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Transcriptomic profiling of the intermediate cell carcinoma of the primary liver cancer

GSE241466 Homo sapiens (human) RNA-seq (gene expression) 25 samples Submitted 2024/08/14 Platform GPL24676
At a glance

RNA-seq (gene expression) · human · 25 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)
Samples
25 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.
Paper
Transcriptomic profiling of intermediate cell carcinoma of the liverHepatology communications · 2024
Summary (written by the submitters)
Introduction: Combined hepatocellular-cholangiocarcinoma (cHCC-CCA) is a mixed-type tumor of hepatocellular carcinoma (HCC) and intrahepatic cholangiocarcinoma (iCCA), which is classified into classical type (i.e., c-CHC) and intermediate cell type (i.e., i-CHC). c-CHC harbors both HCC and iCCA cells, whereas i-CHC is comprised of intermediate cell types lacking classical regions of HCC or iCCA cells.
Read the full summary ↓
Notwithstanding the unique pathological feature of i-CHC, its molecular characteristics is not fully elucidated yet. Methods: To obtain molecular insights on the i-CHC, RNA-sequencing (RNA-Seq) and whole genome sequencing (WGS) profiling were performed on the tissues of i-CHC, HCC, and iCCA, respectively. Results: i-CHC showed unique transcriptomic features differing from HCC and iCCA, showing higher expression of Notch signaling and frequent splicing events of intron-retention (IR). Noticeably, we found that i-CHC had DNA-copy number loss and concomitant transcriptional suppression of METTL16, which may contribute to the aggressive progression of i-CHC via Notch activation. Conclusions: We suggest that i-CHC had unique transcriptomic features, providing new insights into the pathobiology of i-CHC.
Published in
Transcriptomic profiling of intermediate cell carcinoma of the liver
Jang B, Kwon SM, Kim JH et al. · Hepatology communications 2024 · PMID 39101773 · doi:10.1097/HC9.0000000000000505
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 GSE241466_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 PRJNA1008226 and SRA study SRP456536. Searching any of these in the dataset finder brings you back here.

Study design
A cohort of 25 individual samples

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

How we read this: Sample titles run YSINT2 … YSINT26 and carry no group information.

Samples in this study
Datasets on a similar topic

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Metadata from NCBI GEO, cached and refreshed periodically — the NCBI page above is authoritative. Downloads link straight to NCBI/ENA; nothing is proxied through BioTransfer.