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5,287 results for “colorectal cancer”
Deep learning models to detect microsatellite instability in colorectal cancer from histological images
<p>This repository contains trained deep learning models (based on shufflenet) for detecting microsatellite instability (MSI) in histological images of colorectal cancer. Expected input is 512x512x3, output is categorical (MSI vs. not MSI).</p> <p>The models are provided as MAT (Matlab R2019a) files. All models are described in detail in the publication "Clinical-grade detection of microsatellite instability in colorectal cancer by deep learning: an international multicenter study"</p> <p>More information on the original model: <a href="https://www.mathworks.com/help/deeplearning/ref/shufflenet.html">https://www.mathworks.com/help/deeplearning/ref/shufflenet.html</a></p>
Synthetic histology images of colorectal cancer, generated by conditional generative adversarial networks
<p>These are generated (synthetic) histology images of colorectal cancer. These images were generated by conditional GANs and are in two classes: MSIH (microsatellite instable high) and nonMSIH. There are two sets: one set with 10K images per class and another one with 75K images per class. All images are RGB, 512x512 px at a resolution of 0.5 micrometers per pixel. For more information, please stay tuned for our upcoming manuscript on www.kather.ai. </p>
Data from: High sensitivity isoelectric focusing to establish a signaling biomarker for the diagnosis of human colorectal cancer
Background: The progression of colorectal cancer (CRC) involves recurrent amplifications/mutations in the epidermal growth factor receptor (EGFR) and downstream signal transducers of the Ras pathway, KRAS and BRAF. Whether genetic events predicted to result in increased and constitutive signaling indeed lead to enhanced biological activity is often unclear and, due to technical challenges, unexplored. Here, we investigated proliferative signaling in CRC using a highly sensitive method for protein detection. The aim of the study was to determine whether multiple changes in proliferative signaling in CRC could be combined and exploited as a "complex biomarker" for diagnostic purposes. Methods: We used robotized capillary isoelectric focusing as well as conventional immunoblotting for the comprehensive analysis of epidermal growth factor receptor signaling pathways converging on extracellular regulated kinase 1/2 (ERK1/2), AKT, phospholipase Cγ1 (PLCγ1) and c-SRC in normal mucosa compared with CRC stage II and IV. Computational analyses were used to test different activity patterns for the analyzed signal transducers. Results: Signaling pathways implicated in cell proliferation were differently dysregulated in CRC and, unexpectedly, several were downregulated in disease. Thus, levels of activated ERK1 (pERK1), but not pERK2, decreased in stage II and IV while total ERK1/2 expression remained unaffected. In addition, c-SRC expression was lower in CRC compared with normal tissues and phosphorylation on the activating residue Y418 was not detected. In contrast, PLCγ1 and AKT expression levels were elevated in disease. Immunoblotting of the different signal transducers, run in parallel to capillary isoelectric focusing, showed higher variability and lower sensitivity and resolution. Computational analyses showed that, while individual signaling changes lacked predictive power, using the combination of changes in three signaling components to create a "complex biomarker" allowed with very high accuracy, the correct diagnosis of tissues as either normal or cancerous. Conclusions: We present techniques that allow rapid and sensitive determination of cancer signaling that can be used to differentiate colorectal cancer from normal tissue.
Data from: Common genetic variation in ETV6 is associated with colorectal cancer susceptibility
Genome-wide association studies (GWAS) have identified multiple susceptibility loci for colorectal cancer, but much of heritability remains unexplained. To identify additional susceptibility loci for colorectal cancer, here we perform a GWAS in 1,023 cases and 1,306 controls and replicate the findings in seven independent samples from China, comprising 5,317 cases and 6,887 controls. We find a variant at 12p13.2 associated with colorectal cancer risk (rs2238126 in ETV6, P = 2.67 × 10-10). We replicate this association in an additional 1,046 cases and 1,076 controls of European ancestry (P = 0.034). The G allele of rs2238126 confers earlier age at onset of colorectal cancer (P = 1.98 × 10-6) and reduces the binding affinity of transcriptional enhancer MAX. The mRNA level of ETV6 is significantly lower in colorectal tumors than in paired normal tissues. Our findings highlight the potential importance of genetic variation in ETV6 conferring susceptibility to colorectal cancer.
