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Danita M. Pearson

Researcher at University of Cambridge

Publications -  21
Citations -  2693

Danita M. Pearson is an academic researcher from University of Cambridge. The author has contributed to research in topics: Astrocytoma & DNA methylation. The author has an hindex of 18, co-authored 21 publications receiving 2444 citations.

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Tandem duplication producing a novel oncogenic BRAF fusion gene defines the majority of pilocytic astrocytomas.

TL;DR: This is the first report of BRAF activation through rearrangement as a frequent feature in a sporadic tumor, and the frequency and specificity of this change underline its potential both as a therapeutic target and as a diagnostic tool.
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IDH1 mutations are present in the majority of common adult gliomas but rare in primary glioblastomas

TL;DR: The data indicate that IDH1 mutation combined with either TP53 mutation or total 1p/19q loss is a frequent and early change in the majority of oligodendroglial tumors, diffuse astrocytomas, anaplastic astro CYTomas, and secondary glioblastomas but not in primary gliOBlastomas.
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Oncogenic RAF1 rearrangement and a novel BRAF mutation as alternatives to KIAA1549:BRAF fusion in activating the MAPK pathway in pilocytic astrocytoma

TL;DR: The number of cases with an identified ‘hit’ on the Ras/Raf-signalling pathway is brought to 36 from the series of 44 (82%), confirming its central importance to the development of pilocytic astrocytomas.
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Hi-C as a tool for precise detection and characterisation of chromosomal rearrangements and copy number variation in human tumours.

TL;DR: The use of Hi-C is described as a tool for detection of both balanced and unbalanced chromosomal rearrangements in primary human tumour samples, with the potential to define chromosome breakpoints to bp resolution.
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A distinct region of the MGMT CpG island critical for transcriptional regulation is preferentially methylated in glioblastoma cells and xenografts

TL;DR: Results indicate that several CpG sites within DMR2 play a critical role in the transcriptional control of MGMT, making DMR1 the optimal target for methylation testing, but methylation levels need to be measured at a number of individual CpGs within D MR2 to confidently predict transcriptional silencing and thus sensitivity to alkylating agents.