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Title:
JCM | Free Full-Text | Molecular and Metabolic Subtypes Correspondence for Pancreatic Ductal Adenocarcinoma Classification
Description:
Pancreatic ductal adenocarcinoma (PDAC), the most common form of pancreatic cancer, is an extremely lethal disease due to late diagnosis, aggressiveness and lack of effective therapies. Considering its intrinsic heterogeneity, patient stratification models based on transcriptomic and genomic signatures, with partially overlapping subgroups, have been established. Besides molecular alterations, PDAC tumours show a strong desmoplastic response, resulting in profound metabolic reprogramming involving increased glucose and amino acid consumption, as well as lipid scavenging and biosynthesis. Interestingly, recent works have also revealed the existence of metabolic subtypes with differential prognosis within PDAC, which correlated to defined molecular subclasses in patients: lipogenic subtype correlated with a classical/progenitor signature, while glycolytic tumours associated with the highly aggressive basal/squamous profile. Bioinformatic analyses have demonstrated that the representative genes of each metabolic subtype are up-regulated in PDAC samples and predict patient survival. This suggests a relationship between the genetic signature, metabolic profile, and aggressiveness of the tumour. Considering all this, defining metabolic subtypes represents a clear opportunity for patient stratification considering tumour functional behaviour independently of their mutational background.
Website Age:
20 years and 8 months (reg. 2003-12-19).
Title:
JCM | Free Full-Text | Molecular and Metabolic Subtypes Correspondence for Pancreatic Ductal Adenocarcinoma Classification
Description:
Pancreatic ductal adenocarcinoma (PDAC), the most common form of pancreatic cancer, is an extremely lethal disease due to late diagnosis, aggressiveness and lack of effective therapies. Considering its intrinsic heterogeneity, patient stratification models based on transcriptomic and genomic signatures, with partially overlapping subgroups, have been established. Besides molecular alterations, PDAC tumours show a strong desmoplastic response, resulting in profound metabolic reprogramming involving increased glucose and amino acid consumption, as well as lipid scavenging and biosynthesis. Interestingly, recent works have also revealed the existence of metabolic subtypes with differential prognosis within PDAC, which correlated to defined molecular subclasses in patients: lipogenic subtype correlated with a classical/progenitor signature, while glycolytic tumours associated with the highly aggressive basal/squamous profile. Bioinformatic analyses have demonstrated that the representative genes of each metabolic subtype are up-regulated in PDAC samples and predict patient survival. This suggests a relationship between the genetic signature, metabolic profile, and aggressiveness of the tumour. Considering all this, defining metabolic subtypes represents a clear opportunity for patient stratification considering tumour functional behaviour independently of their mutational background.
Website Age:
20 years and 8 months (reg. 2003-12-19).
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Keywords {🔍}
pdac, pancreatic, cancer, google, scholar, crossref, metabolic, subtypes, subtype, cells, genes, glycolytic, version, green, cell, molecular, expression, pubmed, adenocarcinoma, metabolism, classical, table, kras, jul, aug, ductal, tumours, tumour, prognosis, lipid, survival, glucose, classification, lipogenic, high, pathways, basal, gene, patients, sep, stratification, biosynthesis, glycolysis, showed, zhao, related, signature, clinical, article, signatures,
Topics {✒️}
k-ras-driving pdac-bearing mice tgf-β-mediated epithelial-mesenchymal transition branched-chain α-ketoacid myc/pgc-1α balance determines branched-chain amino acids genome-wide chromatin immunoprecipitation-sequencing graded patient-derived xenografts tgf-β/smad4 signaling 3-hydroxy-3-methylglutaryl-coa synthase 1 tgf-β tumor suppression writing—original draft preparation transforming growth factor-beta mitogen-activated protein kinases recurrence-free survival rates overcomes growth arrest/senescence oncogenic k-ras enhances mismatch repair-deficient tumours jun amino-terminal kinases stress-activated protein kinases [google scholar] morton proton-coupled symport transporters high-gradient extracellular compartment low-gradient cytoplasmic compartment single-cell rnaseq analyses chan-seng-yue ecm-rich subtype appeared emt-related gene snail disease-free survival analyses beatriz parejo-alonso atp-independent glucose transporter author contributions conceptualisation pancreatic ductal adenocarcinomas glycolysis–cholesterol synthesis axis k-ras k-ras stromal-rich pdac tumours mdpi stays neutral pancreatic ductal adenocarcinoma kras-regulated metabolic pathway fatty acid synthase transcriptional network tp63δn tumorigenic ductal cells pilar espiau-romera positive feedback loop acquire fatty acids �immune-rich” group characterised lipid-derived messengers amino acid consumption tgf-β pathway advanced pancreatic adenocarcinoma intermediate cellular phenotypes
Questions {❓}
- Pancreatic ductal adenocarcinoma epidemiology and risk assessment: Could we prevent?
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