Searching for the roots of brain cancer

Savage, Neil

doi:10.1038/d41586-018-06709-2

Cited by 14 publications

(14 citation statements)

References 8 publications

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“…Gliomas are primary brain malignancies, which are derived from neuroglial stem or progenitor cells (Weller et al, 2015). Ionizing radiation, inherited genotype, and smoking are among the known risk factors for brain cancers including glioma (Savage, 2018). Although several therapeutic approaches including surgery, irradiation, and temozolomide therapy bring some remission in glioma treatment, tumor relapse is still inevitable and unrelenting, eventually causing patient death (Sanai and Berger, 2018).…”

Section: Introductionmentioning

confidence: 99%

RETRACTED: Long Non-coding RNA LINC00320 Inhibits Tumorigenicity of Glioma Cells and Angiogenesis Through Downregulation of NFKB1-Mediated AQP9

Chang

Bian

Xiong

et al. 2020

Front. Cell. Neurosci.

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The inhibitory effect of long intergenic non-coding RNA 00320 (LINC00320) in glioma cell proliferation has been proposed in a recent study. However, the mechanisms by which LINC00320 regulate aquaporin 9 (AQP9) in glioma require further exploration. Hence, this study aims to investigate effects of LINC00320 on tumorigenicity of glioma cells and angiogenesis of microvascular endothelial cells (MVECs). Expression of LINC00320 and AQP9 in glioma tissues and cells was measured by reverse transcription–quantitative polymerase chain reaction and Western blot analysis. The relationship among LINC00320, nuclear factor κB subunit 1 (NFKB1) and AQP9 was examined by RNA immunoprecipitation, dual-luciferase reporter gene, and chromatin immunoprecipitation assays. The participation of LINC00320 and AQP9 in glioma cell proliferation and MVEC angiogenesis was analyzed using gain- and loss-of-function approaches. Finally, a nude mouse orthotopic xenograft model of glioma was established to investigate the effects of LINC00320 and AQP9 on glioma growth in vivo. LINC00320 was under-expressed and AQP9 was over-expressed in glioma tissues. Further mechanistic investigation showed that LINC00320 downregulated AQP9 by inhibiting the recruitment of NFKB1 to the promoter region of AQP9. LINC00320 overexpression or AQP9 silencing inhibited the proliferation of glioma cells and angiogenesis of MVECs. Also, upregulation of LINC00320 restrained tumor growth and angiogenesis in xenograft mice by downregulating AQP9. Taken together, LINC00320 acts as a tumor suppressor in glioma, thus presenting a novel therapeutic target.

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Section: Introductionmentioning

confidence: 99%

RETRACTED: Long Non-coding RNA LINC00320 Inhibits Tumorigenicity of Glioma Cells and Angiogenesis Through Downregulation of NFKB1-Mediated AQP9

Chang

Bian

Xiong

et al. 2020

Front. Cell. Neurosci.

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“…The National Comprehensive Cancer Network guideline recommends chemoradiation with or without tumortreating fields (TTF) for the adjuvant treatment of primary glioblastoma (GBM). However, the prognosis of GBM remains poor, mainly due to the high risk of recurrence and resistance to chemoradiotherapy (2)(3)(4). In addition, gliomas do not have clear boundaries and are characterized by high degrees of infiltration via diffusion and a high proliferation rate, thereby complicating surgical resection (5).…”

Section: Introductionmentioning

confidence: 99%

A Prognostic DNA Damage Repair Genes Signature and Its Impact on Immune Cell Infiltration in Glioma

