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Temporal genomic analysis of melanoma rejection identifies regulators of tumor immune evasion [scc]

ABSTRACT: Temporal genomic analysis of melanoma rejection identifies regulators of tumor immune evasion [scc]

PROVIDER: PRJNA1036175 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26684673_1.fastq.gz	Fastqsanger.gz
	SRR26684673_2.fastq.gz	Fastqsanger.gz
	SRR26684674_1.fastq.gz	Fastqsanger.gz
	SRR26684674_2.fastq.gz	Fastqsanger.gz
	SRR26684675_1.fastq.gz	Fastqsanger.gz

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Temporal genomic analysis of melanoma rejection identifies regulators of tumor immune evasion

Project description:Temporal genomic analysis of melanoma rejection identifies regulators of tumor immune evasion

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Temporal genomic analysis of melanoma rejection identifies regulators of tumor immune evasion [scc35]

Project description:Temporal genomic analysis of melanoma rejection identifies regulators of tumor immune evasion [scc35]

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Temporal genomic analysis of melanoma rejection identifies regulators of tumor immune evasion [scc]

Project description:Decreased intra-tumor heterogeneity (ITH) correlates with increased patient survival and immunotherapy response. However, the mechanism underlying this association remains inconclusive since additional factors dictate tumor aggressiveness. Here, we study the mechanisms responsible for the immune escape of tumors bearing low ITH. We compare homogeneous, genetically similar single-cell clones that are rejected vs. non-rejected after transplantation. We followed the growth of these clone-derived tumors over time using single-cell RNA sequencing and immunophenotyping. Non-rejected clones show high infiltration of tumor-associated macrophages (TAM), increased Mif expression, lower T-cell infiltration, and increased T-cell exhaustion. Mif KO led to smaller tumors and reversed these immune phenotypes, validating its role in the growth of low ITH tumors. Mif secretion by these tumor cells causes TAM infiltration, thus contributing to an immunosuppressive environment that supports aggressive growth. We validated this result in melanoma patient data, confirming that high levels of MIF distinguish aggressive from non-aggressive ITHs.

2023-12-12 | GSE247058 | GEO

Temporal genomic analysis of melanoma rejection identifies regulators of tumor immune evasion.

Project description:Decreased intra-tumor heterogeneity (ITH) correlates with increased patient survival and immunotherapy response. However, even highly homogenous tumors may display variability in their aggressiveness, and how immunologic-factors impinge on their aggressiveness remains understudied. Here we studied the mechanisms responsible for the immune-escape of murine tumors with low ITH. We compared the temporal growth of homogeneous, genetically-similar single-cell clones that are rejected vs. those that are not-rejected after transplantation in-vivo using single-cell RNA sequencing and immunophenotyping. Non-rejected clones showed high infiltration of tumor-associated-macrophages (TAMs), lower T-cell infiltration, and increased T-cell exhaustion compared to rejected clones. Comparative analysis of rejection-associated gene expression programs, combined with in-vivo CRISPR knockout screens of candidate mediators, identified Mif (macrophage migration inhibitory factor) as a regulator of immune rejection. Mif knockout led to smaller tumors and reversed non-rejection-associated immune composition, particularly, leading to the reduction of immunosuppressive macrophage infiltration. Finally, we validated these results in melanoma patient data.

| S-EPMC10705560 | biostudies-literature

Temporal genomic analysis of melanoma rejection identifies regulators of tumor immune evasion

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

2023-12-12 | GSE247059 | GEO

Temporal genomic analysis of melanoma rejection identifies regulators of tumor immune evasion [scc35]

2023-12-12 | GSE247057 | GEO

Pseudo-temporal ordering of individual cells reveals regulators of differentiation

Project description:Single-cell expression profiling by RNA-Seq promises to exploit cell-to-cell variation in gene expression to reveal regulatory circuitry governing cell differentiation and other biological processes. Here, we describe Monocle, a novel unsupervised algorithm for ordering cells by progress through differentiation that dramatically increases temporal resolution of expression measurements. This reordering unmasks switch-like changes in expression of key regulatory factors, reveals sequentially organized waves of gene regulation, and exposes regulators of cell differentiation. A functional screen confirms that a number of these regulators dramatically alter the efficiency of myoblast differentiation, demonstrating that single-cell expression analysis with Monocle can uncover new regulators even in well-studied systems.

2014-03-23 | GSE52529 | GEO

ST779-MRSA with a pseudo SCCmec-SCC-SCC (CRISPR)

Project description:WHole genome sequencing of a ST779-MRSA isolate identified a novel composite SCC element we have termed a pseudo SCCmec-SCC-SCC(CRISPR) element

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Expression data from rejection and non-rejection kidney transplant patients

Project description:Acute renal allograft rejection is an important complication in kidney transplantation. Accurate diagnosis of rejection events is necessary for timely response and treatment. We illustrate the usefulness and biological relevance of selected multivariate approaches to detect rejection from genomic and proteomic signals. The data was used to study gene expression changes using whole genome microarray analysis of peripheral blood from subjects with acute rejection (n=20) and non-rejecting controls (n=20) to obtain insight into the molecular and biological causation of acute renal allograft rejection when combined with proteomics (iTRAQ) data for the same patients/time-points.

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MicroRNAs as Regulators of the Immune Response during Allograft Rejection

Project description:MicroRNAs are small non-coding RNA molecules that regulate the post-transcriptional expression of target genes. In addition to being involved in many biologic processes including development, cell differentiation, proliferation, and apoptosis, microRNAs are important regulators in innate and adaptive immune responses. Distinct sets of expressed miRNAs are found in different cell types and tissues and aberrant expression of microRNAs is associated with many disease states. MicroRNA expression was examined in a model of heterotopic heart transplantation by microarray analyses and a unique profile was detected in rejecting allogeneic transplants (BALB/C to C57BL/6) as compared to syngeneic transplants (C57BL/6 to C57BL/6). The microRNA miR-182 was significantly increased in rejecting cardiac allografts and in mononuclear cells that infiltrate the grafts. Forkhead Box (FOX) proteins are a family of important transcription factors and FOXO1 is a target of miR-182. As miR-182 increases after transplant, there is a concomitant post-transcriptional decrease in FOXO1 expression in heart allografts that is localized to both the cardiomyocytes and CD3+ T cells. The microRNA miR-182 is significantly increased in both PBMC and plasma during graft rejection suggesting potential as a biomarker of graft status. Our results identify microRNAs that may regulate alloimmune responses and graft outcomes. In total 14 microRNA microarrays data. For heart graft: each sample column corresponds to the expression profile of 3 pooled syngeneic or 3 pooled allogeneic heart grafts or 3 pooled normal heart. For graft infiltrating lymphocytes (GILs): each sample column corresponds to the expression profile of 3 pooled syngeneic or 3 pooled allogeneic GILs or 3 pooled normal PBMC.

2012-12-30 | E-GEOD-32545 | biostudies-arrayexpress

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