Relevant bibliographies by topics / Cancer stem cells, pancreatic ductal adenocarcinoma, tumor microenvironment, extracellular matrix

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  1. Journal articles
  2. Dissertations / Theses

Academic literature on the topic 'Cancer stem cells, pancreatic ductal adenocarcinoma, tumor microenvironment, extracellular matrix'

Author: Grafiati
Published: 11 March 2023
Last updated: 31 July 2025

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Journal articles on the topic "Cancer stem cells, pancreatic ductal adenocarcinoma, tumor microenvironment, extracellular matrix"

1

Truong, Linh-Huyen, and Siim Pauklin. "Pancreatic Cancer Microenvironment and Cellular Composition: Current Understandings and Therapeutic Approaches." Cancers 13, no. 19 (2021): 5028. http://dx.doi.org/10.3390/cancers13195028.

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Pancreatic ductal adenocarcinoma (PDAC) remains one of the most lethal human solid tumors, despite great efforts in improving therapeutics over the past few decades. In PDAC, the distinct characteristic of the tumor microenvironment (TME) is the main barrier for developing effective treatments. PDAC TME is characterized by a dense stroma, cancer-associated fibroblasts, and immune cells populations that crosstalk to the subpopulations of neoplastic cells that include cancer stem cells (CSCs). The heterogeneity in TME is also exhibited in the diversity and dynamics of acellular components, inclu
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Allgoewer, Chantal, Markus Breunig, Meike Hohwieler, Medhanie Mulaw, and Alexander Kleger. "Abstract C010: Single-cell profiling unleashes KRAS-driven redrafting of the tumor microenvironment before cancer onset." Cancer Research 84, no. 17_Supplement_2 (2024): C010. http://dx.doi.org/10.1158/1538-7445.pancreatic24-c010.

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Abstract Pancreatic cancer is a highly lethal and aggressive disease, commonly characterized by a unique tumor microenvironment, where mutant KRAS signaling plays a pivotal role in its pathophysiology. To deepen our understanding of KRAS-dependent signaling in earliest tumor development, oncogenic KRAS (KRASG12D) expression was induced in human stem cell-derived pancreatic ductal-like organoids (PDLOs), followed by time-resolved single-cell RNA and bulk ATAC sequencing. This unique precancerous state model facilitated a comprehensive characterization of early oncogenic events at cellular resol
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Parvaneh, Shahram, Vanda Miklós, Zoltán Gábor Páhi, et al. "Chemoresistance in Pancreatic Cancer: The Role of Adipose-Derived Mesenchymal Stem Cells and Key Resistance Genes." International Journal of Molecular Sciences 26, no. 1 (2025): 390. https://doi.org/10.3390/ijms26010390.

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Drug resistance is a significant challenge in pancreatic ductal adenocarcinoma (PDAC), where stromal elements such as adipose-derived mesenchymal stem cells (ASCs) contribute to a chemoresistant tumor microenvironment (TME). This study explored the effects of oxaliplatin (OXP) and 5-fluorouracil (5-FU) on PDAC cells (Capan-1) and ASCs to investigate the mechanisms of chemoresistance. While OXP and 5-FU reduced Capan-1 viability in a dose- and time-dependent manner, ASCs demonstrated high resistance, maintaining > 90% viability even at cytotoxic doses. Transcriptomic analyses revealed OXP-in
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Han, Bo, Zhi Yang, Shuqing Zhao, et al. "Abstract 1234: Mechanical control of cancer-associated adipocyte plasticity orchestrates pancreatic cancer progression." Cancer Research 85, no. 8_Supplement_1 (2025): 1234. https://doi.org/10.1158/1538-7445.am2025-1234.

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Abstract Cancer-associated adipocytes (CAAs) are key components of the pancreatic tumor microenvironment, yet how their phenotype and function are regulated by environmental conditions remains poorly understood. Here, we demonstrate that oxygen tension and matrix stiffness dramatically alter CAA behavior and their subsequent effects on pancreatic ductal adenocarcinoma (PDAC) progression. Under normoxic conditions and soft matrix, CAAs exhibit an activated phenotype characterized by extended podia formation and enhanced secretion of matrix-degrading enzymes, particularly MMP-2 and MMP-9, leadin
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Wang, Dan, Yuqiang Li, Heming Ge, Tarik Ghadban, Matthias Reeh, and Cenap Güngör. "The Extracellular Matrix: A Key Accomplice of Cancer Stem Cell Migration, Metastasis Formation, and Drug Resistance in PDAC." Cancers 14, no. 16 (2022): 3998. http://dx.doi.org/10.3390/cancers14163998.

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Pancreatic ductal adenocarcinoma (PDAC) is rich in dense fibrotic stroma that are composed of extracellular matrix (ECM) proteins. A disruption of the balance between ECM synthesis and secretion and the altered expression of matrix remodeling enzymes lead to abnormal ECM dynamics in PDAC. This pathological ECM promotes cancer growth, survival, invasion, and alters the behavior of fibroblasts and immune cells leading to metastasis formation and chemotherapy resistance, which contribute to the high lethality of PDAC. Additionally, recent evidence highlights that ECM, as a major structural compon
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Wiedmann, Lena, Francesca De Angelis Rigotti, Nuria Vaquero-Siguero, et al. "Abstract 960: HAPLN1 increases peritoneal carcinomatosis by inducing tumor cell hyperplasticity." Cancer Research 82, no. 12_Supplement (2022): 960. http://dx.doi.org/10.1158/1538-7445.am2022-960.

