Towards the DNA methylation haplotype map of 11 common solid cancers
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ABSTRACT:
PROVIDER: PRJNA875426 | ENA |
REPOSITORIES: ENA
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Project description:Aberrant DNA methylation is an epigenetic hallmark of cancer, known to play an essential role in cancer initiation, progression and drug resistance. Traditional analyses focus on mean methylation that measures the aggregated signal across a group of cells and neglect intra-sample heterogeneity. Sequencing-based techniques such as whole genome bisulfite sequencing (WGBS) are now widely used to measure DNA methylation on each read at single-nucleotide resolution. A single read fragment stems from a single chromosome of a single cell and represents a DNA methylation haplotype (mHap). In this study, we have profiled 110 fresh frozen tumor samples that cover 11 most common solid cancer types using WGBS and constructed a comprehensive DNA methylation haplotype map.
2024-08-23 | GSE212391 | GEO
Project description:Cancers disrupt host homeostasis in various manners but the identity of host factors underlying such disruption remains largely unknown. Here we show that nicotinamide-N-methyltransferase (NNMT) is a novel host factor that mediates metabolic dysfunction in the livers of cancer-bearing mice. Multiple solid cancers distantly increase expression of Nnmt and its product 1-methylnicotinamide (MNAM) in the liver. Multi-omics analyses reveal suppression of the urea cycle accompanied by accumulation of amino acids, and enhancement of uracil biogenesis in the livers of cancer-bearing mice. Importantly, genetic deletion of Nnmt leads to alleviation of these metabolic abnormalities, and buffers cancer-dependent weight loss and reduction of the voluntary wheel-running activity. Our data also demonstrate that MNAM is capable of affecting urea cycle metabolites in the liver. These results suggest that cancers up-regulate the hepatic NNMT pathway to rewire liver metabolism towards uracil biogenesis rather than nitrogen disposal via the urea cycle, thereby disrupting host homeostasis. Anionic polar metabolites (i.e., organic acids, sugar phosphates, nucleotides,etc.) were analyzed via IC/HR/MS/MS. Cationic polar metabolites (i.e., amino acids, bases, nucleosides, NAM, SAM, MNAM, SAH, me2PY, me4PY, etc) were analyzed via PFPP-LC/HR/MS/MS.
2022-05-11 | ST002163 | MetabolomicsWorkbench
Project description:We report a map of H3K4me3 - an activiting expression histone modification in C6 rat glioma cells. The data was obtained using whole genome high throughput technology. The sequencing was performed on Solid 5500xl platform.
2015-05-07 | GSE46822 | GEO
Project description:We report a map of H3K4me3 - an activiting expression histone modification in C6 rat glioma cells. The data was obtained using whole genome high throughput technology. The sequencing was performed on Solid 5500xl platform. Examination of H3K4me3 histone modification in C6 rat glioma cell line
2015-05-07 | E-GEOD-46822 | biostudies-arrayexpress
Project description:Multi-omics of Bladder Cancers of Solid Organ Transplant Recipients
| PRJNA865854 | ENA
Project description:Multi-omics of Bladder Cancers of Solid Organ Transplant Recipients
| PRJNA865855 | ENA
Project description:Cancers disrupt host homeostasis in various manners but the identity of host factors underlying such disruption remains largely unknown. Here we show that nicotinamide-N-methyltransferase (NNMT) is a novel host factor that mediates metabolic dysfunction in the livers of cancer-bearing mice. Multiple solid cancers distantly increase expression of Nnmt and its product 1-methylnicotinamide (MNAM) in the liver. Multi-omics analyses reveal suppression of the urea cycle accompanied by accumulation of amino acids, and enhancement of uracil biogenesis in the livers of cancer-bearing mice. Importantly, genetic deletion of Nnmt leads to alleviation of these metabolic abnormalities, and buffers cancer-dependent weight loss and reduction of the voluntary wheel-running activity. Our data also demonstrate that MNAM is capable of affecting urea cycle metabolites in the liver. These results suggest that cancers up-regulate the hepatic NNMT pathway to rewire liver metabolism towards uracil biogenesis rather than nitrogen disposal via the urea cycle, thereby disrupting host homeostasis. Anionic polar metabolites (i.e., organic acids, sugar phosphates, nucleotides, etc.) were analyzed via IC/HR/MS/MS. Cationic polar metabolites (i.e., amino acids, bases, nucleosides, NAM, SAM, MNAM, SAH, me2PY, me4PY, etc) were analyzed via PFPP-LC/HR/MS/MS.
