Project description:This SuperSeries is composed of the following subset Series: GSE39013: Stability of miRNA in FFPE tumour samples exhibiting degraded mRNA [Cervix samples series 1] GSE39014: Stability of miRNA in FFPE tumour samples exhibiting degraded mRNA [Cervix samples series 2] GSE39015: Stability of miRNA in FFPE tumour samples exhibiting degraded mRNA [Cervix samples miRNA] GSE39016: Stability of miRNA in FFPE tumour samples exhibiting degraded mRNA [Bladder samples] GSE39066: Stability of miRNA in FFPE tumour samples exhibiting degraded mRNA [cell lines] Refer to individual Series
Project description:Using murine models that exclude variation in host genetics, environmental factors and tumour mutation burden, limiting variation between animals to naturally diverse TCRβ repertoires, we applied bulk TCRseq to study TCRβ repertoire dynamics in ICT responders and non-responders
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.
Project description:Skeletal homeostasis if profoundly altered in response to multiple-myeloma tumour burden. Osteocytes are pivotal regulatory cells in skeletal homeostasis. This dataset was used to examine the differences in the osteocyte-specific transcriptome that may underlie the changes in skeletal homeostasis that occur with multiple myeloma tumour burden. We performed total-RNA transcriptome sequencing on the isolated osteocytes from tumour-burdened and naive bone samples, as well as the marrow from these samples. With this experimental design we can identify genes that are changed specifically in osteocytes in the presence of multiple myeloma tumour burden.
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.
Project description:Genome-wide DNA methylation analysis of colorectal tumour samples from 44 FFPE tumour and 15 FFPE normal mucosa samples was performed to invesgitate genome-wide DNA methylation signatures that can distinguish MLH1 epimutation carrier CRCs. This was further applied to resolve clinically challenging CRCs including MLH1 promoter VUS carriers and MLH1 methylated EOCRCs
Project description:To screen the related miRNAs in the occurence and development of sebaceous gland carcinoma(SGC) of the eyelid , we have employed Human Agilient microarray expression profiling as a discovery platform to identify differentially expressed miRNAs for SGC and TP53 mtation related miRNAs. Human formalin-fixed paraffin-embedded (FFPE) SGC tissues and para-carcinoma sebaceous gland(SG) FFPE samples from SGC patients were screened using microarray assay. Human FFPE SGC tissues containing TP53 mutation and human FFPE SGC tissues without TP53 mutation were screened using microarray. The overlap of two sets of microarray differentially upregulated miRNAs were selected as our research object.
Project description:162 FFPE samples, representing six different tumour types, were profiled in triplicate across three independent laboratories. OncoScan¬ FFPE assay data was then analysed for reproducibility of genome-wide copy number, loss of heterozygosity and somatic mutations.
