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Anticancer activity of RAS-GTP inhibition in cholangiocarcinoma [Human_Abr24]

GSE318388 Homo sapiens (human) RNA-seq (gene expression) 12 samples Submitted 2026/03/30 Platform GPL30173
At a glance

RNA-seq (gene expression) · human · 12 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
CholangiocarcinomaThis series is part of our curated briefing on it.
Samples
12 samples: 3 × HUCCT1_C vs 3 × HUCCT1_T vs 3 × KKU213A_C vs 3 × KKU213A_TGroups 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; the raw sequencing reads from ENA. Which of these hold counts depends on the study, so check the file list.
Paper
Anticancer activity of RAS-GTP inhibition in cholangiocarcinomaCancer cell · 2026
Summary (written by the submitters)
About 25% of cholangiocarcinoma (CCA) patients harbor KRAS mutations, being potentially amenable to direct KRAS inhibitors. Here, we investigated the activity of RAS(ON) multi-selective inhibitors, which target the active, GTP-bound state of both mutant and wild-type variants of canonical RAS isoforms, in CCA preclinical models and patients.
Read the full summary ↓
RAS(ON) multi-selective inhibitors yield strong anticancer responses in cell- and patient-derived xenografts and in immunocompetent allograft models. Consistently, we describe responses to the RAS(ON) multi-selective inhibitor daraxonrasib in two KRASG12X patients with advanced CCA. RAS-GTP inhibition also potentiates the activity of the current standard-of-care CCA therapy to prolong survival in cell-derived human xenografts and mouse allografts. Furthermore, we demonstrate that both intrinsic and acquired resistance to RAS(ON) multi-selective inhibitors mainly rely on reconstitution of RAS signalling. Overall, our findings indicate that KRAS mutant CCA is addicted to RAS signalling for proliferation and support the potential clinical evaluation of RAS-GTP inhibition in CCA.
Published in
Anticancer activity of RAS-GTP inhibition in cholangiocarcinoma
Entrialgo-Cadierno R, Morali K, Feliu I et al. · Cancer cell 2026 · PMID 42030930 · doi:10.1016/j.ccell.2026.03.020
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 GSE318388_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 PRJNA1418666 and SRA study SRP674594. Searching any of these in the dataset finder brings you back here.

Study design
3 × HUCCT1_C vs 3 × HUCCT1_T vs 3 × KKU213A_C vs 3 × KKU213A_T

Supports a between-group comparison across 12 samples.

How we read this: 4 replicated groups read from 12 sample titles; they account for 12 of them. 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
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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.