International Glioma Case-Control Study
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA377600 | ENA |
REPOSITORIES: ENA
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Project description:<p>The main goals of the GICC Study were: 1) to identify novel genetic risk variants for glioma, as well as validate variants implicated by previous genome-wide association studies of glioma; and 2) to explore biologically relevant gene-gene and gene-environment interactions in glioma susceptibility. The GICC Study includes participants from the following centers: Brigham and Women's Hospital (Boston, Massachusetts), Case Western Reserve University (Cleveland, Ohio), Columbia University (New York, New York), the Danish Cancer Society Research Centre (Copenhagen, Denmark), Duke University (Durham, North Carolina), the University of Texas MD Anderson Cancer Center (Houston, Texas), Memorial Sloan Kettering Cancer Center (New York, New York), the Mayo Clinic (Rochester, Minnesota), NorthShore HealthSystem (Chicago, Illinois), Umea University (Umea, Sweden), the University of California, San Francisco (San Francisco, California), the University of Southern California (Los Angeles, California), and the Institute of Cancer Research (London, United Kingdom).</p>
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Project description:The MD Anderson Colorectal Cancer Case Control Study
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Project description:Background: Patients with high-grade gliomas are at high risk of venous thromboembolism (VTE). MicroRNAs (miRNAs) are small non-coding RNAs with multiple roles in tumor biology, hemostasis and platelet function. We aimed to explore the association between plasma miRNAs and risk of VTE in high-grade glioma. Results: We conducted a nested-case control study within 152 patients with WHO grade IV glioma that had been included in the Vienna Cancer and Thrombosis Study (CATS), a prospective cohort study focused on risk factors for VTE in newly diagnosed or recurrent cancer. At study inclusion a single blood draw was taken, and patients were thereafter followed for a maximum of two years. During that time, 24 patients (16%) developed VTE. Of the other 128 patients, we randomly selected 24 age- and sex-matched controls. After sample quality control, the final group size was 21 VTE-patients and 23 without VTE. Small RNA next-generation sequencing of plasma was performed. We observed that hsa-miR-451a was globally the most abundant miRNA. Notably, 51% of all miRNAs showed a correlation with platelet count. The analysis of miRNAs differentially regulated in VTE patients – with and without platelet adjustment – identified potential VTE biomarker candidates such as has-miR- 221-3p. Conclusion: We here provide one of the largest and deepest peripheral blood miRNA datasets of high-grade glioma patients so far. Further, we confirm previous observations of a considerable impact of platelet count on the blood miRNome. And, finally, we present first VTE biomarker candidates that can serve as the starting point for future confirmatory research.
2023-12-31 | GSE222666 | GEO
Project description:Gliomas are the most devastating of primary adult malignant brain tumors. These tumors are highly infiltrative and can arise from cells with extensive self-renewal capability and chemoresistance, frequently termed glioma-propagating cells (GPCs). GPCs are thus the plausible culprits of tumor recurrence. Treatment strategies that eradicate GPCs will greatly improve disease outcome. Such findings support the use of GPCs as in vitro cellular systems for small molecule screening. However, the nuances in utilizing GPCs as a cellular screening platform are not trivial. These slow-growing cells are typically cultured as suspension, spheroid structures in serum-free condition supplemented with growth factors. Consequently, replenishment of growth factors throughout the screening period must occur to maintain cells in their undifferentiated state, as the more lineage-committed, differentiated cells are less tumorigenic. We will present a case study of a small molecule screen conducted with GPCs and explain how unique sphere activity assays were implemented to distinguish drug efficacies against the long-term, self-renewing fraction, as opposed to transient-amplifying progenitors, latter of which are detected in conventional viability assays. We identified Pololike kinase 1 as a regulator of GPC survival. Finally, we leveraged on public glioma databases to illustrate GPC contribution to disease progression and patient survival outcome.
2012-08-02 | GSE36782 | GEO