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The transcriptional landscape and mutational profile of lung adenocarcinoma

GSE40419 Homo sapiens (human) RNA-seq (gene expression) 164 samples Submitted 2012/09/06 Platform GPL11154
At a glance

RNA-seq (gene expression) · human · 164 samples

What it is
RNA-seq (gene expression)Gene activity measured by sequencing. The summary does not mention single-cell work, so this is most likely bulk: one average per sample, the usual starting point for comparing groups.
Organism
Homo sapiens (human)
Topic
Lung cancerThis series is part of our curated briefing on it.
Samples
164 samples
Data you can get
A processed table (series matrix) and supplementary files from NCBI; the raw sequencing reads from ENA. Which of these hold counts depends on the study, so check the file list.
Summary (written by the submitters)
Understanding the molecular signatures of cancer is important to apply appropriate targeted therapies. Here we present the first large scale RNA sequencing study of lung adenocarcinoma demonstrating its power to identify somatic point mutations as well as transcriptional variants such as gene fusions, alternative splicing events and expression outliers.
Read the full summary ↓
Our results reveal the genetic basis of 200 lung adenocarcinomas in Koreans including deep characterization of 87 surgical specimens by transcriptome sequencing. We identified driver somatic mutations in cancer genes including EGFR, KRAS, NRAS, BRAF, PIK3CA, MET and CTNNB1. New cancer genes, such as LMTK2, ARID1A, NOTCH2 and SMARCA4, were also suggested as candidates for novel drivers in lung adenocarcinoma. We found 45 fusion genes, 8 of which were chimeric tyrosine kinases involving ALK, RET, ROS1, FGFR2, AXL and PDGFRA. Of 17 recurrent alternative splicing events, we identified exon 14 skipping in the proto-oncogene MET as highly likely to be a cancer driver. The number of somatic mutations and expression outliers varied markedly between individual cancers and was strongly correlated with smoking history of cancer patients. In addition, we identified genomic blocks where genes were frequently up- or down-regulated together that could be explained by copy number alterations in the cancer tissue. We also found an association between lymph node metastasis and somatic mutations in TP53. Our findings broaden our understanding of lung adenocarcinoma and may also lead to new diagnostic and therapeutic approaches. * Raw data files were submitted to EBI-SRA under accession number ERP001058.
This dataset
Download · which file do I need?

Direct links to NCBI and ENA, 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, or the whole study as GSE40419_RAW.tar (it can run to tens of gigabytes).

3 · Start from the raw reads

Raw sequencing reads

The original FASTQ files, straight from the sequencer, held at ENA. Large, and you align them yourself, so only choose this if you need to re-process the study from scratch.

What the files usually look like: For RNA-seq the counts are usually a table among the supplementary files (look for 'counts', 'expression', 'FPKM' or 'TPM' in the file name). The series matrix of a sequencing study is sometimes nearly empty.

Also filed as BioProject PRJEB3132 and SRA study ERP001058. Searching any of these in the dataset finder brings you back here.

Samples in this study

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