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Status |
Public on Nov 30, 2017 |
Title |
Lckpr-TCL1A+/- T-cells; ‘exponential phase’ 3 |
Sample type |
genomic |
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Source name |
splenic isolates from T-cell leukemia / lymphoma bearing Lckpr-hTCL1A+/- mice
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Organism |
Mus musculus |
Characteristics |
tissue: spleen Stage: late genotype: Lckpr-TCL1A+/-
|
Extracted molecule |
genomic DNA |
Extraction protocol |
Murine T-cell leukemia. Sample preparation: We hybridized DNA samples (QIAamp DNA Kit, Qiagen) onto the Affymetrix MOUSEDIVm520650 chip. We compared 4 controls (DNA isolated from normal liver tissues of age- and background-matched wild-type mice) to 3 ‘chronic phase’ and 5 ‘exponential phase’ (defining features in 4.2) splenic isolates from T-cell leukemia / lymphoma bearing Lckpr-hTCL1A+/- mice. DNA was restriction digested, PCR amplified, fragmented, labeled and hybridized to each array according to the manufacturer's instructions.
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Label |
biotin
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Label protocol |
As per manufacturer (Affymetrix)
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Hybridization protocol |
As per manufacturer (Affymetrix)
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Scan protocol |
The Arrays were then washed using Affymetrix fluidics stations, and scanned using the Gene Chip Scanner 3000.
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Data processing |
Bioinformatics: Arrays were pre-processed and separately analyzed (‘chronic phase’ vs. ctrl., ‘exponential phase’ vs. ctrl.) with the ‘mouseDivGeno’ R-package. primary data description: Murine TCL1A-driven T-PLL-like expansions generally revealed a lower sCNA abundance and recurrence (average 70.7 sCNAs in chronic phase (n=3) and 74.8 sCNAs in exponential phase (n=5; CN<1.8 or >2.2)).
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Submission date |
Nov 29, 2017 |
Last update date |
Jan 23, 2018 |
Contact name |
Giuliano Crispatzu |
Organization name |
University of Cologne (UoC), Germany
|
Department |
CECAD
|
Street address |
Joseph-Stelzmann-Straße 26
|
City |
Cologne |
ZIP/Postal code |
50931 |
Country |
Germany |
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Platform ID |
GPL13147 |
Series (2) |
GSE107510 |
The molecular basis of T-PLL is an actionable perturbation of TCL1/ATM- and epigenetically instructed damage responses [murine SNP array] |
GSE107513 |
The molecular basis of T-PLL is an actionable perturbation of TCL1/ATM- and epigenetically instructed damage responses |
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