Ontology highlight
ABSTRACT:
PROVIDER: PRJNA532762 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR8893590_1.fastq.gz | Fastqsanger.gz | |||
| SRR8893590_2.fastq.gz | Fastqsanger.gz | |||
| SRR8893600_1.fastq.gz | Fastqsanger.gz | |||
| SRR8893600_2.fastq.gz | Fastqsanger.gz | |||
| SRR8893591_1.fastq.gz | Fastqsanger.gz |
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Project description:Stability Analysis of a Mathematical Model for Glioma-Immune Interaction under Optimal Therapy
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Abstract
We investigate a mathematical model using a system of coupled ordinary differential equations, which describes the interplay of malignant glioma cells, macrophages, glioma specific CD8+T cells and the immunotherapeutic drug Adoptive Cellular Immunotherapy (ACI). To better understand under what circumstances the glioma cells can be eliminated, we employ the theory of optimal control. We investigate the dynamics of the system by observing biologically feasible equilibrium points and their stability analysis before administration of the external therapy ACI. We solve an optimal control problem with an objective functional which minimizes the glioma cell burden as well as the side effects of the treatment. We characterize our optimal control in terms of the solutions to the optimality system, in which the state system coupled with the adjoint system. Our model simulation demonstrates that the strength of treatment u1(t) plays an important role to eliminate the glioma cells. Finally, we derive an optimal treatment strategy and then solve it numerically.
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Project description:Isocitrate dehydrogenase (IDH)-mutant gliomas are malignant brain tumors that typically arise in early- to mid-adulthood and nearly always recur following treatment. However, the genetic and cellular state changes that drive IDH-mutant glioma progression under treatment remain incompletely understood. Here, we integrated single-nucleus transcriptomic profiles, chromatin accessibility profiles and bulk DNA/RNA sequencing from 75 temporally separated gliomas across 35 patients comprising both the oligodendroglioma and astrocytoma IDH-mutant glioma tumor types. We show that malignant cell states transcriptionally resemble stages of normal glial-neuronal lineage development or a reactive mesenchymal-like state, mirroring states previously described in IDH-wildtype glioblastoma. Malignant cell states displayed distinct chromatin accessibility profiles that were comparable between both IDH-mutant glioma types. The abundance of less differentiated malignant cells increased with grade and with genetic alterations such as PDGFRA amplification. Longitudinal analysis highlighted two major malignant cell state transition patterns. First, reduced lineage differentiation and increased proliferative malignant cells at recurrence were pronounced in gliomas that acquired recurrence-associated genetic events, including treatment-associated hypermutation, increased copy number changes, and cell cycle alterations. Second, increased mesenchymal-like state abundance occurred independently of acquired genetic alterations and instead coincided with heightened macrophage expression. Overall, our findings provide an integrative model that traces the cell-intrinsic and extrinsic factors that shape cellular states during IDH-mutant glioma disease progression.
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