Open Access Green möglich sobald Postprint bei der ZB eingereicht worden ist.
Matrix metalloproteinase 1 (MMP1) is associated with early-onset lung cancer.
Cancer Epidemiol. Biomarkers Prev. 17, 1127-1135 (2008)
Matrix metalloproteinases (MMP) play a key role in the breakdown of extracellular matrix and in inflammatory processes. MMP1 is the most highly expressed interstitial collagenase degrading fibrillar collagens. Overexpression of MMP1 has been shown in tumor tissues and has been suggested to be associated with tumor invasion and metastasis. Nine haplotype tagging and additional two intronic single nucleotide polymorphisms (SNP) of MMP1 were genotyped in a case control sample, consisting of 635 lung cancer cases with onset of disease below 51 years of age and 1,300 age- and sex-matched cancer-free controls. Two regions of linkage disequilibrium (LD) of MMP1 could be observed: a region of low LD comprising the 5' region including the promoter and a region of high LD starting from exon 1 to the end of the gene and including the 3' flanking region. Several SNPs were identified to be individually significantly associated with risk of early-onset lung cancer. The most significant effect was seen for rs1938901 (P = 0.0089), rs193008 (P = 0.0108), and rs996999 (P = 0.0459). For rs996999, significance vanished after correction for multiple testing. For each of these SNPs, the major allele was associated with an increase in risk with an odds ratio between 1.2 and 1.3 (95% confidence interval, 1.0-1.5). The haplotype analysis supported these findings, especially for subgroups with high smoking intensity. In summary, we identified MMP1 to be associated with an increased risk for lung cancer, which was modified by smoking.
Altmetric
Weitere Metriken?
Zusatzinfos bearbeiten
[➜Einloggen]
Publikationstyp
Artikel: Journalartikel
Dokumenttyp
Wissenschaftlicher Artikel
Schlagwörter
Matrix Metalloproteinase 1; MMP1; lung cancer
ISSN (print) / ISBN
1055-9965
e-ISSN
1538-7755
Zeitschrift
Cancer Epidemiology, Biomarkers & Prevention
Quellenangaben
Band: 17,
Heft: 5,
Seiten: 1127-1135
Verlag
American Association for Cancer Research (AACR)
Begutachtungsstatus
Peer reviewed
Institut(e)
Institute of Epidemiology (EPI)