An alternative splicing signature defines the basal-like phenotype and predicts worse clinical outcome in pancreatic cancer.

doi:10.1016/j.xcrm.2024.101411

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Community

Back to search

Article

An alternative splicing signature defines the basal-like phenotype and predicts worse clinical outcome in pancreatic cancer.

Cell reports. Medicine - 20 Feb 2024

Ruta Veronica, Naro Chiara, Pieraccioli Marco, Leccese Adriana, Archibugi Livia, Cesari Eleonora, Panzeri Valentina, Allgöwer Chantal, Arcidiacono Paolo Giorgio, Falconi Massimo, Carbone Carmine, Tortora Giampaolo, Borrelli Federica, Attili Fabia, Spada Cristiano, Quero Giuseppe, Alfieri Sergio, Doglioni Claudio, Kleger Alexander, Capurso Gabriele, Sette Claudio

Abstract excerpt

Pancreatic ductal adenocarcinoma (PDAC) is characterized by extremely poor prognosis. PDAC presents with molecularly distinct subtypes, with the basal-like one being associated with enhanced chemoresistance. Splicing dysregulation contributes to PDAC; however, its involvement in subtype specification remains elusive. Herein, we uncover a subtype-specific splicing signature associated with prognosis in PDAC and...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Alternative Splicing

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Cancer Genomics and Diagnostics

Share to Carcinoma, Pancreatic Ductal

Share to Cell Line

Share to Pancreatic and Hepatic Oncology Research

Share to Pancreatic Neoplasms

Share to Phenotype

Share to Single-cell and spatial transcriptomics

Source

Open in PubMed Open full text

Identifiers

PMID: 38325381
DOI: 10.1016/j.xcrm.2024.101411
PMCID: PMC10897606

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

An alternative splicing signature defines the basal-like phenotype and predicts worse clinical outcome in pancreatic cancer.PMID 38325381Read ↗

Clinical Impact of Molecular Subtyping of Pancreatic CancerSemantic proximity Read ↗

The tumor microenvironment drives transcriptional phenotypes and their plasticity in metastatic pancreatic cancerSemantic proximity Read ↗

GATA6 Expression Distinguishes Classical and Basal-like Subtypes in Advanced Pancreatic CancerSemantic proximity Read ↗

An integrative RNA spliceosomic landscape of pancreatic neuroendocrine tumors unveils novel clinicomolecular associationsSemantic proximity Read ↗

Clinical and Genomic Features of Classical and Basal Transcriptional Subtypes in Pancreatic Cancer.Semantic proximity Read ↗

Single-cell analysis of patient-derived PDAC organoids reveals cell state heterogeneity and a conserved developmental hierarchySemantic proximity Read ↗

Determination of permissive and restraining cancer-associated fibroblast (DeCAF) subtypesSemantic proximity Read ↗

Molecular mechanisms of RACK1-driven metastasis in pancreatic ductal adenocarcinoma revealed by single-cell RNA sequencingSemantic proximity Read ↗

Integrative analysis of spatial and single-cell transcriptome data from human pancreatic cancer reveals an intermediate cancer cell population associated with poor prognosisSemantic proximity Read ↗

A Luminal–Basal Stratification of the Native Human Pancreatic Duct is Differentially Represented in Pancreatic CancersSemantic proximity Read ↗

Spliceosomic dysregulation unveils <i>NOVA1</i> as an actionable therapeutic target in pancreatic neuroendocrine tumorsSemantic proximity Read ↗

Dysregulated splicing factor SF3B1 unveils a dual therapeutic vulnerability to target pancreatic cancer cells and cancer stem cells with an anti-splicing drugSemantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.