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Genes regulating B cell development are mutated in acute lymphoid leukaemia

GSE5511 Homo sapiens (human) Genome variation profiling by SNP array; SNP genotyping by SNP array 1099 samples Submitted 2009/09/02 Platform GPL2005Platform GPL3720Platform GPL2004
At a glance

human · 1099 samples

Organism
Homo sapiens (human)
Topic
Acute lymphoblastic leukemiaThis series is part of our curated briefing on it.
Samples
1099 samples: 1099 samples, each with a distinct title — no replicated groupsGroups are read from the sample names, not from the paper. Check the list below.
Data you can get
A processed table (series matrix) and supplementary files from NCBI.
Summary (written by the submitters)
Chromosomal aberrations are a hallmark of acute lymphoid leukaemia (ALL) but alone fail to induce leukaemia. To identify cooperating oncogenic lesions, we performed genome-wide analysis of leukaemic blasts from 242 paediatric ALL patients using high-resolution single nucleotide polymorphism arrays and genomic DNA sequencing. Our analyses revealed deletion, amplification, point mutation and structural rearrangement in genes encoding key regulators of B lymphocyte development and differentiation in 40% of B-progenitor ALL.
Read the full summary ↓
PAX5 was the most frequent target of somatic mutation, being altered in 31.7% of cases. The identified PAX5 mutations resulted in haploinsufficiency or the generation of hypomorphic alleles. Deletions were also detected in E2A, EBF, LEF1, Ikaros, and Aiolos. These findings demonstrate that direct disruption of pathways controlling B cell development and differentiation contributes to B-progenitor ALL pathogenesis. Moreover, these data demonstrate the power of high-resolution, genome-wide approaches to identify critical new molecular lesions in cancer. Keywords: disease state analysis *** Due to privacy concerns, the primary SNP array data is no longer available with unrestricted access. Individuals wishing to obtain this data for research purposes may request access using the Web links below. ***
This dataset
Download · which file do I need?

Direct links to NCBI, no account and no request form. Pick by what you want to do: take the small processed table to look, the supplementary files to re-analyse, or the original raw data to start over.

1 · Just have a look

Processed table

The series matrix: one table of values per sample as the submitters processed it. The smallest download, and it opens in Excel or R. Start here to see what the data look like.

2 · Re-analyse it

Supplementary files

The count tables and other files the authors uploaded. Take only the samples you need.

All supplementary files ↗
3 · The original raw files

Whole study · RAW.tar

Everything the authors deposited as one archive (GSE5511_RAW.tar), including the raw array or instrument files. Can be large; the picker in step 2 takes just the samples you need.

Also filed as BioProject PRJNA96241. Searching any of these in the dataset finder brings you back here.

Study design
1099 samples, each with a distinct title — no replicated groups

Any grouping that defines a comparison lives in the sample characteristics, which GEO records separately from the titles.

How we read this: Read from the first 400 of 1099 sample titles: 400 distinct titles with little repetition. These groups are guessed from the sample names, not taken from the paper, so check them against the sample list below before relying on them.

Samples in this study

+ 1059 more — browse all 1099 samples with per-sample file links →

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