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DNA methylation loss coupled with mitotic cell division promotes immune evasion of tumours with high mutation load [RNA-seq]

ABSTRACT: DNA methylation loss coupled with mitotic cell division promotes immune evasion of tumours with high mutation load [RNA-seq]

PROVIDER: PRJNA557841 | ENA |

REPOSITORIES: ENA

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DNA methylation loss coupled with mitotic cell division promotes immune evasion of tumours with high mutation load

Project description:Mitotic cell division increases tumour mutation burden and copy number load with a positive and inverse correlation, respectively, with the clinical benefit of immunotherapy. Markers of cell division correlate also with genomic demethylation involving methylation loss in late-replicating partial methylation domains. Here we find that immunomodulatory pathway genes are concentrated in these domains and transcriptionally repressed in demethylated tumours with CpG island promoter hypermethylation. Global methylation loss correlated with immune evasion signatures independently of mutation burden and aneuploidy. Methylome data of our cohort (n = 60) and a published cohort (n = 81) in lung cancer and a melanoma cohort (n = 40) consistently demonstrated that genomic methylation alterations counteract the contribution of high mutation burden and increase immunotherapeutic resistance. Higher predictive power was observed for methylation loss than mutation burden. We also found that genomic hypomethylation correlates with the immune escape signatures of aneuploid tumours. Hence, DNA methylation alterations implicate epigenetic modulation as a combination regimens for precision immunotherapy.

2019-07-31 | GSE119144 | GEO

DNA methylation loss coupled with mitotic cell division promotes immune evasion of tumours with high mutation load [RNA-seq]

Project description:Mitotic cell division increases tumour mutation burden and copy number load, predictive markers of the clinical benefit of immunotherapy. Cell division correlates also with genomic demethylation involving methylation loss in late-replicating partial methylation domains. Here we find that immunomodulatory pathway genes are concentrated in these domains and transcriptionally repressed in demethylated tumours with CpG island promoter hypermethylation. Global methylation loss correlated with immune evasion signatures independently of mutation burden and aneuploidy. Methylome data of our cohort (n = 60) and a published cohort (n = 81) in lung cancer and a melanoma cohort (n = 40) consistently demonstrated that genomic methylation alterations counteract the contribution of high mutation burden and increase immunotherapeutic resistance. Higher predictive power was observed for methylation loss than mutation burden. We also found that genomic hypomethylation correlates with the immune escape signatures of aneuploid tumours. Hence, DNA methylation alterations implicate epigenetic modulation in precision immunotherapy.

2019-08-02 | GSE135222 | GEO

DNA methylation loss coupled with mitotic cell division promotes immune evasion of tumours with high mutation load

Project description:DNA methylation loss coupled with mitotic cell division promotes immune evasion of tumours with high mutation load

| PRJNA488256 | ENA

DNA Methylation loss coupled with mitotic cell division promotes immune evasion of tumours with high mutation load

| EGAS00001003731 | EGA

Project description:DNA methylation loss coupled with mitotic cell division promotes immune evasion of tumours with high mutation load

| PRJNA488496 | ENA

DNA methylation loss promotes immune evasion of tumours with high mutation and copy number load.

Project description: Not available

| S-EPMC6753140 | biostudies-literature

KP lung tumours

Project description:KP lung tumours

| PRJNA577056 | ENA

BRD4 marks chromatin on cell cycle genes activates their transcription and orchestrates mitotic cell division

Project description:BRD4 marks chromatin on cell cycle genes activates their transcription and orchestrates mitotic cell division

2022-01-31 | GSE153572 | GEO

Cohesin removal reprograms mitotic gene expression upon mitotic entry

Project description:Cohesin removal reprograms mitotic gene expression upon mitotic entry

| PRJNA587151 | ENA

Effect of oestrogen treatment on growth of human angiomyolipoma xenograft tumours

Project description:SV7tert AML cells were obtained from ATCC and cultured in Dulbecco's modified essential medium (DMEM), glutamine (4mmol) and 10% foetal bovine serum (FBS). Two million SV7tertAML cells were subcutaneously injected into nude mice either with or without subcutaneous oestrogen pellets (n=4 per group); oestrogen was added using 0.36mg 60 day release oestrogen pellets implanted sub-cutaneously. Mice were housed in pathoflex isolators at 26°C, on 12 hour light / dark cycles. Irradiated RB2 diet and autoclaved water provided ad libertum. All oestrogen treated mice inoculated with SV7tertAML cells developed subcutaneous tumours which required termination of the animals at six weeks due to tumour load. These primary tumours were removed and fragments placed subcutaneously in further nude mice which went on to develop tumours both in the presence and absence of oestrogen. Mice were weighed weekly and their clinical condition closely monitored by a trained observer. Mice were terminated individually when the tumour cross-sectional area reached 250mm2 or sooner, which has previously been seen to be below the limit of 10% of initial body weight set by the UKCCCR guidelines. Tumours were removed and a portion flash frozen in liquid nitrogen. RNA was extracted from five tumours from oestrogen treated and control animals. Equal quantities of RNA was pooled and quality checked by Agilent Bioanylyser. Experimenter name = Simon Johnson Experimenter institute = Queens Medical Centre Keywords: estrogen treatment, angiomyolipoma xenograft tumors

2007-09-19 | GSE5868 | GEO

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