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

An allosteric PGAM1 inhibitor effectively suppresses pancreatic ductal adenocarcinoma

29 Oct 2019

Abstract excerpt

Glycolytic enzyme phosphoglycerate mutase 1 (PGAM1) plays a critical role in cancer metabolism by coordinating glycolysis and biosynthesis. A well-validated PGAM1 inhibitor, however, has not been reported for treating pancreatic ductal adenocarcinoma (PDAC), which is one of the deadliest malignancies worldwide. By uncovering the elevated PGAM1 expressions were statistically related to worse prognosis of PDAC in a...

Read the complete abstract on PubMed

Topics

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

Share to Cancer, Hypoxia, and Metabolism
Share to Epigenetics and DNA Methylation
Share to Pancreatic and Hepatic Oncology Research

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 31662475
DOI: 10.1073/pnas.1914557116

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 5 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

An allosteric PGAM1 inhibitor effectively suppresses pancreatic ductal adenocarcinomaPMID 31662475Read ↗

Glycometabolic rearrangements–aerobic glycolysis in pancreatic ductal adenocarcinoma (PDAC): roles, regulatory networks, and therapeutic potentialSemantic proximity Read ↗

Integrated transcriptomics, proteomics and metabolomics-based analysis uncover TAM2-associated glycolysis and pyruvate metabolic remodeling in pancreatic cancerSemantic proximity Read ↗

Metabolomic profiling of pancreatic adenocarcinoma reveals key features driving clinical outcome and drug resistance.Semantic proximity Read ↗

FV-429 induces apoptosis by regulating nuclear translocation of PKM2 in pancreatic cancer cellsSemantic proximity Read ↗

Metabolic reprogramming by driver mutation-tumor microenvironment interplay in pancreatic cancer: new therapeutic targets.Semantic proximity Read ↗

Metabolomic profiling of pancreatic adenocarcinoma reveals fundamental clinical featuresSemantic proximity Read ↗

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

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

PKM2 modulates chemotherapy sensitivity by regulating autophagy and predicts the prognosis and immunity in pancancerSemantic proximity Read ↗

Knockdown of PGM1 Synergistically Enhances Anticancer Effects of Orlistat in Gastric Cancer Under Glucose DeprivationSemantic proximity Read ↗

The biological role of metabolic reprogramming in pancreatic cancerSemantic proximity Read ↗

Glycolysis-Based Genes Associated with the Clinical Outcome of Pancreatic Ductal Adenocarcinoma Identified by The Cancer Genome Atlas Data AnalysisSemantic proximity Read ↗

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