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Journal articles 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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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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2

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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5

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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10

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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Vaish, Utpreksha, Tejeshwar Jain, Abhi C. Are, and Vikas Dudeja. "Cancer-Associated Fibroblasts in Pancreatic Ductal Adenocarcinoma: An Update on Heterogeneity and Therapeutic Targeting." International Journal of Molecular Sciences 22, no. 24 (2021): 13408. http://dx.doi.org/10.3390/ijms222413408.

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Pancreatic ductal adenocarcinoma (PDAC) is a leading cause of cancer-related morbidity and mortality in the western world, with limited therapeutic strategies and dismal long-term survival. Cancer-associated fibroblasts (CAFs) are key components of the pancreatic tumor microenvironment, maintaining the extracellular matrix, while also being involved in intricate crosstalk with cancer cells and infiltrating immunocytes. Therefore, they are potential targets for developing therapeutic strategies against PDAC. However, recent studies have demonstrated significant heterogeneity in CAFs with respec

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Awaji, Mohammad, and Rakesh Singh. "Cancer-Associated Fibroblasts’ Functional Heterogeneity in Pancreatic Ductal Adenocarcinoma." Cancers 11, no. 3 (2019): 290. http://dx.doi.org/10.3390/cancers11030290.

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Pancreatic ductal adenocarcinoma (PDAC) is a leading cause of cancer-related deaths in the USA. Desmoplasia and inflammation are two major hallmarks of PDAC. Desmoplasia, composed of extracellular matrix (ECM), cancer-associated fibroblasts (CAFs), and infiltrating immune and endothelial cells, acts as a biophysical barrier to hinder chemotherapy and actively contributes to tumor progression and metastasis. CAFs represent a multifunctional subset of PDAC microenvironment and contribute to tumor initiation and progression through ECM deposition and remodeling, as well as the secretion of paracr

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13

Chu, Xiangyu, Yinmo Yang, and Xiaodong Tian. "Crosstalk between Pancreatic Cancer Cells and Cancer-Associated Fibroblasts in the Tumor Microenvironment Mediated by Exosomal MicroRNAs." International Journal of Molecular Sciences 23, no. 17 (2022): 9512. http://dx.doi.org/10.3390/ijms23179512.

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Pancreatic ductal adenocarcinoma (PDAC) is one of the most malignant digestive tumors, characterized by a low rate of early diagnosis, strong invasiveness, and early metastasis. The abundant stromal cells, dense extracellular matrix, and lack of blood supply in PDAC limit the penetration of chemotherapeutic drugs, resulting in poor efficacy of the current treatment regimens. Cancer-associated fibroblasts (CAFs) are the major stromal cells in the tumor microenvironment. Tumor cells can secrete exosomes to promote the generation of activated CAFs, meanwhile exosomes secreted by CAFs help promote

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Yamamoto, Keisuke, Dosuke Iwadate, Hiroyuki Kato, Yousuke Nakai, Keisuke Tateishi, and Mitsuhiro Fujishiro. "Targeting the Metabolic Rewiring in Pancreatic Cancer and Its Tumor Microenvironment." Cancers 14, no. 18 (2022): 4351. http://dx.doi.org/10.3390/cancers14184351.

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Pancreatic ductal adenocarcinoma (PDAC) is an aggressive malignancy with only a few effective therapeutic options. A characteristic feature of PDAC is its unique tumor microenvironment (TME), termed desmoplasia, which shows extensive fibrosis and extracellular matrix deposition, generating highly hypoxic and nutrient-deprived conditions within the tumor. To thrive in this harsh TME, PDAC undergoes extensive metabolic rewiring that includes the altered use of glucose and glutamine, constitutive activation of autophagy-lysosomal pathways, and nutrient acquisition from host cells in the TME. Nota

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Padinharayil, Hafiza, Vikrant Rai, and Alex George. "Mitochondrial Metabolism in Pancreatic Ductal Adenocarcinoma: From Mechanism-Based Perspectives to Therapy." Cancers 15, no. 4 (2023): 1070. http://dx.doi.org/10.3390/cancers15041070.

