Genomic evolution of low and high grade glioma
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA634166 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Genomic evolution of low and high grade glioma
| PRJNA634165 | ENA
Project description:We carried out the analyses of chromosome variations between low-grade and high-grade gliomas in Chinese population. We found out the differences in chromosomes, cytobands, genes, pathways and GO functions. To identify the glioma tissue-specific genomic alterations and compare the genomic variations between low-grade and high-grade gliomas.
2015-01-03 | E-GEOD-34888 | biostudies-arrayexpress
Project description:RNA sequencing was performed on paraffin embedded mouse low grade glioma tumor tissue
2022-09-12 | GSE172391 | GEO
Project description:We describe the case of a low grade glioma in a 37 year old male patient showing an amplification of KRAS
2016-11-18 | GSE89982 | GEO
Project description:IDH1-R132H Low Grade Glioma animal brain tumors
| PRJNA374999 | ENA
Project description:RNA seq of mouse low grade glioma tumors
| PRJNA723204 | ENA
Project description:Ribba2012 - Low-grade gliomas, tumour growth inhibition model
Using longitudinal mean tumour diameter (MTD) data, this model describe the size evolution of low-grade glioma (LGG) in patients treated with chemotherapy or radiotherapy.
This model is described in the article:
A tumour growth inhibition model for low-grade glioma treated with chemotherapy or radiotherapy
Ribba B, Kaloshi G, Peyre M, Ricard D, Calvez V, Tod M, Cajavec-Bernard B, Idbaih A, Psimaras D, Dainese L, Pallud J, Cartalat-Carel S, Delattre JY, Honnorat J, Grenier E, Ducray F.
Clin. Cancer Res. 2012 Sep; 18(18): 5071-5080
Abstract:
PURPOSE: To develop a tumor growth inhibition model for adult diffuse low-grade gliomas (LGG) able to describe tumor size evolution in patients treated with chemotherapy or radiotherapy.
EXPERIMENTAL DESIGN: Using longitudinal mean tumor diameter (MTD) data from 21 patients treated with first-line procarbazine, 1-(2-chloroethyl)-3-cyclohexyl-l-nitrosourea, and vincristine (PCV) chemotherapy, we formulated a model consisting of a system of differential equations, incorporating tumor-specific and treatment-related parameters that reflect the response of proliferative and quiescent tumor tissue to treatment. The model was then applied to the analysis of longitudinal tumor size data in 24 patients treated with first-line temozolomide (TMZ) chemotherapy and in 25 patients treated with first-line radiotherapy.
RESULTS: The model successfully described the MTD dynamics of LGG before, during, and after PCV chemotherapy. Using the same model structure, we were also able to successfully describe the MTD dynamics in LGG patients treated with TMZ chemotherapy or radiotherapy. Tumor-specific parameters were found to be consistent across the three treatment modalities. The model is robust to sensitivity analysis, and preliminary results suggest that it can predict treatment response on the basis of pretreatment tumor size data.
CONCLUSIONS: Using MTD data, we propose a tumor growth inhibition model able to describe LGG tumor size evolution in patients treated with chemotherapy or radiotherapy. In the future, this model might be used to predict treatment efficacy in LGG patients and could constitute a rational tool to conceive more effective chemotherapy schedules.
This model is hosted on BioModels Database
and identified
by: BIOMD0000000521
.
To cite BioModels Database, please use: BioModels Database: An enhanced, curated and annotated resource
for published quantitative kinetic models
.
To the extent possible under law, all copyright and related or
neighbouring rights to this encoded model have been dedicated to the public
domain worldwide. Please refer to CC0 Public Domain
Dedication
for more information.
