Correction: Author Correction: Somatic chromosomal engineering identifies BCAN-NTRK1 as a potent glioma driver and therapeutic target

Cook, Peter J.; Thomas, Rozario; Kannan, Ram; León, Esther; Drilon, Alexander; Rosenblum, Marc K.; Scaltriti, Maurizio; Benezra, Robert; Ventura, Andrea

doi:10.1038/ncomms16187

Cited by 5 publications

(2 citation statements)

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“…Sulbactam Inhibits Cell Proliferation. In recent years, more drugs were developed besides TMZ, such as entrectinib, 14 lomustine, 15 paxalisib, 16 and larotrectinib. 17 The sulfatase activity determination with the probe was not inhibited by the abovementioned drugs (Figure 4C), indicating that these drugs treating GBM are not through the sulfatase pathway, while sulbactam has an obvious inhibitory effect, declaring that sulbactam is a therapeutic candidate worthy of further development.…”

Section: ■ Results and Discussionmentioning

confidence: 99%

New Protocol-Guided Exploitation of a Lysosomal Sulfatase Inhibitor to Suppress Cell Growth in Glioblastoma Multiforme

et al. 2021

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Glioblastoma multiforme (GBM) is a highly invasive and aggressive malignant glioma. Current treatment modalities are unable to significantly prolong survival in patients diagnosed with glioblastoma, so more effective strategies of antitumor treatments are in urgent demand. Here, we found that lysosomal sulfatase expression was significantly correlated with poor prognosis of GBM. Hence, a new probe, MNG, was developed with a new protocol utilizing glucose groups to detect lysosomal sulfatase. It also exhibits potential for monitoring GBM cells, depending on the hyperactive lysosomal sulfatase expression of tumor cells. Meantime, we identified that sulbactam as the first reported lysosomal sulfatase inhibitor inhibits the tumor growth of GBM. Collectively, our work highlights that lysosomal sulfatase was detected using a new protocol and its potential as a therapeutic target in GBM and reveals a distinct mechanism that sulbactam inhibits cell proliferation related to lysosomal sulfatase, indicating that sulbactam could be a promising therapeutic agent against GBM.

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Section: ■ Results and Discussionmentioning

confidence: 99%

New Protocol-Guided Exploitation of a Lysosomal Sulfatase Inhibitor to Suppress Cell Growth in Glioblastoma Multiforme

et al. 2021

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“…After integrating brain-specific genes with CSF proteins, we revealed that there are five brain-specific proteins that can be detected in CSF ( Specifically, BCAN, a member of the lectican family of chondroitin sulfate proteoglycans, is highly expressed in glioma and may promote cell motility of brain tumor cells [64,65]. In addition, the fusion event between BCAN and NTRK1 (BCAN-NTRK1) is a potential glioma driver and therapeutic target [66].…”

Section: Resultsmentioning

confidence: 99%

Computational identification and characterization of glioma candidate biomarkers through multi-omics integrative profiling

Liu

Wang

et al. 2020

Biol Direct

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Background: Glioma is one of the most common malignant brain tumors and exhibits low resection rate and high recurrence risk. Although a large number of glioma studies powered by high-throughput sequencing technologies have led to massive multi-omics datasets, there lacks of comprehensive integration of glioma datasets for uncovering candidate biomarker genes. Results: In this study, we collected a large-scale assemble of multi-omics multi-cohort datasets from worldwide public resources, involving a total of 16,939 samples across 19 independent studies. Through comprehensive molecular profiling across different datasets, we revealed that PRKCG (Protein Kinase C Gamma), a brain-specific gene detectable in cerebrospinal fluid, is closely associated with glioma. Specifically, it presents lower expression and higher methylation in glioma samples compared with normal samples. PRKCG expression/methylation change from high to low is indicative of glioma progression from low-grade to high-grade and high RNA expression is suggestive of good survival. Importantly, PRKCG in combination with MGMT is effective to predict survival outcomes in a more precise manner. Conclusions: PRKCG bears the great potential for glioma diagnosis, prognosis and therapy, and PRKCG-like genes may represent a set of important genes associated with different molecular mechanisms in glioma tumorigenesis. Our study indicates the importance of computational integrative multi-omics data analysis and represents a datadriven scheme toward precision tumor subtyping and accurate personalized healthcare.

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Molecular Biology, Genetics, and Translational Models of Human Cancer

Traub¹,

Scheufele²,

Viswanathan³

et al. 2022

Holland‐Frei Cancer Medicine

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Overview Cancer is a disease of abnormal cellular behavior and characterized by molecular aberrations that promote cellular proliferation and survival. Neoplastic progression ultimately produces tumor masses that compromise local organ function, and the invasion and metastasis of malignant cells away from their tissue of origin and spread throughout the body cause a diverse array of pathophysiologic sequelae that compromise the quality and length of life of patients. A background knowledge of cancer pathogenesis and cancer models should help oncologists understand the developing approaches for optimal patient care, including the new concept of personalized medicine. This article is a basic, “methods‐oriented” survey of molecular biology directed toward the clinician or trainee who wants a fundamental understanding of this discipline. It describes the principles that underlie the procedures used most commonly by molecular biologists and provides examples of clinically relevant situations that draw on particular techniques. Molecular biology already plays an important role in clinical cancer medicine, both in terms of diagnosis (e.g., in the analysis of tumors for prognostic or pathogenetic information) and in treatment (e.g., in the production of pharmacologic and biologic agents, such as recombinant growth factors and monoclonal antibodies). We will begin with an overview of genes, gene expression, and gene cloning. Our discussion of techniques will follow the flow of genetic information as we explain the procedures used to analyze gene expression at the levels of DNA, ribonucleic acid ( RNA ), and protein. We conclude with a discussion of current cancer modeling systems in vitro and in vivo . Good general overviews of these topics can be found in several books. 1–3

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Correction: Author Correction: Somatic chromosomal engineering identifies BCAN-NTRK1 as a potent glioma driver and therapeutic target

Cited by 5 publications

References 0 publications

New Protocol-Guided Exploitation of a Lysosomal Sulfatase Inhibitor to Suppress Cell Growth in Glioblastoma Multiforme

New Protocol-Guided Exploitation of a Lysosomal Sulfatase Inhibitor to Suppress Cell Growth in Glioblastoma Multiforme

Computational identification and characterization of glioma candidate biomarkers through multi-omics integrative profiling

Molecular Biology, Genetics, and Translational Models of Human Cancer

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