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Pancreatic ductal adenocarcinoma (PDAC), the fourteenth most common malignancy, is a major contributor to cancer-related death with the utmost case fatality rate among all malignancies. Functional mitochondria, regardless of their complex ecosystem relative to normal cells, are essential in PDAC progression. Tumor cells’ potential to produce ATP as energy, despite retaining the redox potential optimum, and allocating materials for biosynthetic activities that are crucial for cell growth, survival, and proliferation, are assisted by mitochondria. The polyclonal tumor cells with different metabo

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Chang, Chun-Yi, and Chien-Chi Lin. "Hydrogel Models with Stiffness Gradients for Interrogating Pancreatic Cancer Cell Fate." Bioengineering 8, no. 3 (2021): 37. http://dx.doi.org/10.3390/bioengineering8030037.

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Pancreatic ductal adenocarcinoma (PDAC) is the most common type of pancreatic cancer and has seen only modest improvements in patient survival rate over the past few decades. PDAC is highly aggressive and resistant to chemotherapy, owing to the presence of a dense and hypovascularized fibrotic tissue, which is composed of stromal cells and extracellular matrices. Increase deposition and crosslinking of matrices by stromal cells lead to a heterogeneous microenvironment that aids in PDAC development. In the past decade, various hydrogel-based, in vitro tumor models have been developed to mimic a

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Geismann, Schäfer, Gundlach та ін. "NF-κB Dependent Chemokine Signaling in Pancreatic Cancer". Cancers 11, № 10 (2019): 1445. http://dx.doi.org/10.3390/cancers11101445.

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Pancreatic cancer is one of the carcinomas with the worst prognoses, as shown by its five-year survival rate of 9%. Although there have been new therapeutic innovations, the effectiveness of these therapies is still limited, resulting in pancreatic ductal adenocarcinoma (PDAC) becoming the second leading cause of cancer-related death in 2020 in the US. In addition to tumor cell intrinsic resistance mechanisms, this disease exhibits a complex stroma consisting of fibroblasts, immune cells, neuronal and vascular cells, along with extracellular matrix, all conferring therapeutic resistance by sev

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18

Huang, Huocong, and Rolf A. Brekken. "Recent advances in understanding cancer-associated fibroblasts in pancreatic cancer." American Journal of Physiology-Cell Physiology 319, no. 2 (2020): C233—C243. http://dx.doi.org/10.1152/ajpcell.00079.2020.

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Pancreatic ductal adenocarcinoma (PDA) is a devastating disease with a poor survival rate. It is resistant to therapy in part due to its unique tumor microenvironment, characterized by a desmoplastic reaction resulting in a dense stroma that constitutes a large fraction of the tumor volume. A major contributor to the desmoplastic reaction are cancer-associated fibroblasts (CAFs). CAFs actively interact with cancer cells and promote tumor progression by different mechanisms, including extracellular matrix deposition, remodeling, and secretion of tumor promoting factors, making CAFs an attractiv

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19

Ahmad, Ramiz S., Timothy D. Eubank, Slawomir Lukomski, and Brian A. Boone. "Immune Cell Modulation of the Extracellular Matrix Contributes to the Pathogenesis of Pancreatic Cancer." Biomolecules 11, no. 6 (2021): 901. http://dx.doi.org/10.3390/biom11060901.

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Pancreatic ductal adenocarcinoma (PDAC) is a highly lethal malignancy with a five-year survival rate of only 9%. PDAC is characterized by a dense, fibrotic stroma composed of extracellular matrix (ECM) proteins. This desmoplastic stroma is a hallmark of PDAC, representing a significant physical barrier that is immunosuppressive and obstructs penetration of cytotoxic chemotherapy agents into the tumor microenvironment (TME). Additionally, dense ECM promotes hypoxia, making tumor cells refractive to radiation therapy and alters their metabolism, thereby supporting proliferation and survival. In

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20

Hessmann, Elisabeth, Soeren M. Buchholz, Ihsan Ekin Demir, et al. "Microenvironmental Determinants of Pancreatic Cancer." Physiological Reviews 100, no. 4 (2020): 1707–51. http://dx.doi.org/10.1152/physrev.00042.2019.

