ArticleJournal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer2015
Epigenetic Repression of CCDC37 and MAP1B Links Chronic Obstructive Pulmonary Disease to Lung Cancer.
Article in Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 58 citations in OpenAlex.
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- Therapeutic monoclonal antibody targeting of neuronal pentraxin receptor to control metastasis in gastric cancer.Molecular cancer · 2020Article
- Identification of novel epigenetic abnormalities as sputum biomarkers for lung cancer risk among smokers and COPD patients.Lung cancer (Amsterdam, Netherlands) · 2020Article
- Identification of prognostic signature of non-small cell lung cancer based on TCGA methylation data.Scientific reports · 2020Article
- Epigenetic Regulation of RIP3 Suppresses Necroptosis and Increases Resistance to Chemotherapy in NonSmall Cell Lung Cancer.Translational oncology · 2020Article
- Chronic obstructive pulmonary disease (COPD) and lung cancer: common pathways for pathogenesis.Journal of thoracic disease · 2019Review
- Identification and analysis of long non-coding RNA related miRNA sponge regulatory network in bladder urothelial carcinoma.Cancer cell international · 2019Article
- Survival associated with chronic obstructive pulmonary disease among SEER-Medicare beneficiaries with non-small-cell lung cancer.International journal of chronic obstructive pulmonary disease · 2019Article
- Gene Promoter Hypermethylation Detected in Sputum Predicts FEVAmerican journal of respiratory and critical care medicine · 2018Article
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
introductionLung cancer and chronic obstructive pulmonary disease (COPD) share environmental risk factors. COPD also increases the risk of lung cancer; however, the molecular mechanisms are unclear.
methodsAn epigenome-wide association study of lung tumors and cancer-free lung tissue (CFLT) pairs from non-small-cell lung cancer cases with (n = 18) or without (n = 17) COPD was conducted using the HumanMethylation450 beadchip (HM450K). COPD-associated methylation of top-ranked genes was confirmed in a larger sample set, independently validated, and their potential as sputum-based biomarkers was investigated.
resultsMethylation of CCDC37 and MAP1B was more prevalent in lung tumors from COPD than non-COPD cases [54 of 71 (76%) versus 20 of 46 (43%), p = 0.0013] and [48 of 71 (68%) versus 17 of 46 (37%), p = 0.0035], respectively, after adjustment for age, sex, smoking status, and tumor histology. HM450K probes across CCDC37 and MAP1B promoters showed higher methylation in tumors than CFLT with the highest methylation seen in tumors from COPD cases (p < 0.05). These results were independently validated using The Cancer Genome Atlas data. CCDC37 methylation was more prevalent in sputum from COPD than non-COPD smokers (p < 0.005) from two cohorts. CCDC37 and MAP1B expression was dramatically repressed in tumors and CFLT from COPD than non-COPD cases, p less than 0.02.
conclusionsThe reduced expression of CCDC37 and MAP1B associated with COPD likely predisposes these genes to methylation that in turn, may contribute to lung cancer.
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