In:
Clinical Cancer Research, American Association for Cancer Research (AACR), Vol. 16, No. 14_Supplement ( 2010-07-15), p. B4-B4
Abstract:
Lung cancer is the most common cause of cancer death worldwide. Smoking is known as the strongest single factor for the development of lung cancer. However, there are inherited genetic factors that cause different responses to cigarette smoking exposure among individuals. We tried to identify these differences in heavy smokers by examining copy number variations (CNVs) between lung cancer patients and healthy controls. Analysis by array comparative genomic hybridization (aCGH) showed 26 significant (P & lt;0.05) clones with either copy number gains or losses. 3 genes, KCTD11, FGF11, and PTPRH on chromosomal regions 17p13.1 (KCTD11 and FGF11) and 19q13.42 (PTPRH) were selected (P & lt;0.001) and tested by realtime quantitative PCR (qPCR) with 34 healthy controls and 54 lung cancer patients for large-scale analysis. KCTD11, a known tumor suppressor gene, showed copy number losses in cancer patients. In addition, as the years of smoking increased, odds ratios were also increased (0R=0.8,2.2, and 16.0), implying that it is a susceptible gene to lung cancer when an individual smokes. Therefore, KCTD11 is a promising candidate for a predictive marker to identify individuals with high, inherited genetic risk for the development of lung cancer. Citation Information: Clin Cancer Res 2010;16(14 Suppl):B4.
Type of Medium:
Online Resource
ISSN:
1078-0432
,
1557-3265
DOI:
10.1158/1078-0432.TCMUSA10-B4
Language:
English
Publisher:
American Association for Cancer Research (AACR)
Publication Date:
2010
detail.hit.zdb_id:
1225457-5
detail.hit.zdb_id:
2036787-9
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