CNTNAP3

Last update 08 May 2025

Basic Info

Synonyms

CASPR3, Cell recognition molecule Caspr3, CNTNAP3

+ [5]

Introduction-

100 Clinical Results associated with CNTNAP3

100 Translational Medicine associated with CNTNAP3

0 Patents (Medical) associated with CNTNAP3

Literatures (Medical) associated with CNTNAP3

01 Jun 2022·Psychiatry and Clinical Neurosciences

Peripheral transcriptome of clinical high‐risk psychosis reflects symptom alteration and helps prognosis prediction

Letter

Author: Wang, Weidi ; Yu, Shunying ; Zhang, Tianhong ; Fu, Yingmei ; Xu, Qingqing ; Lin, Guan Ning ; Ning, Ailing ; Yuan, Ruixue ; Song, Weichen ; Wang, Jijun ; Xu, Lihua

A review.We removed 10 samples with RNA integrity number (RIN) <6. With peripheral expression data and clin. assessment at both baseline and at 1- and 2-yr follow-up, we built a model to evaluate the psychotic symptom alteration by differential expression anal. and step regression, then explored the biol. functions associated with this model by gene set enrichment anal.(GSEA).We obtained RNA expression data of the peripheral blood from 56 patients collected at baseline and at 1-yr follow-up.In the leave-one-out and cross-validation tests, the model with top two (SYP and IFNW1 [interferon omega 1])or top three (by including gene CNTNAP3) genes achieved AUC scores between 0.80 and 0.92 (Fig.1d).

01 Jan 2022·Anti-Cancer DrugsQ4 · MEDICINE

Effective treatment of a BRAF V600E-mutant epithelioid glioblastoma patient by vemurafenib: a case report

Q4 · MEDICINE

Article

Author: Zhang, Zhu ; Yang, Runwei ; Zheng, Haojie ; Liu, Yawei ; Huang, Guanglong ; Zhang, Xian ; Peng, Junxiang ; Qi, Songtao ; Li, Zhiyong ; Lin, Zhiying ; Xu, Haiyan

Epithelioid glioblastoma (E-GBM) is a recently described variant of glioblastoma (GBM) which is associated with short survival and now added as a provisional entity to WHO 2016 classification of central nervous system tumors. About half of these tumors show the BRAF mutant. Therefore, this is a target of special interest for this group of patients. Meanwhile, unlike conventional glioblastoma, E-GBM lacks specific prognostic markers. We described a case of a long-term surviving 37-years-old men patient diagnosed with a BRAF V600E and TERT mutated E-GBM with wild-type in the isocitrate dehydrogenase gene (IDH wild-type). The tumor displayed atypical exophytic growth, an obvious proliferation of vascular endothelial cells, especially tumor tissue can be seen under subarachnoid space. Notably, tumor tissue was found under subarachnoid space. After postoperative conventional treatment options were exhausted, vemurafenib treatment was initiated. The patient remained clinically stable, and follow-up magnetic resonance images were consistent with stable disease for the following fifteen months up to now. Whole-exome sequencing analysis and RNA-seq results of formalin-fixed and paraffin-embedded tissue revealed nine mutant genes (AHNAK2, BFSP1, BRAF, CNTNAP3, DNHD1, MTOR, NFATC3, NOM1). For E-GBM patients, the use of BRAF inhibitors combined with inhibitors of these seven genes may be a useful remedial treatment option.

01 Aug 2021·Molecular Case Studies

Case of multifocal glioblastoma with four fusion transcripts of ALK, FGFR2, NTRK2, and NTRK3 genes stresses the need for tumor tissue multisampling for transcriptomic analysis

Article

Author: Makovskaia, Luidmila ; Moisseev, Aleksey ; Hartmann, Christian ; Garazha, Andrew ; Giese, Alf ; Kar, Souvik ; Sorokin, Maxim ; Kim, Ella ; Buzdin, Anton ; Samii, Amir

Glioblastoma multiforme (GBM) is the most malignant brain tumor with patient mortality rate close to 100%, 5-yr survival rate of ∼5%, and a median survival of 14 mo. GBMs have notorious histomorphologic and molecular heterogeneities thus giving hope for development of future personalized therapies. We describe here a case of a 48-yr-old male patient with three-nodular GBM. To address the question of intratumoral molecular heterogeneity, a comparative analysis of gene expression was performed by using multiple samples collected from different tumor sites with the aid of intraoperative magnetic resonance imaging (MRI). Sixteen GBM biosamples from parietal, temporal, and temporo-polar localizations were collected from primary, recurrent, and second recurrent tumors and were obtained and investigated by RNA sequencing. Our investigations revealed that biosamples derived from different tumor sites differ in their gene expression profiles with classical or mesenchymal signatures associated with clinically distinct molecular subtypes of GBM found within the same tumor. The results also showed significant differences in the expression of genes specific for targeted therapeutics. Our investigations have enabled the identification of four novel fusion transcripts—KIF5C-NTRK3, AC016907.2-ALK, CNTNAP3-NTRK2, and ZNF135-FGFR2—each present in only one sample. We found no differences between untreated and recurrent stages in the expression levels of genes involved in fusion transcripts, suggesting the lack of association between fusion transcript and treatment response. In contrast, longitudinal changes in the expression of VEGF and MGMT genes were concordant with the tumor response to bevacizumab and temozolomide. Our study underscores the importance of integrating a multisampling approach and RNA sequencing and demonstrates the predictive merit of an integrated approach for differentiating genomic aberrations associated with untreated or post-treatment recurrent GBMs.

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CNTNAP3

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