Littérature scientifique sur le sujet « Cancer stem cells, pancreatic ductal adenocarcinoma, tumor microenvironment, extracellular matrix »
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Articles de revues sur le sujet "Cancer stem cells, pancreatic ductal adenocarcinoma, tumor microenvironment, extracellular matrix"
Truong, Linh-Huyen, et Siim Pauklin. « Pancreatic Cancer Microenvironment and Cellular Composition : Current Understandings and Therapeutic Approaches ». Cancers 13, no 19 (8 octobre 2021) : 5028. http://dx.doi.org/10.3390/cancers13195028.
Texte intégralWang, Dan, Yuqiang Li, Heming Ge, Tarik Ghadban, Matthias Reeh et Cenap Güngör. « The Extracellular Matrix : A Key Accomplice of Cancer Stem Cell Migration, Metastasis Formation, and Drug Resistance in PDAC ». Cancers 14, no 16 (18 août 2022) : 3998. http://dx.doi.org/10.3390/cancers14163998.
Texte intégralWiedmann, Lena, Francesca De Angelis Rigotti, Nuria Vaquero-Siguero, Elisa Donato, Elisa Espinet, Andreas Trumpp, Andreas Fischer et Juan Rodriguez-Vita. « Abstract 960 : HAPLN1 increases peritoneal carcinomatosis by inducing tumor cell hyperplasticity ». Cancer Research 82, no 12_Supplement (15 juin 2022) : 960. http://dx.doi.org/10.1158/1538-7445.am2022-960.
Texte intégralSun, Hongzhi, Bo Zhang et Haijun Li. « The Roles of Frequently Mutated Genes of Pancreatic Cancer in Regulation of Tumor Microenvironment ». Technology in Cancer Research & ; Treatment 19 (1 janvier 2020) : 153303382092096. http://dx.doi.org/10.1177/1533033820920969.
Texte intégralSperb, Nadine, Miltiadis Tsesmelis et Thomas Wirth. « Crosstalk between Tumor and Stromal Cells in Pancreatic Ductal Adenocarcinoma ». International Journal of Molecular Sciences 21, no 15 (31 juillet 2020) : 5486. http://dx.doi.org/10.3390/ijms21155486.
Texte intégralSeifert, Adrian M., Julian List, Max Heiduk, Rahel Decker, Janusz von Renesse, Ann-Christin Meinecke, Daniela E. Aust, Thilo Welsch, Jürgen Weitz et Lena Seifert. « Gamma-delta T cells stimulate IL-6 production by pancreatic stellate cells in pancreatic ductal adenocarcinoma ». Journal of Cancer Research and Clinical Oncology 146, no 12 (31 août 2020) : 3233–40. http://dx.doi.org/10.1007/s00432-020-03367-8.
Texte intégralAwaji, Mohammad, et Rakesh Singh. « Cancer-Associated Fibroblasts’ Functional Heterogeneity in Pancreatic Ductal Adenocarcinoma ». Cancers 11, no 3 (1 mars 2019) : 290. http://dx.doi.org/10.3390/cancers11030290.
Texte intégralVaish, Utpreksha, Tejeshwar Jain, Abhi C. Are et Vikas Dudeja. « Cancer-Associated Fibroblasts in Pancreatic Ductal Adenocarcinoma : An Update on Heterogeneity and Therapeutic Targeting ». International Journal of Molecular Sciences 22, no 24 (14 décembre 2021) : 13408. http://dx.doi.org/10.3390/ijms222413408.
Texte intégralYamamoto, Keisuke, Dosuke Iwadate, Hiroyuki Kato, Yousuke Nakai, Keisuke Tateishi et Mitsuhiro Fujishiro. « Targeting the Metabolic Rewiring in Pancreatic Cancer and Its Tumor Microenvironment ». Cancers 14, no 18 (7 septembre 2022) : 4351. http://dx.doi.org/10.3390/cancers14184351.
Texte intégralPadinharayil, Hafiza, Vikrant Rai et Alex George. « Mitochondrial Metabolism in Pancreatic Ductal Adenocarcinoma : From Mechanism-Based Perspectives to Therapy ». Cancers 15, no 4 (8 février 2023) : 1070. http://dx.doi.org/10.3390/cancers15041070.
Texte intégralThèses sur le sujet "Cancer stem cells, pancreatic ductal adenocarcinoma, tumor microenvironment, extracellular matrix"
Biondani, Giulia. « Pancreatic cancer stem cell characterization and study of the microenvironment impact on their biological features ». Doctoral thesis, 2016. http://hdl.handle.net/11562/939505.
Texte intégralIt has been reported that cancer stem cells (CSCs) are responsible for tumor initiation, metastasis, chemoresistance, and relapse. Furthermore, the tumor microenvironment of pancreatic ductal adenocarcinoma (PDAC) is rich of extracellular matrix (ECM), which supports tumor growth and chemotherapy resistance. The aim of this thesis was to obtain and characterize CSCs derived from PDAC established cell lines. PDAC CSCs were generally more resistant to the action of five anti-cancer drugs than parental cell lines and were characterized by an increased expression of the stem cell markers EpCAM and CD44v6, and a decreased expression of the epithelial state marker E-cadherin. Furthermore, PDAC CSCs were more tumorigenic and possessed a higher metastatic activity than parental cells when injected into nude mice. When cultured on the top of several matrices, CSCs and the parental cells acquired a different morphology. In particular, only CSCs developed tube-like structures in the presence of Matrigel, and showed an increased expression of the endothelial cell markers CD34, CD31, and CD144, and of the pro-angiogenic factors IGFBP1 and eNOS. Furthermore, PDAC CSCs demonstrated a higher angiogenic profile with respect to the parental cells, as demonstrated by the secretion of several pro-angiogenic factors. When injected into nude mice, PDAC CSCs gave rise to tumors with a more intense vascular network with vessels with larger caliper than the tumors generated by parental cells. Additionally, when directly co-cultured with microenvironment bone marrow-mesenchymal stem cells (BM-MSCs), PDAC cells showed a decreased expression of the stem cell markers EpCAM and CD24. Taken together these results demonstrate that CSCs derived from PDAC cell lines possess all the characteristics of the clinically relevant tumor, rendering them a model to deeply understand PDAC biology. Three-dimensional cell culture models are of crucial relevance to study the role of the microenvironment on tumor biology and of the capability of PDAC CSCs for the sprouting of new vessels at the initial phases of tumor development. Finally, BM-MSCs may play a role in the regulation of PDAC cellular differentiation.