2024-09-02 | BIOMD0000000521 | BioModels
Project description:Glioma vascular cells (GVC) from high-grade IV gliomas (HG) are molecularly and functionally distinct from normal brain EC, and secrete higher levels of pro-tumorigenic factors that promote glioma growth and progression. However, it remains unclear whether GVC from Low- Grade II/II gliomas (LG) also express pro-tumorigenic factors, and to what extent they functionally contribute to glioma growth. Here, we profile the transcriptomes of GVC from IDH-mutant (mIDH) LG and IDH-wildtype (wIDH) HG and show that they exhibit significant molecular and functional heterogeneity. LG-GVC show enrichment of extracellular matrix and cell cycle-related gene sets and sensitivity to anti-angiogenic drugs, whereas HG-GVC display an increase in immune response-related gene sets and anti-angiogenic resistance. Strikingly, conditioned media from LG-GVC inhibits the growth of wIDH glioblastoma cells, whereas HG-GVC promotes growth. In vivo co-transplantation of LG-GVC with tumor cells reduces growth, whereas HG-GVC enhances tumor growth in orthotopic xenografts. We identify ASPORIN (ASPN), a small leucine-rich repeat proteoglycan, enriched in LG-GVC as a growth suppressor of wIDH glioblastoma cells in vitro and in vivo. Together, these findings indicate that GVC from LG and HG gliomas are heterogeneous and differentially regulate tumor growth.
2024-07-10 | GSE236569 | GEO
Project description:Glioma vascular cells (GVC) from high-grade IV gliomas (HG) are molecularly and functionally distinct from normal brain EC, and secrete higher levels of pro-tumorigenic factors that promote glioma growth and progression. However, it remains unclear whether GVC from Low- Grade II/II gliomas (LG) also express pro-tumorigenic factors, and to what extent they functionally contribute to glioma growth. Here, we profile the transcriptomes of GVC from IDH-mutant (mIDH) LG and IDH-wildtype (wIDH) HG and show that they exhibit significant molecular and functional heterogeneity. LG-GVC show enrichment of extracellular matrix and cell cycle-related gene sets and sensitivity to anti-angiogenic drugs, whereas HG-GVC display an increase in immune response-related gene sets and anti-angiogenic resistance. Strikingly, conditioned media from LG-GVC inhibits the growth of wIDH glioblastoma cells, whereas HG-GVC promotes growth. In vivo co-transplantation of LG-GVC with tumor cells reduces growth, whereas HG-GVC enhances tumor growth in orthotopic xenografts. We identify ASPORIN (ASPN), a small leucine-rich repeat proteoglycan, enriched in LG-GVC as a growth suppressor of wIDH glioblastoma cells in vitro and in vivo. Together, these findings indicate that GVC from LG and HG gliomas are heterogeneous and differentially regulate tumor growth.
2024-07-10 | GSE236568 | GEO
Project description:Glioma vascular cells (GVC) from high-grade IV gliomas (HG) are molecularly and functionally distinct from normal brain EC, and secrete higher levels of pro-tumorigenic factors that promote glioma growth and progression. However, it remains unclear whether GVC from Low- Grade II/II gliomas (LG) also express pro-tumorigenic factors, and to what extent they functionally contribute to glioma growth. Here, we profile the transcriptomes of GVC from IDH-mutant (mIDH) LG and IDH-wildtype (wIDH) HG and show that they exhibit significant molecular and functional heterogeneity. LG-GVC show enrichment of extracellular matrix and cell cycle-related gene sets and sensitivity to anti-angiogenic drugs, whereas HG-GVC display an increase in immune response-related gene sets and anti-angiogenic resistance. Strikingly, conditioned media from LG-GVC inhibits the growth of wIDH glioblastoma cells, whereas HG-GVC promotes growth. In vivo co-transplantation of LG-GVC with tumor cells reduces growth, whereas HG-GVC enhances tumor growth in orthotopic xenografts. We identify ASPORIN (ASPN), a small leucine-rich repeat proteoglycan, enriched in LG-GVC as a growth suppressor of wIDH glioblastoma cells in vitro and in vivo. Together, these findings indicate that GVC from LG and HG gliomas are heterogeneous and differentially regulate tumor growth.
2024-07-10 | GSE236570 | GEO