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Hypermethylation of CCND2 May Reflect a Smoking-Induced Precancerous Change in the Lung.

Salskov A, Hawes SE, Stern JE, Feng Q, Jordan CD, Wiens L, Rasey J, Lu H, Kiviat NB, Vesselle H - J Oncol (2011)

Bottom Line: CCND2 hypermethylation was also associated with increased age and upper lobe sample location.BVES, CDH13, CDKN2A (p16), CDKN2B, DAPK1, IGFBP3, IGSF4, KCNH5, KCNH8, MGMT, OPCML, PCSK6, RASSF1, RUNX, and TMS1 were rarely hypermethylated (<2%) in all subjects.Hypermethylation of CCND2 may reflect a smoking-induced precancerous change in the lung.

View Article: PubMed Central - PubMed

Affiliation: Division of Nuclear Medicine, Department of Radiology, Box 357115, School of Medicine, University of Washington, Seattle, WA 98195-7115, USA.

ABSTRACT
It remains unknown whether tobacco smoke induces DNA hypermethylation as an early event in carcinogenesis or as a late event, specific to overt cancer tissue. Using MethyLight assays, we analyzed 316 lung tissue samples from 151 cancer-free subjects (121 ever-smokers and 30 never-smokers) for hypermethylation of 19 genes previously observed to be hypermethylated in nonsmall cell lung cancers. Only APC (39%), CCND2 (21%), CDH1 (7%), and RARB (4%) were hypermethylated in >2% of these cancer-free subjects. CCND2 was hypermethylated more frequently in ever-smokers (26%) than in never-smokers (3%). CCND2 hypermethylation was also associated with increased age and upper lobe sample location. APC was frequently hypermethylated in both ever-smokers (41%) and never-smokers (30%). BVES, CDH13, CDKN2A (p16), CDKN2B, DAPK1, IGFBP3, IGSF4, KCNH5, KCNH8, MGMT, OPCML, PCSK6, RASSF1, RUNX, and TMS1 were rarely hypermethylated (<2%) in all subjects. Hypermethylation of CCND2 may reflect a smoking-induced precancerous change in the lung.

No MeSH data available.


Related in: MedlinePlus

Hypermethylation of four genes in noncancerous lung tissues. Percent of subjects with hypermethylation of four genes (APC, CCND2, CDH1, and RARB), stratified by smoking status.  Samples were considered to be positive for any hypermethylation at PMR >0%.  To provide population statistics, one lung tissue sample per subject was randomly selected.  The 15 other genes tested were hypermethylated in <2% of all subjects.
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fig1: Hypermethylation of four genes in noncancerous lung tissues. Percent of subjects with hypermethylation of four genes (APC, CCND2, CDH1, and RARB), stratified by smoking status. Samples were considered to be positive for any hypermethylation at PMR >0%. To provide population statistics, one lung tissue sample per subject was randomly selected. The 15 other genes tested were hypermethylated in <2% of all subjects.

Mentions: Considering one random tissue block per subject, only APC (39%), CCND2 (21%), CDH1 (7%), and RARB (4%) were hypermethylated in more than 2% of subjects (Figure 1). All 15 remaining genes (BVES, CDH13, CDKN2A (p16), CDKN2B, DAPK1, IGFBP3, IGSF4, KCNH5, KCNH8, MGMT, OPCML, PCSK6, RASSF1, RUNX, and TMS1) were hypermethylated in less than 2% of subjects. CCND2 was hypermethylated significantly more frequently in ever-smokers compared to never-smokers (26% versus 3%, P < .001). APC was hypermethylated somewhat more frequently in ever-smokers (41% versus 30%), but this did not achieve statistical significance (P = .3).


Hypermethylation of CCND2 May Reflect a Smoking-Induced Precancerous Change in the Lung.

Salskov A, Hawes SE, Stern JE, Feng Q, Jordan CD, Wiens L, Rasey J, Lu H, Kiviat NB, Vesselle H - J Oncol (2011)

Hypermethylation of four genes in noncancerous lung tissues. Percent of subjects with hypermethylation of four genes (APC, CCND2, CDH1, and RARB), stratified by smoking status.  Samples were considered to be positive for any hypermethylation at PMR >0%.  To provide population statistics, one lung tissue sample per subject was randomly selected.  The 15 other genes tested were hypermethylated in <2% of all subjects.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC3090638&req=5

fig1: Hypermethylation of four genes in noncancerous lung tissues. Percent of subjects with hypermethylation of four genes (APC, CCND2, CDH1, and RARB), stratified by smoking status. Samples were considered to be positive for any hypermethylation at PMR >0%. To provide population statistics, one lung tissue sample per subject was randomly selected. The 15 other genes tested were hypermethylated in <2% of all subjects.
Mentions: Considering one random tissue block per subject, only APC (39%), CCND2 (21%), CDH1 (7%), and RARB (4%) were hypermethylated in more than 2% of subjects (Figure 1). All 15 remaining genes (BVES, CDH13, CDKN2A (p16), CDKN2B, DAPK1, IGFBP3, IGSF4, KCNH5, KCNH8, MGMT, OPCML, PCSK6, RASSF1, RUNX, and TMS1) were hypermethylated in less than 2% of subjects. CCND2 was hypermethylated significantly more frequently in ever-smokers compared to never-smokers (26% versus 3%, P < .001). APC was hypermethylated somewhat more frequently in ever-smokers (41% versus 30%), but this did not achieve statistical significance (P = .3).

Bottom Line: CCND2 hypermethylation was also associated with increased age and upper lobe sample location.BVES, CDH13, CDKN2A (p16), CDKN2B, DAPK1, IGFBP3, IGSF4, KCNH5, KCNH8, MGMT, OPCML, PCSK6, RASSF1, RUNX, and TMS1 were rarely hypermethylated (<2%) in all subjects.Hypermethylation of CCND2 may reflect a smoking-induced precancerous change in the lung.

View Article: PubMed Central - PubMed

Affiliation: Division of Nuclear Medicine, Department of Radiology, Box 357115, School of Medicine, University of Washington, Seattle, WA 98195-7115, USA.

ABSTRACT
It remains unknown whether tobacco smoke induces DNA hypermethylation as an early event in carcinogenesis or as a late event, specific to overt cancer tissue. Using MethyLight assays, we analyzed 316 lung tissue samples from 151 cancer-free subjects (121 ever-smokers and 30 never-smokers) for hypermethylation of 19 genes previously observed to be hypermethylated in nonsmall cell lung cancers. Only APC (39%), CCND2 (21%), CDH1 (7%), and RARB (4%) were hypermethylated in >2% of these cancer-free subjects. CCND2 was hypermethylated more frequently in ever-smokers (26%) than in never-smokers (3%). CCND2 hypermethylation was also associated with increased age and upper lobe sample location. APC was frequently hypermethylated in both ever-smokers (41%) and never-smokers (30%). BVES, CDH13, CDKN2A (p16), CDKN2B, DAPK1, IGFBP3, IGSF4, KCNH5, KCNH8, MGMT, OPCML, PCSK6, RASSF1, RUNX, and TMS1 were rarely hypermethylated (<2%) in all subjects. Hypermethylation of CCND2 may reflect a smoking-induced precancerous change in the lung.

No MeSH data available.


Related in: MedlinePlus