Molecular markers in glioma

Ludwig, Kirsten; Kornblum, Harley I.

doi:10.1007/s11060-017-2379-y

Cited by 326 publications

(258 citation statements)

References 62 publications

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“…3D). This was also highlighted by differential expression of putative marker genes for GBM subtypes 18 across patient samples ( Supplementary Fig. 2C).…”

Section: Scrna-seq Reveals Transcriptional Heterogeneity Between Tumomentioning

confidence: 78%

Modeling glioblastoma invasion using human brain organoids and single-cell transcriptomics

Krieger

Tirier

Park

et al. 2019

Preprint

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AbstractGlioblastoma multiforme (GBM) are devastating neoplasms with high invasive capacity. GBM has been difficult to study in vitro. Therapeutic progress is also limited by cellular heterogeneity within and between tumors. To address these challenges, we present an experimental model using human cerebral organoids as a scaffold for patient-derived glioblastoma cell invasion. By tissue clearing and confocal microscopy, we show that tumor cells within organoids extend a network of long microtubes, recapitulating the in vivo behavior of GBM. Single-cell RNA-seq of GBM cells before and after co-culture with organoid cells reveals transcriptional changes implicated in the invasion process that are coherent across patient samples, indicating that GBM cells reactively upregulate genes required for their dispersion. Functional therapeutic targets are identified by an in silico receptor-ligand pairing screen detecting potential interactions between GBM and organoid cells. Taken together, our model has proven useful for studying GBM invasion and transcriptional heterogeneity in vitro, with applications for both pharmacological screens and patient-specific treatment selection at a time scale amenable to clinical practice.

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“…3D). This was also highlighted by differential expression of putative marker genes for GBM subtypes 18 across patient samples ( Supplementary Fig. 2C).…”

Section: Scrna-seq Reveals Transcriptional Heterogeneity Between Tumomentioning

confidence: 78%

Modeling glioblastoma invasion using human brain organoids and single-cell transcriptomics

Krieger

Tirier

Park

et al. 2019

Preprint

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“…2,3 Owing to the indistinct symptoms and lack of an effective diagnostic method for early detection, patients with GC are typically diagnosed at an advanced stage and have a dismal prognosis. 5,6 Taking this into consideration, it is necessary to seek more effective biological markers for the diagnosis and treatment of GC. 5,6 Taking this into consideration, it is necessary to seek more effective biological markers for the diagnosis and treatment of GC.…”

Section: Introductionmentioning

confidence: 99%

Retracted: Knockdown of long noncoding RNA urothelial carcinoma–associated 1 inhibits cell viability, migration, and invasion by regulating microRNA‐182 in gastric carcinoma

Qin

Jia

Xie

et al. 2018

J of Cellular Biochemistry

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“…15 In addition, more well-known molecular markers including MGMT, IDH, EGFR, p53, Rb, and RAF are identified in gliomas. 16 Here, we reported that PTPN2 was upregulated in glioma cells. PTPN2 silence could significantly inhibit glioma progression.…”

Section: Discussionmentioning

confidence: 81%

“…For instance, a number of circulating biomarkers have been identified in glioma patients . In addition, more well‐known molecular markers including MGMT, IDH, EGFR, p53, Rb, and RAF are identified in gliomas . Here, we reported that PTPN2 was upregulated in glioma cells.…”

Section: Discussionmentioning

confidence: 99%

PTPN2 induced by inflammatory response and oxidative stress contributed to glioma progression

Wang

Jiang

et al. 2019

J of Cellular Biochemistry

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Malignant glioma remains the most frequent form of primary brain tumors all over the world. The gliomagenesis is characterized by various molecular processes such as neoplastic transformation, dysregulation of the cell cycle, and angiogenesis. Among these biomolecular events, the existence of inflammation and oxidative stress pathways in the development of glioma has been reported. PTPN2 is associated with several inflammatory disorders. However, the biological role of PTPN2 in inflammation responses and oxidative stress pathways involved in glioma remains poorly known. Here, we focused on its function in glioma development. Here, we observed that PTPN2 was significantly increased in glioma especially in a grade‐dependent manner. Meanwhile, interferon‐γ and tumor necrosis factor‐α, which have been identified as crucial inflammation cytokines, were able to trigger PTPN2 expression in a dose‐dependent course in T98G cells. Then, we found that PTPN2 was oxidated and inactivated by H2O2. Meanwhile, H2O2 induced glioma cell colony formation capacity and increased ki‐67 expression confirmed by flow cytometry assay. Finally, T98G cells were transfected with PTPN2 shRNA and it was shown that knockdown of PTPN2 obviously inhibited T98G cell colony formation and induced cell apoptosis. In summary, our findings indicated that PTPN2 could be induced by inflammatory response and oxidative stress and its deficiency depressed glioma cell growth.

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Molecular markers in glioma

Cited by 326 publications

References 62 publications

Modeling glioblastoma invasion using human brain organoids and single-cell transcriptomics

Modeling glioblastoma invasion using human brain organoids and single-cell transcriptomics

Retracted: Knockdown of long noncoding RNA urothelial carcinoma–associated 1 inhibits cell viability, migration, and invasion by regulating microRNA‐182 in gastric carcinoma

PTPN2 induced by inflammatory response and oxidative stress contributed to glioma progression

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