2022-05-13 | ST002167 | MetabolomicsWorkbench
Project description:Towards an integrative map of a single cell type's transcription factor landscape
| PRJNA412590 | ENA
Project description:BackgroundA stronger spatial clustering of cancer burden indicates stronger environmental and human behavioral effects. However, which common cancers in China have stronger spatial clustering and knowledge gaps regarding the environmental and human behavioral effects have yet to be investigated. This study aimed to compare the spatial clustering degree and hotspot patterns of 11 common cancers in mainland China and discuss the potential environmental and behavioral risks underlying the patterns.MethodsCancer incidence data recorded at 339 registries in 2014 was obtained from the "China Cancer Registry Annual Report 2017". We calculated the spatial clustering degree of the common cancers using the global Moran's Index and identified the hotspot patterns using the hotspot analysis.ResultsWe found that esophagus, stomach and liver cancer have a significantly higher spatial clustering degree ([Formula: see text]) than others. When by sex, female esophagus, male stomach, male esophagus, male liver and female lung cancer had significantly higher spatial clustering degree ([Formula: see text]). The spatial clustering degree of male liver was significantly higher than that of female liver cancer ([Formula: see text]), whereas the spatial clustering degree of female lung was significantly higher than that of male lung cancer ([Formula: see text]). The high-risk areas of esophagus and stomach cancer were mainly in North China, Huai River Basin, Yangtze River Delta and Shaanxi Province. The hotspots for liver and male liver cancer were mainly in Southeast China and south Hunan. Hotspots of female lung cancer were mainly located in the Pearl River Delta, Shandong, North and Northeast China. The Yangtze River Delta and the Pearl River Delta were high-risk areas for multiple cancers.ConclusionsThe top highly clustered cancer types in mainland China included esophagus, stomach and liver cancer and, by sex, female esophagus, male stomach, male esophagus, male liver and female lung cancer. Among them, knowledge of their spatial patterns and environmental and behavioral risk factors is generally limited. Potential factors such as unhealthy diets, water pollution and climate factors have been suggested, and further investigation and validation are urgently needed, particularly for male liver cancer. This study identified the knowledge gap in understanding the spatial pattern of cancer burdens in China and offered insights into targeted cancer monitoring and control.
| S-EPMC9377081 | biostudies-literature
Project description:The contribution of the majority of frequently mutated genes to tumourigenesis is not fully defined. Many aggressive human cancers, such as triple negative breast cancers (TNBCs), have a poor prognosis and lack tractable biomarkers and targeted therapeutic options. Here, we systematically characterize loss-of-function mutations to generate a functional map of novel driver genes in a 3-dimensional model of breast cancer heterogeneity that more readily recapitulates the unfavourable tumour microenvironment in vivo. This identified the histone acetyltransferase CREBBP as a potent tumour suppressor gene whose silencing provided a 3D-specific growth advantage only under oxygen and nutrient deplete conditions. CREBBP protein expression was altered in a substantial proportion of TNBCs as well as several other solid tumours, including endometrial, bladder, ovarian and squamous lung cancers. In multiple primary tumours and cell models, loss of CREBBP activity resulted in upregulation of the FOXM1 transcriptional network. Strikingly, treatment with a range of CDK4/6 inhibitors (CDK4/6i), that indirectly target FOXM1 activity, selectively impaired growth in both CREBBP-altered spheroids and cell line xenografts and patient derived models from multiple tumour types. This study is the first to provide rationale for CREBBP as a biomarker for CDK4/6i response in cancer representing a new treatment paradigm for tumours that harbour CREBBP alterations that have limited therapeutic options.
2022-03-23 | PXD012098 | Pride