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Consensus molecular subtype transition during progression of colorectal cancer [Tumor Signaling 360™ Panel]

ABSTRACT: Consensus molecular subtype transition during progression of colorectal cancer [Tumor Signaling 360™ Panel]

PROVIDER: PRJNA994464 | ENA |

REPOSITORIES: ENA

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Consensus molecular subtype transition during progression of colorectal cancer [Tumor Signaling 360™ Panel]

Project description:The consensus molecular subtype (CMS) classification divides colorectal cancer (CRC) into four distinct subtypes based on RNA-expression profiles. The biological differences between CMSs are already present in CRC precursor lesions, but not all CMSs pose the same risk of malignant transformation. To fully understand the path to malignant transformation and to determine whether CMS is a fixed entity during progression, genomic and transcriptomic data from two regions of the same CRC lesion were compared: the precursor and carcinoma region. In total, 24 patients that underwent endoscopic removal of T1-2 CRC were included. Regions were subtyped for CMS and DNA mutation analysis was performed. Additionally, a set of 85 benign adenomas was CMS subtyped. This analysis revealed that almost all benign adenomas were classified as CMS3 (91.8%). In contrast, CMS2 was the most prevalent subtype in precursor regions (66.7%), followed by CMS3 (29.2%). CMS4 was absent in precursor lesions and originated at the carcinoma stage. Importantly, CMS switching occurred in a substantial number of cases and almost all (6 out of 7) CMS3 precursor regions showed a shift to a different subtype in the carcinoma part of the lesion, which in 4 cases was classified as CMS4. In conclusion, our data indicate that CMS3 is related to a more indolent type of precursor lesions that less likely progresses to CRC and when this occurs it often associates with a subtype change that includes the more aggressive mesenchymal CMS4. In contrast, an acquired CMS2 signature appeared to be rather fixed during early CRC development. Combined our data shows that subtype changes occur during progression and that CMS3 switching is related to changes in the genomic background through acquisition of a novel driver mutation (TP53) or selective expansion of a clone, but also occurred independent of such genetic changes.

2023-07-13 | GSE237248 | GEO

NanoString Human PC3 nCounter PanCancer IO 360 panel

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Consensus molecular subtype transition during progression of colorectal cancer

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miRCURY LNA™ Universal RT microRNA PCR, Urine Exosome Focus Panel

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NanoSTRING nCounter Mouse Tumor Signaling 360 Panel for mouse ileum tissue

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NanoSTRING nCounter Human tumor Signaling 360 Panel for xenograft tumor tissue

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Consensus molecular subtype transition during progression of colorectal cancer [NanoClassifier Gene Set]

Project description:Consensus molecular subtype transition during progression of colorectal cancer [NanoClassifier Gene Set]

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Spatial analysis reveals distinct immune phenotypes and tertiary lymphoid structure-like aggregates in pediatric acute myeloid leukemia [Nanostring PanCancer IO 360]

Project description:Comparison of immune-infiltrated bone marrow samples (n=6) with immune-depleted bone marrow samples (n=17) of pediatric acute myeloid leukemia patients using the Nanostring PanCancer IO 360 panel.

2024-08-27 | GSE228481 | GEO

Gene expression related to tumor infiltrating lymphocytes status and BRAFV600E status in naive melanoma cancer patients

Project description:Gene expression profiling of a total of 770 genes included in the PanCancer IO 360™ panel+ 20 genes of interest were studied in 198 melanomas cases and correlated to TILS and BRAF600E mutation status

2022-08-31 | GSE193802 | GEO

Consensus Molecular Subtype predicts differential vulnerability of colorectal cancer to the survivin suppressant YM155 I

Project description:Tumor heterogeneity is a major challenge to the treatment of colorectal cancer (CRC). Recently, a transcriptome-based classification was developed, segregating CRC into four consensus molecular subtypes (CMS) with distinct biological and clinical characteristics. Here, we applied the CMS classification on CRC cell lines to identify novel subtype-specific drug vulnerabilities. We combined publicly available transcriptome data from multiple resources to assign 159 CRC cell lines to CMS. By integrating results from large scale drug screens, we discovered that CMS1 cancer is highly vulnerable to the survivin suppressor YM155. We confirmed our results using an independent panel of CRC cell lines and demonstrate a 100-fold higher sensitivity of CMS1 lines. This vulnerability was specific to YM155 and not observed for commonly used chemotherapeutic agents. In CMS1 cancer, low concentrations of YM155 induced apoptosis and expression signatures associated with NFkappaB and ER stress mediated apoptosis signaling. Using a genome-wide CRISPR/Cas9 screen, we discovered a novel role of genes involved in LDL-receptor recycling as modulators of YM155 response in CMS1 CRC. Our work shows that combining drug response data with CMS classification in cell lines can reveal specific vulnerabilities and propose YM155 as novel CMS1 specific drug.

2018-07-03 | GSE116529 | GEO

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