اینتروداکشن پروژه ارشد (81069)

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شرح پروژه

سلام
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از دستورالعمل عکس پیروی شود

بین ۳۵ تا ۴۰

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دانشگاه خیلی حساسه

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چطوری قبلا  هتروجنیسیتی بررسی میشده قبلا از  single cell rna seq

موضوع احتمالا هتروجنیسیتی تو گلایوبلاستموما باشه ولی هنوز تصمیم نگرفتیم

Elucidating the molecular mechanisms underlying intra-tumor heterogeneity and cell plasticity in Glioblastoma by integrating omics approaches 

Glioblastoma (GBM) is an aggressive brain cancer occurring in children and adults. Despite intense treatment regimens, patients affected by GBM usually relapse and have an exceedingly poor prognosis. Recent evidence suggests that resistance in GBM stems from intra-tumoral cellular plasticity, whereby GBM cells transition across phenotypic states. Therefore, the aim of this project is to decipher the molecular mechanisms underlying plasticity in GBM, towards the identification of novel vulnerabilities to target.

Objective 1: Characterization of GBM intra-tumoral heterogenicity by single-cell RNA-sequencing.

As a model that mimics GBM patients’ heterogeneity, a tridimensional culture system derived from GBM primary samples will be used. Firstly, a single cell RNA sequencing (scRNAseq) experiment will be performed on three different samples to identify markers of subpopulations. As well as standard clustering procedures and the description of transcriptomic profiles of the heterogenic populations, single cell copy number variation analysis will be applied to check for the presence of differentclonal populations. Moreover, to phenotypically characterize tumor heterogeneity and validate scRNAseq results, fluorescence-activated cell sorting (FACS) assays will be applied.

Objective 2: Characterization of phenotypically plastic states.

FACS-sorting will be employed to physically separate the identified subpopulations, based upon the transcriptomics signatures identified within the first aim. We will assess whether subpopulations of cells purified for a given phenotypic state would regain the phenotypic equilibrium proportions of the parental population in our patient-derived model systems, as proof-of-concept plasticity in this model.

Objective 3: Identification of key molecular mechanisms responsible for tumor plasticity.

To gain insight of the mechanisms governing this plastic behavior, experiments of bulk RNAseq and bulk proteomics, will be performed on GBM subpopulations, immediately after sorting. The aim is to detect changes in transcriptional profiles associated with a differential protein expression that could explain the plasticity phenotype. Furthermore, ATAC-seq and Cut&Tagexperiments will be crucial to better understand the molecular mechanism from an epigenetic point of view. Functional enrichment and integration of the various omics approaches will be performed.

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