Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA353380 | ENA |
REPOSITORIES: ENA
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Project description:Retinoblastoma (RB) is an intraocular childhood tumor which, if left untreated, leads to blindness and mortality. Nucleolin (NCL) protein which is differentially expressed on the tumor cell surface, binds ligands and regulates carcinogenesis and angiogenesis. We found that NCL is over expressed in RB tumor tissues and cell lines compared to normal retina. We studied the effect of nucleolin-aptamer (NCL-APT) to reduce proliferation in RB tumor cells. Aptamer treatment on the RB cell lines (Y79 and WERI-Rb1) led to significant inhibition of cell proliferation. Locked nucleic acid (LNA) modified NCL-APT administered subcutaneously (s.c.) near tumor or intraperitoneally (i.p.) in Y79 xenografted nude mice resulted in 26 and 65% of tumor growth inhibition, respectively. Downregulation of inhibitor of apoptosis proteins, tumor miRNA-18a, altered serum cytokines, and serum miRNA-18a levels were observed upon NCL-APT treatment. Desorption electrospray ionization mass spectrometry (DESI MS)-based imaging of cell lines and tumor tissues revealed changes in phosphatidylcholines levels upon treatment. Thus, our study provides proof of concept illustrating NCL-APT-based targeted therapeutic strategy and use of DESI MS-based lipid imaging in monitoring therapeutic responses in RB.
2016-11-15 | GSE89818 | GEO
Project description:Intratumoral heterogeneity (ITH) challenges the molecular characterization of clear cell renal cell Carcinoma (ccRCC) with percutaneous biopsies and is a confounding factor in selection of molecular-targeted versus immune-based therapy. Magnetic Resonance (MR) Imaging can noninvasively assess the spatial landscape of the entire tumor. To validate MRI for ITH assessment, we implemented a radiogenomic platform through a systematic imaging based co-localization approach for multi region tissue acquisition from single tumors. We investigated if the spatial changes in imaging can predict the molecular changes using transcriptome and histopathological correlatives. Our study confirmed imaging heterogeneity as a predictor of molecular heterogeneity in ccRCC.
| EGAS00001003846 | EGA
Project description:Purpose The heterogeneity of squamous cell carcinoma tissue complicates diagnosis and an individualized therapy to a great extent. Therefore it is of utmost importance to spatially characterize this tissue heterogeneity and to identify appropriate biomarkers. Matrix assisted laser desorption/ionization (MALDI) mass spectrometry imaging (MSI) can analyze spatially resolved tissue biopsies on a molecular level. Experimental design MALDI MSI of snap frozen tissues as well as of formalin-fixed and paraffin-embedded (FFPE) tissue samples from patients with head and neck cancer (HNC) were used to analyze m/z values localized in tumor and non-tumor regions. Peptide identification was performed by using liquid chromatography (LC)-MS/MS and immunohistochemistry (IHC). Results In both FFPE and frozen tissue specimen seven characteristic masses of the tumor epithelial region were found identified. Using LC-MS/MS, the peaks were identified as Vimentin, Keratin type II, Nucleolin, Heat shock protein 90, Prelamin-A/C, Junction plakoglobin and PGAM1. Finally, Vimentin, Nucleolin and PGAM1 were verified with IHC. Conclusions and Clinical Relevance The combination of MALDI MSI, LC-MS/MS and subsequent IHC is an appropriate tool to characterize the molecular heterogeneity of tissue as well as to identify new representative biomarkers for a more individualized therapy.
2018-11-14 | PXD009144 | Pride
Project description:Immune checkpoint blockade (ICB) therapy does not benefit the majority of treated patients, and those who respond to the therapy can become resistant to it. Here we report the design and performance of systemically administered activity sensors conjugated to anti-programmed cell death protein 1 (αPD1) antibodies for the monitoring of antitumour responses to ICB therapy. RNA sequencing analysis revealed that differential expression of tumour and immune proteases underpins ICB response and resistance. We then designed a library of mass-barcoded sensors that, when cleaved by proteases, are released into urine, where they can be detected by mass spectrometry. By using syngeneic mouse models of colorectal cancer, we show that random-forest classification trained on mass-spectrometry signatures can be used to detect early antitumour responses and to discriminate resistance to ICB therapy driven by loss-of-function mutations in either the B2m or Jak1 genes. Our data supports the use of activity-based biomarkers that leverage protease dysregulation for response assessment and classification of refractory tumours.
2022-02-15 | GSE192796 | GEO
Project description:Cyanobacterial identification by native mass spectrometry
| PRJEB45336 | ENA
Project description:MMP qualitative and quantitative mass spectrometry
| PRJNA92213 | ENA
Project description:Retinoblastoma are childhood eye tumors arising from retinal precursor cells. Two distinct retinoblastoma subtypes with different clinical behavior have been described based on gene expression and methylation profiling. Using consensus clustering of DNA methylation analysis from retinoblastomas, we identified a MYCN-driven cluster of subtype 2 retinoblastomas characterized by DNA hypomethylation and high expression of genes involved in protein synthesis. Subtype 2 retinoblastomas outside the MYCN-driven cluster were characterized by high expression of genes from mesodermal development, including NKX2-5. Knockdown of MYCN expression in retinoblastoma cell models caused growth arrest and reactivated a subtype 1-specific photoreceptor signature. These molecular changes suggest that removing the driving force of MYCN oncogenic activity rescues molecular circuitry driving subtype 1 biology. The MYCN-RB gene signature generated from the cell models better identified MYCN-driven retinoblastoma than MYCN amplification and could identify cases that may benefit from MYCN-targeted therapy. MYCN drives tumor progression in a molecularly defined retinoblastoma subgroup, and inhibiting MYCN activity could restore a more differentiated and less aggressive tumor biology
2024-05-31 | GSE267015 | GEO
Project description:Retinoblastoma are childhood eye tumors arising from retinal precursor cells. Two distinct retinoblastoma subtypes with different clinical behavior have been described based on gene expression and methylation profiling. Using consensus clustering of DNA methylation analysis from retinoblastomas, we identified a MYCN-driven of subtype 2 retinoblastomas characterized by DNA hypomethylation and high expression of genes involved in protein synthesis. Subtype 2 retinoblastomas outside the MYCN-driven were characterized by high expression of genes from mesodermal development, including NKX2-5. Knockdown of MYCN expression in retinoblastoma cell models caused growth arrest and reactivated a subtype 1-specific photoreceptor signature. These molecular changes suggest that removing the driving force of MYCN oncogenic activity rescues molecular circuitry driving subtype 1 biology. The MYCN-RB gene signature generated from the cell models better identified MYCN-driven retinoblastoma than MYCN amplification and could identify cases that may benefit from MYCN-targeted therapy. MYCN drives tumor progression in a molecularly defined retinoblastoma subgroup, and inhibiting MYCN activity could restore a more differentiated and less aggressive tumor biology
2024-05-31 | GSE268136 | GEO
Project description:We present a spatial omics approach that merges and expands the capabilities of independently performedin situassays on a single tissue section. Our spatial multimodal analysis combines histology, mass spectrometry imaging, and spatial transcriptomics to facilitate precise measurements of mRNA transcripts and low-molecular weight metabolites across tissue regions. We demonstrate the potential of our method using murine and human brain samples in the context of dopamine and Parkinson’s disease.
2023-05-21 | GSE232910 | GEO