Disrupted Neurogenesis, Gliogenesis, and Ependymogenesis in the Ccdc85c Knockout Rat for Hydrocephalus Model

Hasan, Md. Mehedi; Konishi, Shizuka; Tanaka, Miyuu; Izawa, Takeshi; Yamate, Jyoji; Kuwamura, Mitsuru

doi:10.2139/ssrn.4367238

Cited by 1 publication

(1 citation statement)

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“…These included, the 3'UTR of CCDC85 at 14q32.3 (3% of gliomas), the 7p12.2 enhancer near VWC2 (2%), the CTCF site within CROCC at 1p36.13 (2%), the open chromatin region at 15q11.2 (1.5%), as well as the brain GeneHancer elements within EGFR (7p11.2; 4%), near VWC2 (7p12.2, 2%), ITGA1 (5q11, 3%), LINC01787 (1p21.1, 3%) and FEZ2 (2p22.2, 6%). While a role for mutation of these non-coding elements in glioma oncogenesis is yet to be established, two have biological plausibility a priori -CCDC85C (coiled-coil domain containing 85c) is implicated in neurogenesis, gliogenesis, and ependymogenesis 20 , and upregulation of ITGA1 (Integrin Subunit Alpha 1) is implicated in de ning temozolomide (TMZ) resistance 21 .…”

Section: Non-coding Driver Mutationsmentioning

confidence: 99%

Genomic landscape of diffuse glioma revealed by whole genome sequencing

Kinnersley,

Jung,

Cornish

et al. 2023

Preprint

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Diffuse gliomas are the commonest malignant primary brain tumour in adults. Herein, we present the most comprehensive analysis of the genomic landscape of adult glioma to date, by whole genome sequencing of 403 tumours. We identify an extended catalogue of recurrent coding and non-coding genetic mutations that represents a source for future studies and provides the most complete high-resolution map of structural variants, copy number changes and global genome features including telomere length, mutational signatures and genomic complexity. Finally, we relate these to clinical outcome. As well as identifying new DNA level drug targets for treatment of glioma findings offer the prospect of improving treatment allocation with targeted therapies.

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Section: Non-coding Driver Mutationsmentioning

confidence: 99%