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DNA methylome and transcriptome landscapes of cancer-associated fibroblasts reveal a smoking-associated malignancy index

ABSTRACT: DNA methylome and transcriptome landscapes of cancer-associated fibroblasts reveal a smoking-associated malignancy index

PROVIDER: PRJNA630700 | ENA |

REPOSITORIES: ENA

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DNA methylome and transcriptome landscapes of cancer-associated fibroblasts reveal a smoking-associated malignancy index

Project description:DNA methylome and transcriptome landscapes of cancer-associated fibroblasts reveal a smoking-associated malignancy index

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DNA methylome and transcriptome landscapes of cancer-associated fibroblasts reveal a smoking-associated malignancy index

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DNA methylome and transcriptome landscapes of cancer-associated fibroblasts reveal a smoking-associated malignancy index

Project description:Unlike the better-studied aberrant epigenome in the tumor, the clinicopathologic impact of DNA methylation in the tumor microenvironment (TME), especially the contribution from cancer-associated fibroblasts (CAFs), remains elusive. CAFs exhibit profound patient-to-patient tumorigenic heterogeneity. We asked whether such heterogeneity may be exploited to quantify the level of TME malignancy. We developed a robust and efficient methylome/transcriptome co-analytical system for CAFs and paired normal fibroblasts (NFs) from non-small-cell lung cancer patients. We found 14,781 CpG sites of CAF/NF differential methylation, of which 3,707 sites showed higher methylation changes in ever-smokers than in nonsmokers. Concomitant CAF/NF differential gene expression analysis pointed to a subset of 54 smoking-associated CpG sites with strong methylation-regulated gene expression. A methylation index that summarizes the β values of these CpGs was built for NF/CAF discrimination (MIND) with high sensitivity and specificity. The potential of MIND in detecting premalignancy across individual patients was shown. MIND succeeded in predicting tumor recurrence in multiple lung cancer cohorts without reliance on patient survival data, suggesting that the malignancy level of TME may be effectively graded by this index. Precision TME grading may provide additional pathological information to guide cancer prognosis and open up more options in personalized medicine.

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Cross-sectional association of salivary proteins with age, sex, body mass index, smoking, and education

Project description:In a cross-sectional approach, we analyzed the influence of age, sex, body mass index (BMI), smoking, and education on salivary protein signatures in whole saliva samples of 187 individuals. Subjects were randomly selected from the population-based Study of Health in Pomerania (SHIP-Trend).

2017-05-16 | PXD006367 | Pride

DNA methylome and transcriptome landscapes of cancer-associated fibroblasts reveal a smoking-associated malignancy index

Project description:This SuperSeries is composed of the SubSeries listed below.

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DNA methylome and transcriptome landscapes of cancer-associated fibroblasts reveal a smoking-associated malignancy index.

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Project description:Cannabis use has been controversial, largely having been designated a controlled substance over the last century. The link between cannabis smoking and disease pathogenesis may best be explored through DNA methylation, an epigentic mechanism. We investigated the relationship between epigenetic age and cannabis smoking in participants within the Canadian Cohort of Obstructive Lung Disease (CanCOLD) cohort (n=93) (ClinicalTrials.gov identifier NCT00920348). Blood samples were profiled for DNA methylation using the Illumina MethylationEPIC BeadChipv1 at two separate laboratories and the blood epigenetic age of each sample was calculated using the Clock Foundation tool (https://dnamage.clockfoundation.org). An ANOVA was used to identify differences in the age acceleration residuals associated with cannabis smoking status (never, former, and current), adjusted for chronological age, sex, body mass index (BMI), batch, cigarette smoking status, and the first two principal components of blood cell proportions. Our observations indicated that current cannabis smoking and higher joint-years exposure are associated with epigenetic age acceleration; cessation, however, may help to normalize in part this age acceleration.

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