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Inhibition of histone methyltransferase EZH2 for immune-interception of colorectal cancer in Lynch syndrome

ABSTRACT: Inhibition of histone methyltransferase EZH2 for immune-interception of colorectal cancer in Lynch syndrome

PROVIDER: PRJNA1164782 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR30786437_1.fastq.gz	Fastqsanger.gz
	SRR30786437_2.fastq.gz	Fastqsanger.gz
	SRR30786438_1.fastq.gz	Fastqsanger.gz
	SRR30786438_2.fastq.gz	Fastqsanger.gz
	SRR30786439_1.fastq.gz	Fastqsanger.gz

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Inhibition of Histone Methyltransferase EZH2 for Immune-Interception of Colorectal Cancer in Lynch Syndrome

Project description:Inhibition of Histone Methyltransferase EZH2 for Immune-Interception of Colorectal Cancer in Lynch Syndrome

| PRJNA1162779 | ENA

Inhibition of histone methyltransferase EZH2 for immune-interception of colorectal cancer in Lynch syndrome

Project description:This study investigates the potential of EZH2 inhibition as a preventive strategy for colorectal cancer in Lynch Syndrome (LS) by modulating the immune system. Using a mouse model of LS and colonic organoids, researchers treated the mice with the EZH2 inhibitor GSK503 and observed increased CD4+ and CD8+ T cells in both spleen and colon tissue. Over a 9-week period, the inhibitor reduced adenoma formation, indicating its preventive efficacy. RNA sequencing and ChIPseq analyses revealed that EZH2 inhibition activated immune and apoptotic markers and decreased H3K27 methylation, leading to changes in gene regulation. These findings suggest that EZH2 inhibitors hold promise for cancer prevention in LS by reprogramming immune responses and gene expression patterns.

2025-02-14 | GSE277940 | GEO

Inhibition of Histone Methyltransferase EZH2 for Immune-Interception of Colorectal Cancer in Lynch Syndrome

2025-02-14 | GSE277544 | GEO

Inhibition of histone methyltransferase EZH2 for immune interception of colorectal cancer in Lynch syndrome.

Project description: Not available

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Naproxen Chemoprevention Promotes Immune Activation In Lynch Syndrome Colorectal Mucosa

Project description:Lynch syndrome (LS) patients are at markedly increased risk for colorectal cancer. It is being increasingly recognized that the immune system plays an essential role in LS tumor development. Therefore, immune interception strategies are emerging as a novel way to prevent cancer in LS. This phase Ib, placebo-controlled, randomized clinical trial and a co-clinical trial using a LS mouse model and patient-derived organoids aims to evaluate the safety and tolerability as well as to discover novel molecular pathways involved in the activity of Naproxen as chemoprevention in LS patients.

2020-06-25 | GSE144381 | GEO

Expression of immune-related genes in the normal colorectal mucosa and colorectal carcinoma samples from Lynch syndrome individuals

Project description:Colorectal carcinomas arising in the context of Lynch syndrome, the most common inherited cancer syndrome, typically show deficiency of the DNA MMR (mismatch repair) system. Lack of functional MMR leads to accumulation of frameshift mutations at micosatellites (microsatellite instability, MSI). High load of highly immunogenic tumor-specific frameshift neoantigens results in strong immune response against Lynch syndrome MSI cancers. Previous studies have shown systemic immune responses against frameshift neoantigens in Lynch syndrome carriers long before tumor manifestation. In the present study, we analyzed the immune profile of normal colorectal mucosa in Lynch syndrome carriers without current or previous cancer history and in Lynch syndrome colorectal cancer patients, as well as of Lynch syndrome colorectal carcinomas. The unsupervised cluster analysis of gene expression data revealed a sharp differentiation between normal mucosa from Lynch syndrome individuals with and without manifest cancer as well as between normal mucosa in general and Lynch syndrome cancer tissue. Deconvolution analysis for predicting the prevalence of immune cell population among the three groups revealed 10 out of 14 investigated populations to be significantly different between the three tissue types (FDR=10%). In contrast to normal mucosa samples, tumor tissue showed overrepresentation of immune-suppressive cell populations, such as regulatory T cells and neutrophils. Taken together with the quantitative T cell density analysis on the basis of immunohistochemical T cell stainings, our data show strong immune infiltration of the normal colorectal mucosa in Lynch syndrome individuals even in the absence of a manifest cancer.

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Genomic profiling of colorectal cancer from patients with Lynch syndrome and Familial colorectal cancer type X with comparison to sporadic microsatelite stable and instable colorectal cancer

Project description:Lynch syndrome and Familial colorectal cancer type X (FCCTX) are clinically diagnosed using the same criteria, but genomic differences exist between these two groups and the genomic profiles share similarities with their sporadic counterparts, mismatch repair (MMR) deficient and proficient tumors, respectively. Array-based comparative genomic hybridization was performed on 91 tumors, comprising 23 Lynch syndrome (AH), 23 FCCTX (AA), 23 sporadic MMR deficient (AM) and 22 sporadic MMR proficient tumors, in order to identify differences between Lynch syndrome and FCCTX.

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Characterization of the EZH2-MMSET histone methyltransferase regulatory axis in cancer

Project description:This SuperSeries is composed of the following subset Series: GSE41651: Characterization of the EZH2-MMSET histone methyltransferase regulatory axis in cancer [expression] GSE41652: Characterization of the EZH2-MMSET histone methyltransferase regulatory axis in cancer [ChIP-seq] Refer to individual Series

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Project description:Heredity is a major cause of ovarian cancer. Lynch syndrome is associated with 10-12% risk of ovarian cancer, diagnosis at young age and a predilection for endometrioid and clear cell tumors. Global gene expression profiling applied to 25 Lynch syndrome-associated and 42 sporadic ovarian cancers revealed 335 differentially expressed genes and involvement of the mTOR and the MAPK/ERK pathways. The clear cell tumors had distinct expression profiles with upregulation of HER2 and apoptosis signaling pathways. The distinct expression profiles provide clues relevant for hereditary tumorigenesis and may be relevant for therapeutic strategies and refined diagnostics in ovarian cancer linked to Lynch syndrome. Ovarian cancers linked to Lynch syndrome (n=25) were compared to a matched series of sporadic ovarian cancers (n=42), selected from a population-based consecutive series in which hereditary was excluded based on family history, normal MMR protein staining and lack of mutations in BRCA1 and BRCA2.

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Identification and Validation of Frameshift Neoantigens for Mismatch-Repair Deficient Lynch Syndrome

Project description:Lynch syndrome (LS) patients develop DNA mismatch repair deficient tumors which generate high loads of neoantigens (neoAgs), thus constituting a well-defined population that can benefit from cancer immune-interception strategies, including neoantigen-based vaccines. Using paired whole-exome sequencing and mRNAseq of colorectal cancers (CRC) (n=13) and pre-cancers (n=61) from our LS patient cohort (N=46), we performed in-silico prediction and immunogenicity ranking of highly recurrent frameshift-neoags, followed by their in-vitro validation. We described the somatic mutation landscape in all cancers and pre-cancers, and showed that mutation burden is positively correlated with neoAgs load. Furthermore, our in-vitro validation showed a 65% validation rate of our top 100 predicted neoags. Consistent with neoAgs burden, our transcriptomic results revealed increased infiltration of CD8+ and CD4+ T-cells in microsatellite unstable samples. Overall, our neoAgs catalog and all other findings, improve our understanding of cancer development in LS and guide us towards the advancement of immunoprevention vaccine strategies.

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