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Abstract Pancreatic Ductal Adenocarcinoma (PDAC) frequently metastasizes into the peritoneum forming peritoneal carcinomatosis, which are so far not treatable effectively. Metastasis-initiating cells need to acquire beneficial traits including cell plasticity, immune evasion, dormancy state control and organ colonization. These characteristics can be summarized in broad terms into two main processes, epithelial-to-mesenchymal transition (EMT) and stemness. Hyaluronic acid (HA), an extracellular matrix component, is a crucial factor in regulating these processes in PDAC, but it is so far not su
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Sun, Hongzhi, Bo Zhang, and Haijun Li. "The Roles of Frequently Mutated Genes of Pancreatic Cancer in Regulation of Tumor Microenvironment." Technology in Cancer Research & Treatment 19 (January 1, 2020): 153303382092096. http://dx.doi.org/10.1177/1533033820920969.

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Pancreatic ductal adenocarcinoma has extremely high malignancy and patients with pancreatic ductal adenocarcinoma have dismal prognosis. The failure of pancreatic ductal adenocarcinoma treatment is largely due to the tumor microenvironment, which is featured by ample stromal cells and complicated extracellular matrix. Recent genomic analysis revealed that pancreatic ductal adenocarcinoma harbors frequently mutated genes including KRAS, TP53, CDKN2A, and SMAD4, which can widely alter cellular processes and behaviors. As shown by accumulating studies, these mutant genes may also change tumor mic
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8

Pratticò, Fabiana, and Ingrid Garajová. "Focus on Pancreatic Cancer Microenvironment." Current Oncology 31, no. 8 (2024): 4241–60. http://dx.doi.org/10.3390/curroncol31080316.

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Pancreatic ductal adenocarcinoma remains one of the most lethal solid tumors due to its local aggressiveness and metastatic potential, with a 5-year survival rate of only 13%. A robust connection between pancreatic cancer microenvironment and tumor progression exists, as well as resistance to current anticancer treatments. Pancreatic cancer has a complex tumor microenvironment, characterized by an intricate crosstalk between cancer cells, cancer-associated fibroblasts and immune cells. The complex composition of the tumor microenvironment is also reflected in the diversity of its acellular com
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9

Sperb, Nadine, Miltiadis Tsesmelis, and Thomas Wirth. "Crosstalk between Tumor and Stromal Cells in Pancreatic Ductal Adenocarcinoma." International Journal of Molecular Sciences 21, no. 15 (2020): 5486. http://dx.doi.org/10.3390/ijms21155486.

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Pancreatic ductal adenocarcinoma (PDAC) remains a lethal cancer. The poor prognosis calls for a more detailed understanding of disease biology in order to pave the way for the development of effective therapies. Typically, the pancreatic tumor is composed of a minority of malignant cells within an excessive tumor microenvironment (TME) consisting of extracellular matrix (ECM), fibroblasts, immune cells, and endothelial cells. Research conducted in recent years has particularly focused on cancer-associated fibroblasts (CAFs) which represent the most prominent cellular component of the desmoplas
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Seifert, Adrian M., Julian List, Max Heiduk, et al. "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 (2020): 3233–40. http://dx.doi.org/10.1007/s00432-020-03367-8.

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Abstract Introduction The immunosuppressive tumor microenvironment promotes progression of pancreatic ductal adenocarcinoma (PDAC). γδ T cells infiltrate the pancreatic tumor stroma and support tumorigenesis through αβ T cell inhibition. Pancreatic stellate cell (PSC) activation contributes to pancreatic fibrosis in PDAC, limiting the delivery and efficacy of therapeutic agents. Whether γδ T cells have direct effects on PSC activation is unknown. Methods In this study, we analyzed tumor tissue from 68 patients with PDAC and determined the frequency and location of γδ T cells using immunohistoc
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Dissertations / Theses on the topic "Cancer stem cells, pancreatic ductal adenocarcinoma, tumor microenvironment, extracellular matrix"

1

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.

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E’ stato dimostrato che le cellule staminali tumorali (cancer stem cells, CSC) sono responsabili dello sviluppo neoplastico, della formazione delle metastasi, della resistenza al trattamento con chemioterapici e dello sviluppo di recidive. Inoltre, il microambiente tumorale dell’adenocarcinoma pancreatico duttale (pancreatic ductal adenocarcinoma, PDAC) è ricco di matrice extracellulare, la quale promuove la crescita tumorale e la resistenza alle terapie. Lo scopo di questa tesi è stato l’ottenimento e la successiva caratterizzazione di CSC da linee cellulari di PDAC. Le CSC di PDAC si sono ri
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