:articleTitle | NAD(P)H:quinone oxidoreductase-dependent risk for colorectal cancer and its association with the presence of K-ras mutations in tumors. | lld:pubmed |
| pubmed-article:11023538 | pubmed:affiliation | Department of Surgery, Hospital Clinic, Department of Pharmacology, School of Medicine, Casanova 143, E-08036, Barcelona, Spain. alafuente@med.ub.es | lld:pubmed |
| pubmed-article:11023538 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:11023538 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:11023538 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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