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Pancreatic ductal adenocarcinoma (PDAC) belongs to the most lethal solid tumors in humans. A histological hallmark feature of PDAC is the pronounced tumor microenvironment (TME) that dynamically evolves during tumor progression. The TME consists of different non-neoplastic cells such as cancer-associated fibroblasts, immune cells, endothelial cells, and neurons. Furthermore, abundant extracellular matrix components such as collagen and hyaluronic acid as well as matricellular proteins create a highly dynamic and hypovascular TME with multiple biochemical and physical interactions among the var

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Olaoba, Olamide T., Ming Yang, Temitope I. Adelusi, et al. "Targeted Therapy for Highly Desmoplastic and Immunosuppressive Tumor Microenvironment of Pancreatic Ductal Adenocarcinoma." Cancers 16, no. 8 (2024): 1470. http://dx.doi.org/10.3390/cancers16081470.

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Pancreatic ductal adenocarcinoma (PDAC) is a highly lethal malignancy with a very poor prognosis. Despite advancements in treatment strategies, PDAC remains recalcitrant to therapies because patients are often diagnosed at an advanced stage. The advanced stage of PDAC is characterized by metastasis, which typically renders it unresectable by surgery or untreatable by chemotherapy. The tumor microenvironment (TME) of PDAC comprises highly proliferative myofibroblast-like cells and hosts the intense deposition of a extracellular matrix component that forms dense fibrous connective tissue, a proc

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Song, Xiaoyu, Yuma Nihashi, Yukiko Imai, et al. "Collagen Lattice Model, Populated with Heterogeneous Cancer-Associated Fibroblasts, Facilitates Advanced Reconstruction of Pancreatic Cancer Microenvironment." International Journal of Molecular Sciences 25, no. 7 (2024): 3740. http://dx.doi.org/10.3390/ijms25073740.

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Pancreatic ductal adenocarcinoma (PDAC) is a solid-tumor malignancy. To enhance the treatment landscape of PDAC, a 3D model optimized for rigorous drug screening is essential. Within the PDAC tumor microenvironment, a dense stroma comprising a large extracellular matrix and cancer-associated fibroblasts (CAFs) is well-known for its vital role in modulating tumor growth, cellular heterogeneity, bidirectional paracrine signaling, and chemoresistance. In this study, we employed a fibroblast-populated collagen lattice (FPCL) modeling approach that has the ability to replicate fibroblast contractil

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Al-Musawi, Fatimah, and Chang-il Hwang. "Abstract 1580: Investigating the tumor microenvironment of pancreatic ductal adenocarcinoma with BRCA2 mutation." Cancer Research 84, no. 6_Supplement (2024): 1580. http://dx.doi.org/10.1158/1538-7445.am2024-1580.

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Abstract Pancreatic ductal adenocarcinoma (PDAC) is one of the most aggressive and deadliest cancers with a survival rate of less than 12% at 5 years. It is estimated that around 14% of human PDAC contain mutations in genes involved in DNA Damage Repair (DDR), including BRCA1/2, ATM, and others. Additionally, PDAC has an extensive network of extracellular matrix components surrounding the tumor in the stroma, such as cancer-associated fibroblasts, which promote cancer cell growth. The interactions of the tumor with its tumor microenvironment and stroma can bring vulnerabilities that could be t

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Bansal, Sakshi, Anjali Aggarwal, Vinit Sharma, et al. "Abstract 3447: Neutrophil extracellular traps drive the tumorigenic potential in pancreatic ductal adenocarcinoma." Cancer Research 85, no. 8_Supplement_1 (2025): 3447. https://doi.org/10.1158/1538-7445.am2025-3447.

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Abstract Background: Tumor-infiltrating neutrophils (TINs) have been observed to be linked with poor prognosis in patients with pancreatic ductal adenocarcinoma (PDAC). In the inflammation and oxidative stress-rich tumor microenvironment, neutrophils are likely to undergo neutrophil extracellular traps (NETs) formation which have unique capability of shielding the tumor cells from anti-tumor immune response and facilitate tumor progression. However, the extent of NET infiltration in PDAC and the specific mechanisms by which NETs contribute to tumorigenesis remain unclear. This study aims to in

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Han, Xu, Michelle Burrows, Laura Kim, et al. "Abstract B051: Investigating lipid homeostasis in pancreatic ductal adenocarcinoma under tumor-like stress." Cancer Research 84, no. 2_Supplement (2024): B051. http://dx.doi.org/10.1158/1538-7445.panca2023-b051.

