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Status |
Public on Jan 25, 2023 |
Title |
cnmc842t |
Sample type |
SRA |
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|
Source name |
Primary human patient cnmc842t tumor tissue
|
Organism |
Homo sapiens |
Characteristics |
tissue: Pons DIPG tumor cell type: Primary DIPG cells treatment: None
|
Extracted molecule |
polyA RNA |
Extraction protocol |
Total RNA was extracted using chloroform extraction followed by ethanol precipitation and quantified using Qubit, as described in Nagaraja 2017. After extraction, RNA-seq samples were poly(A) selected using Dynabeads mRNA Purification Kit (Life Tech) before fragmentation using Fragmentation Buffer (Ambion, #AM8740) and Second Strand Synthesis using DNA Pol I (Invitrogen #18010-025). Libraries were sequenced at 1x75 on an Illumina NextSeq 500. RNA-seq samples were poly(A) selected using Dynabeads mRNA Purification Kit (Life Tech) before fragmentation using Fragmentation Buffer (Ambion, #AM8740) and Second Strand Synthesis using DNA Pol I (Invitrogen #18010-025). Libraries were sequenced at 1x75 on an Illumina NextSeq 500.
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Library strategy |
RNA-Seq |
Library source |
transcriptomic |
Library selection |
cDNA |
Instrument model |
Illumina NextSeq 500 |
|
|
Description |
Due to patient privacy concerns, we are witholding raw sequencing files at this time.
|
Data processing |
Reads were mapped to hg19 annotation using Tophat2 (Kim et al 2013) (version 2.0.13). Transcript expression was quantified against RefSeq gene annotations using featureCounts (Liao et al, 2014). Attached files indicate transcript expression via tpm values. Assembly: hg19 Supplementary files format and content: Raw tpm counts of gene expression abundance for cnmc842t and pons02 (in csv format)
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|
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Submission date |
Jan 25, 2023 |
Last update date |
Jan 25, 2023 |
Contact name |
Michelle Monje |
E-mail(s) |
mmonje@stanford.edu
|
Organization name |
Stanford University
|
Street address |
265 Campus Drive, SIM1 G3035
|
City |
Stanford |
State/province |
CA |
ZIP/Postal code |
94305 |
Country |
USA |
|
|
Platform ID |
GPL18573 |
Series (1) |
GSE126319 |
Variant and cell-context specific H3K27M reprogramming results in distinct enhancer architecture and oncogenic states |
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