Data from: Origins of lymphatic and distant metastases in human colorectal cancer
The spread of cancer cells from primary tumors to regional lymph nodes is often associated with reduced survival. One prevailing model to explain this association posits that fatal, distant metastases are seeded by lymph node metastases. This view provides a mechanistic basis for the TNM staging system and is the rationale for surgical resection of tumor-draining lymph nodes. Here we examine the evolutionary relationship between primary tumor, lymph node, and distant metastases in human colorectal cancer. Studying 213 archival biopsy samples from 17 patients, we used somatic variants in hypermutable DNA regions to reconstruct high-confidence phylogenetic trees. We found that in 65% of cases, lymphatic and distant metastases arose from independent subclones in the primary tumor, whereas in 35% of cases they shared common subclonal origin. Therefore, two different lineage relationships between lymphatic and distant metastases exist in colorectal cancer.
Effectiveness of Nutritional Web Application on Nutrition Status Improvement among Patients with Colorectal Cancer
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Comments on "Current status and quality of radiomic studies for predicting KRAS mutations in colorectal cancer patients: A systematic review and meta-analysis"
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Single-cell RNA-seq dataset and code for human colorectal cancer liver metastasis study
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Distinct Intratumoral Microbiome of Young-Onset and Average-Onset Colorectal Cancer
<p>Raw 16S rRNA Amplicon sequencing Data.</p>
Raw data of the article:Proof-of-Concept Study on the Use of Tangerine-Derived Nanovesicles as siRNA Delivery Vehicles toward Colorectal Cancer Cell Line SW480
<p>In the last years, the field of nanomedicine and drug delivery has grown exponentially, providing new platforms to carry therapeutic agents into the target sites. Extracellular vesicles (EVs) are ready-to-use, biocompatible, and non-toxic nanoparticles that are revolutionizing the field of drug delivery. EVs are involved in cell-cell communication and mediate many physiological and pathological processes by transferring their bioactive cargo to target cells. Recently, nanovesicles from plants (PDNVs) are raising the interest of the scientific community due to their high yield and biocompatibility. This study aims to evaluate whether PDNVs may be used as drug delivery systems. We isolated and characterized nanovesicles from tangerine juice (TNVs) that were comparable to mammalian EVs in size and morphology. TNVs carry the traditional EV marker HSP70 and, as demonstrated by metabolomic analysis, contain flavonoids, organic acids, and limonoids. TNVs were loaded with DDHD1-siRNA through electroporation, obtaining a loading efficiency of 13%. We found that the DDHD1-siRNA complex TNVs were able to deliver DDHD1-siRNA to human colorectal cancer cells, inhibiting the target expression by about 60%. This study represents a proof of concept for the use of PDNVs as vehicles of RNA interference (RNAi) toward mammalian cells.</p>
Comprehensive analysis of type 2 diabetes-associated gene polymorphisms in a cohort of 99 anonymized metastatic colorectal cancer patients, including their frequency.
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Molecular and functional profiling unravels targetable vulnerabilities in colorectal cancer
<p>Colorectal Cancer (CRC) is a highly heterogeneous group of diseases, with distinctive genetic and epigenetic alterations. CRC tumors bearing KRAS or BRAF mutations still remain resistant to new therapies. Thus, this augments the necessity to reveal new therapeutic targets in mutKRAS/BRAF, which may account for up to 50% of the total CRC patients. To this end, we investigated primary untreated CRC tumors (WES & RNA-Seq) from 28 Greek patients for their systematic molecular characterization and stratification into diverse groups based on their microsatellite instability (MSI) status and KRAS/BRAF genetic variations, in order to unravel novel targets and putative personalized treatment interventions. The raw data of this project (WES & RNA-Seq) have been uploaded in the EGA European Genome-Phenome Archive (EGAD00001011262 and EGAD00001011263).</p>
Increased Expression of Sorbitol Dehydrogenase in Colorectal Cancer Predicts BetterPrognosis (raw data)
<p>COAD/READ/COADREAD_rnaseq_fpkm.txt files contain TCGA RNA-Seq data in FPKM normalisation form for colorectal adenocarcinoma (COAD), rectum adenocarcinoma (READ) or combined (COADREAD).</p> <p>COAD/READ/COADREAD_rnaseq_tpm.txt files contain TCGA RNA-Seq data in TPM normalisation form for colorectal adenocarcinoma (COAD), rectum adenocarcinoma (READ) or combined (COADREAD).</p> <p>COAD/READ/COADREAD_clinical_raw.xlsx files contain TCGA clinical data for patients with colorectal adenocarcinoma (COAD), rectum adenocarcinoma (READ) or combined (COADREAD).</p> <p>COAD/READ/COADREAD_rnaseq_clinical_raw.xlsx files contain corresponding information of TCGA clinical data and RNA-Seq data for patients with colorectal adenocarcinoma (COAD), rectum adenocarcinoma (READ) or combined (COADREAD).</p> <p>Local_cohort_tumour/adenoma_qPCR_rawdata.xlsx files contain our experimental results of qPCR CT values for SORD and GAPDH (as internal ref), shown as separate values for duplicate wells and average values.</p> <p>Local_cohort_tumour_clinical_rawdata.xlsx contains clinical information and calculated SORD relative expression of our recruited patients.</p>
Targeting Myc-driven stress vulnerability in mutant KRAS colorectal cancer (Ruan et al.)