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Abstract Pancreatic ductal adenocarcinoma (PDAC) is a highly aggressive malignancy with a 5-year survival rate of only 10%. One hallmark of PDAC’s tumor microenvironment is dense desmoplasia, due to abnormal accumulation of extracellular matrix and proliferative fibroblasts. During tumorigenesis, pancreatic stellate cells (PSCs) obtain myofibroblast-like signatures and contribute to the fibrotic environment of PDAC. Desmoplasia-induced hypovascularity severely limits oxygen and nutrient delivery. Our laboratory revealed that hypoxia is prominent even at the pancreatic intraepithelial neoplasia

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Xiao, Weikun, Chae-Young Eun, Xinyu Zhang, et al. "Abstract 1567: Increased extracellular matrix stiffness induces hypersecretion of chemoresistance-promoting cancer associated fibroblast-derived exosomes in pancreatic cancer." Cancer Research 82, no. 12_Supplement (2022): 1567. http://dx.doi.org/10.1158/1538-7445.am2022-1567.

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Abstract Pancreatic ductal adenocarcinoma (PDAC) is one of the most lethal types of cancer with few effective treatments. Despite recent advances in in other cancers, the five-year survival rate of PDAC is still only 10%, with most patients succumbing to their disease within the first year. One of the main factors responsible for this poor outcome is the development of chemoresistance in nearly all clinical cases. While the intrinsic factors that facilitate chemoresistance in the tumor cells have been studied extensively, fewer studies have elucidated how the complex and unique microenvironmen

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Kannabran, Sanchitha, Akshaya Ajan, Leanne Lui, and Zaden Yet. "Decoding the Interplay: Exploring Immunotherapy Resistance in the Tumor Microenvironment." Berkeley Pharma Tech Journal of Medicine 4, no. 1 (2024): 113–42. http://dx.doi.org/10.52243/bptjm.v4i1.64.

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The tumor microenvironment (TME) surrounds the tumor and includes blood vessels, immune cells, fibroblasts, signaling molecules, and the extracellular matrix. This review examines the cellular components and pathways within the TME, highlighting their potential as targets for immunotherapy. It also covers recent advances from the past several years in TME, immunotherapy, and combination therapy. The review emphasizes the role of CD8+ T cells in the TME and their relevance to immunotherapy. It discusses various T cell-targeted treatments, including PD-1/PDL1, CTLA-4, VEGF, Interferon-ɣ, LAG-3,

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Waldron, Richard T., Aurelia Lugea, Hui-Hua Chang, et al. "Upregulated Matrisomal Proteins and Extracellular Matrix Mechanosignaling Underlie Obesity-Associated Promotion of Pancreatic Ductal Adenocarcinoma." Cancers 16, no. 8 (2024): 1593. http://dx.doi.org/10.3390/cancers16081593.

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Diet-induced obesity (DIO) promotes pancreatic ductal adenocarcinoma (PDAC) in mice expressing KRasG12D in the pancreas (KC mice), but the precise mechanisms remain unclear. Here, we performed multiplex quantitative proteomic and phosphoproteomic analysis by liquid chromatography–tandem mass spectrometry and further bioinformatic and spatial analysis of pancreas tissues from control-fed versus DIO KC mice after 3, 6, and 9 months. Normal pancreatic parenchyma and associated proteins were steadily eliminated and the novel proteins, phosphoproteins, and signaling pathways associated with PDAC tu

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Modica, Chiara, Martina Olivero, Francesca Zuppini, Melissa Milan, Cristina Basilico, and Elisa Vigna. "HGF/MET Axis Induces Tumor Secretion of Tenascin-C and Promotes Stromal Rewiring in Pancreatic Cancer." Cancers 13, no. 14 (2021): 3519. http://dx.doi.org/10.3390/cancers13143519.

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Pancreatic ductal adenocarcinoma is an aggressive tumor characterized by the presence of an abundant stromal compartment contributing significantly to the malignant phenotype. Pancreatic stellate cells are peculiar fibroblasts present in the stroma and represent the predominant source of extracellular matrix proteins, pro-inflammatory cytokines, and growth factors, including hepatocyte growth factor (HGF). Exploiting a co-culture system of human pancreatic stellate cells and cancer cells, we demonstrated that fibroblast activation was reduced upon HGF/MET axis inhibition. To unveil the signali

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Finan, Jennifer M., Julie Saugstad, and Jonathan Brody. "Abstract 2495: Investigating pancreatic cancer-derived extracellular vesicle signaling in the tumor microenvironment." Cancer Research 83, no. 7_Supplement (2023): 2495. http://dx.doi.org/10.1158/1538-7445.am2023-2495.

