← BioTransfer GEO Dataset Finder
GEO series

Effect of DOT1L inhibition on gene expression in SW1990 pancreatic cancer cells

GSE303903 Homo sapiens Expression profiling by high throughput sequencing 6 samples Submitted 2026/07/28 Platform GPL34284
Summary
Histone methyltransferase DOT1L plays a critical role in the regulation of gene expression through methylation of histone H3 at lysine 79 (H3K79), a modification associated with active transcription. However, its function in pancreatic ductal adenocarcinoma (PDAC) remains incompletely understood. In this study, we investigated the transcriptional impact of DOT1L in SW1990 pancreatic cancer cells using EPZ-5676, a selective DOT1L inhibitor. Treatment with EPZ-5676 resulted in widespread transcriptional changes, indicating a key regulatory role of DOT1L in maintaining the gene expression profile of SW1990 cells. Through RNA-seq analysis, we identified differentially expressed genes between the untreated control and EPZ-5676-treated cells, implicating DOT1L in pathways involved in cell proliferation, differentiation, and tumor progression. These findings suggest that DOT1L-mediated H3K79 methylation contributes to the transcriptional landscape of pancreatic cancer cells and may represent a potential therapeutic target.
This dataset
Download

Direct links to NCBI, no account and no request form: the whole study as GSE303903_RAW.tar, processed values as the series matrix, the supplementary file directory, and per-sample supplementary files for any of the 6 samples. Raw sequencing reads are also available from ENA.

Also filed as BioProject PRJNA1298197 and SRA study SRP604241. Searching any of these in the dataset finder brings you back here.

Samples in this study

The sample list for this study is not cached yet. Press Sort into groups and it will be fetched from NCBI.

+ 6 more — browse all 6 samples with per-sample file links →

Similar datasets

Search all human RNA-seq datasets in GEO →

Share this dataset

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.