Cerebrospinal fluid tumor DNA for liquid biopsy in glioma patients’ management: Close to the clinic?

Simonelli, Matteo; Dipasquale, Angelo; Orzan, Francesca; Lorenzi, Elena; Persico, Paola; Navarria, Pierina; Pessina, Federico; Nibali, Marco Conti; Bello, Lorenzo; Santoro, Armando; Boccaccio, Carla

doi:10.1016/j.critrevonc.2020.102879

Cited by 21 publications

(25 citation statements)

References 30 publications

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“…Surgical resection and radiotherapy are the main methods for glioma treatment, but can only treat the symptoms rather than the root cause. Postoperative patients often have recurrence or metastasis, which dramatically reduces the postoperative survival rate [ 3 ]. In recent years, gene therapy for glioma has become a hot research field [ 4 ].…”

Section: Introductionmentioning

confidence: 99%

RETRACTED ARTICLE: Exosomal SNHG16 secreted by CSCs promotes glioma development via TLR7

Zhang

et al. 2021

Stem Cell Res Ther

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Background Glioma is one of the most common central nervous system malignant tumors, accounting for 45~60% of adult intracranial tumors. However, the clinical treatment of glioma is limited. It is of great significance to seek new therapeutic methods for glioma via gene therapy. Methods Long non-coding RNA (lncRNA) SNHG16 expression level was measured by microarray and qRT-PCR assay; ISH was used to identify the location of SNHG16. Cancer stem cells (CSCs) were separated from glioma tissues and identified using immunofluorescence. Exosomes were isolated from CSCs and cancer cells and identified by TEM and western blot. MTT, wound healing, transwell, and colony formation assay were performed to explore the role of SNHG16 or si-SNHG16 from CSCs on progression of glioma cells. RIP was used to verify the interaction between SNHG16 and TLR7. The experiment of Xenograft used for exploring the function of SNHG16/ TLR7/MyD88/NFκB/c-Myc on growth on glioma in vivo. Results Microarray assay showed long non-coding RNA (lncRNA) SNHG16 was upregulated in glioma. Followed qRT-PCR also showed an increase of SNHG16 in glioma tissues; high expression of SNHG16 indicated a poor prognosis in glioma patients. Interestingly, SNHG16 was packaged into exosomes and derived from CSCs. Functional analysis showed exo-SNHG16 secreted by CSCs promoted the progression of glioma cell lines SHG44 and U251. Furthermore, SNHG16 interacted with TLR7 and activated NFκB/c-Myc signaling in glioma cells. And the silencing of TLR7 inhibited the progression of SHG44 and U251 cells by exo-SNHG16 from CSCs. In vivo tumorigenesis experiments showed that exo-SNHG16 induced glioma progression by activating TLR7/MyD88/NFκB/c-Myc signaling. Conclusion Our study suggested CSC-derived exo-SNHG16 promoted cancer progression by activating TLR7/MyD88/NFκB/c-Myc signaling pathway.

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Section: Introductionmentioning

confidence: 99%

RETRACTED ARTICLE: Exosomal SNHG16 secreted by CSCs promotes glioma development via TLR7

Zhang

et al. 2021

Stem Cell Res Ther

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“…Surgical biopsies are the conventional strategy for gathering pathological information from GBM tumors. This fact is troublesome because a surgical biopsy will only provide a limited spatial and temporal snapshot of cancer, failing to reflect the intratumoral heterogeneity, not to mention there are significant risks associated with the procedure [17]. A newer approach is emerging that allows for assessment of the entire genetic landscape and longitudinal tracking, and is much less invasive: the liquid biopsy (Fig.…”

Section: Liquid Biopsy As a Methods For Detecting Heterogeneity And Longitudinal Trackingmentioning

confidence: 99%

The Multifaceted Glioblastoma: From Genomic Alterations to Metabolic Adaptations

Quinones

2021

Advances in Experimental Medicine and Biology

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Glioblastoma multiforme (GBM) develops on glial cells and is the most common as well as the deadliest form of brain cancer. As in other cancers, distinct combinations of genetic alterations in GBM subtypes induce a diversity of metabolic phenotypes, which explains the variability of GBM sensitivity to current therapies targeting its reprogrammed metabolism. Therefore, it is becoming imperative for cancer researchers to account for the temporal and spatial heterogeneity within this cancer type before making generalized conclusions about a particular treatment’s efficacy. Standard therapies for GBM have shown little success as the disease is almost always lethal; however, researchers are making progress and learning how to combine therapeutic strategies most effectively. GBMs can be classified initially into two subsets consisting of primary and secondary GBMs, and this categorization stems from cancer development. GBM is the highest grade of gliomas, which includes glioma I (low proliferative potential), glioma II (low proliferative potential with some capacity for infiltration and recurrence), glioma III (evidence of malignancy), and glioma IV (GBM) (malignant with features of necrosis and microvascular proliferation). Secondary GBM develops from a low-grade glioma to an advanced-stage cancer, while primary GBM provides no signs of progression and is identified as an advanced-stage glioma from the onset. The differences in prognosis and histology correlated with each classification are generally negligible, but the demographics of individuals affected and the accompanying genetic/metabolic properties show distinct differentiation [3].

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“…The tumor cells release small pieces of their DNA or RNA, called cell-free circulating tumor DNA (ctDNA) and circulating microRNA (miRNA), respectively, into body fluids. They are relatively stable and can be used to analyze genetic tumor material found in CTCs, EVs, ctDNA, and miRNA isolated from body fluids [35,39,54,55]. ct-DNA consists of shortsized fragments base pairs) shed by apoptotic tumor cells and harbors genetic and epigenetic aberrations of the corresponding tumors [56].…”

Section: Circulating Tumor Nucleic Acidsmentioning

confidence: 99%

“…ct-DNA consists of shortsized fragments base pairs) shed by apoptotic tumor cells and harbors genetic and epigenetic aberrations of the corresponding tumors [56]. Susceptible PCR-based techniques are used for tracking changes in tumor mutational patterns [39,55,56]. miRNA is a class of widespread short (18-25 nucleotides) non-coding RNA molecules [54] that are determined by reverse transcription and real-time PCR.…”

Section: Circulating Tumor Nucleic Acidsmentioning

confidence: 99%

Diagnosis of Glioma Molecular Markers by Terahertz Technologies

et al. 2021

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This review considers glioma molecular markers in brain tissues and body fluids, shows the pathways of their formation, and describes traditional methods of analysis. The most important optical properties of glioma markers in the terahertz (THz) frequency range are also presented. New metamaterial-based technologies for molecular marker detection at THz frequencies are discussed. A variety of machine learning methods, which allow the marker detection sensitivity and differentiation of healthy and tumor tissues to be improved with the aid of THz tools, are considered. The actual results on the application of THz techniques in the intraoperative diagnosis of brain gliomas are shown. THz technologies’ potential in molecular marker detection and defining the boundaries of the glioma’s tissue is discussed.

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Cerebrospinal fluid tumor DNA for liquid biopsy in glioma patients’ management: Close to the clinic?

Cited by 21 publications

References 30 publications

RETRACTED ARTICLE: Exosomal SNHG16 secreted by CSCs promotes glioma development via TLR7

RETRACTED ARTICLE: Exosomal SNHG16 secreted by CSCs promotes glioma development via TLR7

The Multifaceted Glioblastoma: From Genomic Alterations to Metabolic Adaptations

Diagnosis of Glioma Molecular Markers by Terahertz Technologies

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