Discover Community Create You

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

Article

De novo pyrimidine biosynthesis inhibition synergizes with BCL-XL targeting in pancreatic cancer

30 Jul 2025

Abstract excerpt

Abstract Oncogenic KRAS induces metabolic rewiring in pancreatic ductal adenocarcinoma (PDAC) characterized, in part, by dependency on de novo pyrimidine biosynthesis. Pharmacologic inhibition of dihydroorotate dehydrogenase (DHODH), an enzyme in the de novo pyrimidine synthesis pathway, delays pancreatic tumor growth; however, limited monotherapy efficacy suggests that compensatory pathways may drive resistance....

Read the complete abstract on PubMed

Topics

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

Share to Biochemical and Molecular Research
Share to Cancer, Hypoxia, and Metabolism
Share to Neuroblastoma Research and Treatments

Methodology Data sources Editorial policy Privacy Delete account & data About Contact Helena Bioinformatics

Source

Identifiers

PMID: 40738904
DOI: 10.1038/s41467-025-61242-x

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 23 Oct 2026.

Related research

Semantic proximity does not establish scientific evidence. Graph snapshot: 2026-09-29.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

De novo pyrimidine biosynthesis inhibition synergizes with BCL-XL targeting in pancreatic cancerPMID 40738904Read ↗

De novo pyrimidine biosynthesis inhibition synergizes with BCL-X <sub>L</sub> targeting in pancreatic cancerSemantic proximity Read ↗

DNAJA1 Dysregulates Metabolism Promoting an Antiapoptotic Phenotype in Pancreatic Ductal Adenocarcinoma.Semantic proximity Read ↗

Vertical RAS-pathway inhibition in pancreatic cancer drives therapeutically exploitable mitochondrial alterationsSemantic proximity Read ↗

Exploring the metabolic landscape of pancreatic ductal adenocarcinoma cells using genome-scale metabolic modelingSemantic proximity Read ↗

Bcl-xL Enforces a Slow-Cycling State Necessary for Survival in the Nutrient-Deprived Microenvironment of Pancreatic CancerSemantic proximity Read ↗

Exploring the metabolic landscape of pancreatic ductal adenocarcinoma cells using genome-scale metabolic modelingSemantic proximity Read ↗

USP25 promotes pathological HIF-1-driven metabolic reprogramming and is a potential therapeutic target in pancreatic cancerSemantic proximity Read ↗

Posttranscriptional Upregulation of IDH1 by HuR Establishes a Powerful Survival Phenotype in Pancreatic Cancer Cells.Semantic proximity Read ↗

Cytidine deaminase-dependent mitochondrial biogenesis as a potential vulnerability in pancreatic cancer cellsSemantic proximity Read ↗

ISL2 is an epigenetically silenced tumor suppressor and regulator of metabolism in pancreatic cancerSemantic proximity Read ↗

Dependence on the Pyrimidine Biosynthetic Enzyme DHODH Is a Synthetic Lethal Vulnerability in Mutant KRAS-Driven Cancers.Semantic proximity Read ↗

Fatty acid metabolism provides an essential survival signal in OxPhos and BCR DLBCL cellsSemantic proximity Read ↗

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