CTHRC1 + fibroblasts and SPP1 + macrophages synergistically contribute to pro-tumorigenic tumor microenvironment in pancreatic ductal adenocarcinoma
- Standort
-
Deutsche Nationalbibliothek Frankfurt am Main
- Umfang
-
1 Online-Ressource.
- Sprache
-
Englisch
- Erschienen in
-
CTHRC1 + fibroblasts and SPP1 + macrophages synergistically contribute to pro-tumorigenic tumor microenvironment in pancreatic ductal adenocarcinoma ; volume:14 ; number:1 ; day:29 ; month:7 ; year:2024 ; pages:1-15 ; date:12.2024
Scientific reports ; 14, Heft 1 (29.7.2024), 1-15, 12.2024
- Urheber
-
Li, Evan
Cheung, Hoi Ching (Zoey)
Ma, Shuangge
- Beteiligte Personen und Organisationen
-
SpringerLink (Online service)
- DOI
-
10.1038/s41598-024-68109-z
- URN
-
urn:nbn:de:101:1-2410132114078.865539901731
- Rechteinformation
-
Open Access; Der Zugriff auf das Objekt ist unbeschränkt möglich.
- Letzte Aktualisierung
-
15.08.2025, 07:23 MESZ
Datenpartner
Dieses Objekt wird bereitgestellt von:
Deutsche Nationalbibliothek. Bei Fragen zum Objekt wenden Sie sich bitte an den Datenpartner.
Deutsche Nationalbibliothek. Bei Fragen zum Objekt wenden Sie sich bitte an den Datenpartner.
Beteiligte
- Li, Evan
- Cheung, Hoi Ching (Zoey)
- Ma, Shuangge
- SpringerLink (Online service)
Ähnliche Objekte (12)
Porcine pancreatic ductal epithelial cells transformed with KRASG12D and SV40T are tumorigenic
Cancer-associated fibroblasts in pancreatic ductal adenocarcinoma
Cancer-associated fibroblasts require proline synthesis by PYCR1 for the deposition of pro-tumorigenic extracellular matrix
Presence of periodontitis may synergistically contribute to cancer progression via Treg and IL-6
Targeting Super‐Enhancers via Nanoparticle‐Facilitated BRD4 and CDK7 Inhibitors Synergistically Suppresses Pancreatic Ductal Adenocarcinoma
Increased peri-ductal collagen micro-organization may contribute to raised mammographic density
Concurrent inhibition of pBADS99 synergistically improves MEK inhibitor efficacy in KRASG12D-mutant pancreatic ductal adenocarcinoma
GLUT5-overexpression-related tumorigenic implications
Author Correction: Cancer-associated fibroblasts require proline synthesis by PYCR1 for the deposition of pro-tumorigenic extracellular matrix
CAFs Homologous Biomimetic Liposome Bearing BET Inhibitor and Pirfenidone Synergistically Promoting Antitumor Efficacy in Pancreatic Ductal Adenocarcinoma
Fibroblast activation protein-α-expressing fibroblasts promote the progression of pancreatic ductal adenocarcinoma
Hypoxic regulation of glyceraldehyde-3-phosphate dehydrogenase in HPV-positive non-tumorigenic and tumorigenic cells
Porcine pancreatic ductal epithelial cells transformed with KRASG12D and SV40T are tumorigenic
Cancer-associated fibroblasts in pancreatic ductal adenocarcinoma
Cancer-associated fibroblasts require proline synthesis by PYCR1 for the deposition of pro-tumorigenic extracellular matrix
Presence of periodontitis may synergistically contribute to cancer progression via Treg and IL-6
Targeting Super‐Enhancers via Nanoparticle‐Facilitated BRD4 and CDK7 Inhibitors Synergistically Suppresses Pancreatic Ductal Adenocarcinoma
Increased peri-ductal collagen micro-organization may contribute to raised mammographic density
Concurrent inhibition of pBADS99 synergistically improves MEK inhibitor efficacy in KRASG12D-mutant pancreatic ductal adenocarcinoma
GLUT5-overexpression-related tumorigenic implications
Author Correction: Cancer-associated fibroblasts require proline synthesis by PYCR1 for the deposition of pro-tumorigenic extracellular matrix
CAFs Homologous Biomimetic Liposome Bearing BET Inhibitor and Pirfenidone Synergistically Promoting Antitumor Efficacy in Pancreatic Ductal Adenocarcinoma
Fibroblast activation protein-α-expressing fibroblasts promote the progression of pancreatic ductal adenocarcinoma
Hypoxic regulation of glyceraldehyde-3-phosphate dehydrogenase in HPV-positive non-tumorigenic and tumorigenic cells
Porcine pancreatic ductal epithelial cells transformed with KRASG12D and SV40T are tumorigenic
Cancer-associated fibroblasts in pancreatic ductal adenocarcinoma
Cancer-associated fibroblasts require proline synthesis by PYCR1 for the deposition of pro-tumorigenic extracellular matrix
Presence of periodontitis may synergistically contribute to cancer progression via Treg and IL-6
Targeting Super‐Enhancers via Nanoparticle‐Facilitated BRD4 and CDK7 Inhibitors Synergistically Suppresses Pancreatic Ductal Adenocarcinoma
Increased peri-ductal collagen micro-organization may contribute to raised mammographic density
Concurrent inhibition of pBADS99 synergistically improves MEK inhibitor efficacy in KRASG12D-mutant pancreatic ductal adenocarcinoma
GLUT5-overexpression-related tumorigenic implications
Author Correction: Cancer-associated fibroblasts require proline synthesis by PYCR1 for the deposition of pro-tumorigenic extracellular matrix
CAFs Homologous Biomimetic Liposome Bearing BET Inhibitor and Pirfenidone Synergistically Promoting Antitumor Efficacy in Pancreatic Ductal Adenocarcinoma
Fibroblast activation protein-α-expressing fibroblasts promote the progression of pancreatic ductal adenocarcinoma