<p>Mutant <em>KRAS </em>is a key driver in colorectal cancer (CRC) and promotes Myc translation and Myc-dependent stress adaptation and proliferation. Here, we report that the combination of two FDA-approved drugs Bortezomib and Everolimus (RAD001) (BR) is highly efficacious against mutant <em>KRAS </em>CRC cells. Mechanistically, the combination, not single agent, rapidly depletes Myc protein, not mRNA, and leads to GCN2- and p-eIF2a-dependent cell death through the activation of extrinsic and intrinsic apoptotic pathways. Cell death is selectively induced in mutant <em>KRAS </em>CRC cells with elevated basal Myc and p-eIF2a and is characterized by CHOP induction and transcriptional signatures in proteotoxicity, oxidative stress, metabolic inhibition, and immune activation. BR-induced p-GCN2/p-eIF2a elevation and cell death are strongly attenuated by <em>MYC </em>knockdown and enhanced by <em>MYC </em>overexpression. The BR combination is efficacious against mutant <em>KRAS </em>patient derived organoids (PDO) and xenografts (PDX) by inducing p-eIF2a/CHOP and cell death. Interestingly, an elevated four-gene (DDIT3, GADD45B, CRYBA4 and HSPA1L) stress signature is linked to shortened overall survival in CRC patients. These data support that Myc-dependent stress adaptation drives the progression of mutant <em>KRAS </em>CRC and serves as a therapeutic vulnerability, which can be targeted using dual translational inhibitors.</p>
Cuproptosis-related genes in colorectal cancer: prognostic significance, immune function, methylation, and regulation
<p>Despite recent advances in therapeutic options, colorectal cancer (CRC) continues to be a lethal disease with a poor prognosis. A recently identified mode of cell death, cuproptosis is yet to be understood in the context of CRC. Herein, we identified a cuproptosis-related three-gene signature that correlates with CRC survival in the Cancer Genome Atlas (TCGA) cohort. With this signature, a nomogram was constructed with new prognostic values, and CDKN2A was identified as an independent risk factor for CRC. Furthermore, CDKN2A expression was significantly correlated with both immune cell infiltration and the immune response. A pan-cancer analysis also revealed the prognostic value and immunological correlations of CDKN2A in other tumor types. Additionally, downregulation of CDKN2A was associated with methylation of m6A. Last but not least, we constructed a ceRNA network to discover the lncRNA KCNQ1OT1/miR-125b-5p/CDKN2A regulatory pathway in CRC. In this study, we provided insights into the role of cuproptosis in CRC and identified CDKN2A as an important cuproptosis-related gene. These results need to be verified by further research.</p>
Study on the Regulation Mechanism of TBX5 Gene and Gegen Qinlian Decoction on Colorectal Cancer
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The role of Gper1 in colorectal cancer progression depends on gender and p53 functionality
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Spatial distribution pattern of immune cells is associated with patient prognosis in colorectal cancer
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AEG-1 inhibits proliferation and invasion of colorectal cancer HCT116 cells via the PI3K/AKT/mTOR pathway
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AEG-1 inhibits proliferation and invasion of colorectal cancer HCT116 cells via the PI3K/AKT/mTOR pathway
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Allen Brain Atlas
Allen Brain Atlas is an Allen Institute collection of brain map atlases, datasets, APIs, and analysis tools covering mouse, human, and non-human primate brain resources.
Annotated Behaviour and Observability Dataset (ABODe)
ABODe is a University of Edinburgh DataShare dataset for behavior classification in group-housed mice using home-cage video, identities, bounding boxes, ground-plate positions, and annotator labels.
DANDI Archive for NWB datasets
DANDI is a BRAIN Initiative archive for publishing and sharing neurophysiology data, including electrophysiology, optophysiology, and behavioral data packaged as NWB and related standards.
International Brain Laboratory public data
The International Brain Laboratory public data releases expose standardized mouse decision-making experiments, including Neuropixels recordings, widefield calcium imaging, behavior, and session metadata accessed through the ONE API.
OpenNeuro
OpenNeuro is a free, open platform for sharing neuroimaging datasets, with public search, dataset pages, and download paths for web, S3, DataLad, and the OpenNeuro CLI.