et al. 2021

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ObjectiveGlioma is the most frequent type of malignant cerebral tumors. DNA damage repair genes (DDRGs) play a crucial role in the development of cancer. In this study, we constructed a DDRGs signature and investigated the potential mechanisms involved in this disease.MethodsRNA sequence data, microarray data, and corresponding clinical information of gliomas were downloaded from The Cancer Genome Atlas (TCGA), Chinese Glioma Genome Atlas (CGGA), and Gene Expression Omnibus (GEO). Subsequently, we identified candidate genes by differential analysis and Cox regression analysis. The least absolute shrinkage and selection operator Cox regression model was utilized to construct a DDRGs signature using TCGA training dataset. According to this signature, patients with glioma were divided into low- and high-risk groups. The predictive ability of the signature was validated by prognostic analysis, receiver operating characteristic curves, principal component analysis, and stratification analysis in TCGA testing and CGGA verification datasets. CIBERSORT and single-sample gene set enrichment analysis (ssGSEA) were used to evaluate the immune microenvironment of glioma. Moreover, we conducted GSEA to determine the functions and pathways in the low- and high-risk groups. Finally, a nomogram was constructed by combining the signature and other clinical features.ResultsA total of 1,431 samples of glioma (592 from TCGA, 686 from the CGGA, and 153 from the GEO) and 23 samples of normal brain tissue from the GEO were analyzed in this study. There were 51 prognostic differentially expressed DDRGs. Additionally, five DDRGs (CDK4、HMGB2、WEE1、SMC3 and GADD45G) were selected to construct a DDRGs signature for glioma, stratifying patients into low- and high-risk groups. The survival analysis showed that the DDRGs signature could differentiate the outcome of the low- and high-risk groups, showing that high-risk gliomas were associated with shorter overall survival. The immune microenvironment analysis revealed that more immunosuppressive cells, such as tumor associated macrophages and regulatory T cells, were recruited in the high-risk group. GSEA also showed that high-risk glioma was correlated with the immune and extracellular matrix pathways.ConclusionThe five DDRGs signature and its impact on the infiltration of immunosuppressive cells could precisely predict the prognosis and provide guidance on the treatment of glioma.

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“…If one looks at the cancers protected against by the presence of allergy/atopy or high serum IgE levels, a number of site-specific cancers stand out, these including lung cancer (in the absence of asthma) [37][38][39]45,46]; colorectal cancer, particularly rectal cancer [37,46,51,64,115]; and pancreatic cancer [37,38,50,52,64,116,117], all of which seemed to be protected against by either the presence of allergy/atopic disease or high serum IgE levels. Another cancer overwhelmingly benefiting from the presence of allergy or high serum IgE is glioma [51,53,65,78,97,100,[118][119][120], with additional evidence to suggest that high serum IgE may even prolong survival in glioma patients [78,100]. Therefore, it is possible that IgE could represent a potential novel therapeutic agent for the treatment of such cancers.…”

Section: Figurementioning

confidence: 99%

Insights from IgE Immune Surveillance in Allergy and Cancer for Anti-Tumour IgE Treatments

McCraw

Chauhan

Bax

et al. 2021

Cancers

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IgE, the predominant antibody class of the allergic response, is known for its roles in protecting against parasites; however, a growing body of evidence indicates a significant role for IgE and its associated effector cells in tumour immunosurveillance, highlighted by the field of AllergoOncology and the successes of the first-in-class IgE cancer therapeutic MOv18. Supporting this concept, substantial epidemiological data ascribe potential roles for IgE, allergy, and atopy in protecting against specific tumour types, with a corresponding increased cancer risk associated with IgE immunodeficiency. Here, we consider how epidemiological data in combination with functional data reveals a complex interplay of IgE and allergy with cancer, which cannot be explained solely by one of the existing conventional hypotheses. We furthermore discuss how, in turn, such data may be used to inform future therapeutic approaches, including the clinical management of different patient groups. With epidemiological findings highlighting several high-risk cancer types protected against by high IgE levels, it is possible that use of IgE-based therapeutics for a range of malignant indications may offer efficacy to complement that of established IgG-class antibodies.

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Searching for the roots of brain cancer

Cited by 14 publications

References 8 publications

RETRACTED: Long Non-coding RNA LINC00320 Inhibits Tumorigenicity of Glioma Cells and Angiogenesis Through Downregulation of NFKB1-Mediated AQP9

RETRACTED: Long Non-coding RNA LINC00320 Inhibits Tumorigenicity of Glioma Cells and Angiogenesis Through Downregulation of NFKB1-Mediated AQP9

A Prognostic DNA Damage Repair Genes Signature and Its Impact on Immune Cell Infiltration in Glioma

Insights from IgE Immune Surveillance in Allergy and Cancer for Anti-Tumour IgE Treatments

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