Abundance of LRP12 C-rs9694676 allelic promoter variant in epilepsy-associated gangliogliomas

Robens, Barbara K.; Gembé, Eva; Fassunke, Jana; Becker, Albert; Schoch, Susanne; Grote, Alexander

doi:10.1016/j.lfs.2016.01.049

Cited by 6 publications

(3 citation statements)

References 32 publications

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“…The low-density lipoprotein LRP12 has been postulated to be a receptor for internalizing lipophilic molecules and may have a potential function in signal transduction (50). Also known as suppressor of tumorigenicity 7 protein, LRP12 has also been reported to be differentially expressed in various cancer types including oral squamous cell carcinoma (50), lymphoma (51) and more recently gangliogliomas and low-grade central nervous system tumor types (52). PARK2 is a tumor suppressor gene and when deleted is known to promote tumorigenicity.…”

Section: Discussionmentioning

confidence: 99%

Determination of genetic aberrations and novel transcripts involved in the pathogenesis of oligodendroglioma using array comparative genomic hybridization and next generation sequencing

2018

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The aim of the present study was to determine the genetic aberrations and novel transcripts, particularly the fusion transcripts, involved in the pathogenesis of low-grade and anaplastic oligodendroglioma. In the present study, tissue samples were obtained from patients with oligodendroglioma and additionally from archived tissue samples from the Brain Tumor Tissue Bank of the Brain Tumor Foundation of Canada. Six samples were obtained, three of which were low-grade oligodendroglioma and the other three anaplastic oligodendroglioma. DNA and RNA were extracted from each tissue sample. The resulting genomic DNA was then hybridized using the Agilent CytoSure 4×180K oligonucleotide array. Human reference DNA and samples were labeled using Cy3 cytidine 5′-triphosphate (CTP) and Cy5 CTP, respectively, while human Cot-1 DNA was used to reduce non-specific binding. Microarray-based comparative genomic hybridization data was then analyzed for genetic aberrations using the Agilent Cytosure Interpret software v3.4.2. The total RNA isolated from each sample was mixed with oligo dT magnetic beads to enrich for poly(A) mRNA. cDNAs were then synthesized and subjected to end-repair, poly(A) addition and connected using sequencing adapters using the Illumina TruSeq RNA Sample Preparation kit. The fragments were then purified and selected as templates for polymerase chain reaction amplification. The final library was constructed with fragments between 350–450 base pairs and sequenced using deep transcriptome sequencing on an Illumina HiSeq 2500 sequencer. The array comparative genomic hybridization revealed numerous amplifications and deletions on several chromosomes in all samples. However, the most interesting result was from the next generation sequencing, where one anaplastic oligodendroglioma sample was demonstrated to have five novel fusion genes that may potentially serve a critical role in tumor pathogenesis and progression.

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Section: Discussionmentioning

confidence: 99%

Determination of genetic aberrations and novel transcripts involved in the pathogenesis of oligodendroglioma using array comparative genomic hybridization and next generation sequencing

2018

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“…B.K. Robens определил роль транскрипционной регуляции рецептора LRP12 в патогенезе ганглио глиом [92].…”

Section: иммунологический статус и локальные иммунные реакцииunclassified

Modern conceptions about the pathogenesis of tumor-related epilepsy

Tolstykh

Викторовна²,

Гурчин

et al. 2019

Medical academic journal

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Tumor-related epilepsy is of interest among the symptomatic epilepsy, that develops in 75% of patients with gliomas low-grade (astrocytomas, oligodendrogliomas — Gr II) and more than 95% of patients with glioneuronal tumors (ganglioglioma — Gr I). Currently, the nature of epileptogenic activity in brain tumors is still controversial, and the search for epileptogenic foci that are part of the tumor zone presents certain difficulties. The authors described the structural changes and metabolism in the tumor and peritumoral zone, immunological status, and molecular genetic features of the tumor, which may explain the pathogenesis of tumor-related epilepsy. In turn, the clarification of the mechanisms of epileptogenesis is a prerequisite for the development of therapeutically effective anticonvulsants, and to improve the strategies of complex treatment of tumors associated with epilepsy.

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“…Lrp12 is important during CNS development where it controls the formation of the cortical plate, neuronal polarity, and migration (Schneider et al, 2011 ; Wang et al, 2013b ). It is also involved in tumorigenesis including epilepsy-associated gangliogliomas (Garnis et al, 2004 ; Robens et al, 2016 ). Silencing of Lrp12 in primary neurons leads to increased dendritic branching, silencing of Lrp12 in the mouse brain during brain development leads to cortical dyslamination and seizure sensitization (Grote et al, 2016 ).…”

Section: Very Distinct and Short Receptors Containing Lbrsmentioning

confidence: 99%

Functional Roles of the Interaction of APP and Lipoprotein Receptors

Pohlkamp

Wasser

Herz

2017

Front. Mol. Neurosci.

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The biological fates of the key initiator of Alzheimer’s disease (AD), the amyloid precursor protein (APP), and a family of lipoprotein receptors, the low-density lipoprotein (LDL) receptor-related proteins (LRPs) and their molecular roles in the neurodegenerative disease process are inseparably interwoven. Not only does APP bind tightly to the extracellular domains (ECDs) of several members of the LRP group, their intracellular portions are also connected through scaffolds like the one established by FE65 proteins and through interactions with adaptor proteins such as X11/Mint and Dab1. Moreover, the ECDs of APP and LRPs share common ligands, most notably Reelin, a regulator of neuronal migration during embryonic development and modulator of synaptic transmission in the adult brain, and Agrin, another signaling protein which is essential for the formation and maintenance of the neuromuscular junction (NMJ) and which likely also has critical, though at this time less well defined, roles for the regulation of central synapses. Furthermore, the major independent risk factors for AD, Apolipoprotein (Apo) E and ApoJ/Clusterin, are lipoprotein ligands for LRPs. Receptors and ligands mutually influence their intracellular trafficking and thereby the functions and abilities of neurons and the blood-brain-barrier to turn over and remove the pathological product of APP, the amyloid-β peptide. This article will review and summarize the molecular mechanisms that are shared by APP and LRPs and discuss their relative contributions to AD.

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Abundance of LRP12 C-rs9694676 allelic promoter variant in epilepsy-associated gangliogliomas

Cited by 6 publications

References 32 publications

Determination of genetic aberrations and novel transcripts involved in the pathogenesis of oligodendroglioma using array comparative genomic hybridization and next generation sequencing

Determination of genetic aberrations and novel transcripts involved in the pathogenesis of oligodendroglioma using array comparative genomic hybridization and next generation sequencing

Modern conceptions about the pathogenesis of tumor-related epilepsy

Functional Roles of the Interaction of APP and Lipoprotein Receptors

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