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Abstract In many solid tumors, including pancreatic ductal adenocarcinoma (PDAC), the secretion of extracellular vesicles (EVs) has been shown to support tumor progression, chemotherapeutic resistance, and metastasis. Importantly, PDAC tumors are composed of up to 80% non-tumor cells and an extracellular matrix, yet no studies have been performed to determine whether PDAC EVs are imported preferentially by specific non-tumor cell types. To improve our understanding of this signaling, we aim to define the recipient cells of PDAC EVs and evaluate the functional importance of this internalization

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Song, Xiaoyu, Yuma Nihashi, and Yasuyuki S. Kida. "Abstract B061: Development of a pancreatic ductal adenocarcinoma 3D tumor model for high-throughput drug screening." Cancer Research 84, no. 2_Supplement (2024): B061. http://dx.doi.org/10.1158/1538-7445.panca2023-b061.

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Abstract Pancreatic ductal adenocarcinoma (PDAC) is a persistent malignancy that is difficult to diagnose in its early stage and is one of the leading cancer-related deaths worldwide. Currently, limited therapeutic options are available for PDAC, resulting in an extremely low 5-year survival rate. To speed up the discovery of novel therapeutics, a reliable 3D model that highly simulates the PDAC tumor microenvironment is needed for large-scale drug screening. In this study, we propose a novel 3D model for restoring the PDAC tumor microenvironment by targeting cancer-associated fibroblasts (CAF

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Kulkarni, Tanmay, Sreya Banik, Debabrata Mukhopadhyay, Hani Babiker, and Santanu Bhattacharya. "Tumor-Treating Fields Alter Nanomechanical Properties of Pancreatic Ductal Adenocarcinoma Cells Co-Cultured with Extracellular Matrix." Journal of Functional Biomaterials 16, no. 5 (2025): 160. https://doi.org/10.3390/jfb16050160.

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Tumor-Treating Fields (TTFields), a novel therapeutic avenue, is approved for therapy in Glioblastoma multiforme, malignant pleural mesothelioma, and metastatic non-small cell lung cancer (NSCLC). In pancreatic ductal adenocarcinoma (PDAC), several clinical trials are underway to improve outcomes, yet a significant knowledge gap prevails involving the cell-extracellular matrix (ECM) crosstalk. Herein, we hypothesized that treatment with TTFields influence this crosstalk, which is reflected by the dynamic alteration in nanomechanical properties (NMPs) of cells and the ECM in a co-culture system

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Procacci, Patrizia, Claudia Moscheni, Patrizia Sartori, Michele Sommariva, and Nicoletta Gagliano. "Tumor–Stroma Cross-Talk in Human Pancreatic Ductal Adenocarcinoma: A Focus on the Effect of the Extracellular Matrix on Tumor Cell Phenotype and Invasive Potential." Cells 7, no. 10 (2018): 158. http://dx.doi.org/10.3390/cells7100158.

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The extracellular matrix (ECM) in the tumor microenvironment modulates the cancer cell phenotype, especially in pancreatic ductal adenocarcinoma (PDAC), a tumor characterized by an intense desmoplastic reaction. Because the epithelial-to-mesenchymal transition (EMT), a process that provides cancer cells with a metastatic phenotype, plays an important role in PDAC progression, the authors aimed to explore in vitro the interactions between human PDAC cells and ECM components of the PDAC microenvironment, focusing on the expression of EMT markers and matrix metalloproteinases (MMPs) that are able

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Han, Xu, Michelle Burrows, Yanqing Jiang, et al. "Abstract PR024: Investigating lipid homeostasis in pancreatic ductal adenocarcinoma under tumor-like stress." Cancer Research 82, no. 22_Supplement (2022): PR024. http://dx.doi.org/10.1158/1538-7445.panca22-pr024.

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Abstract Pancreatic ductal adenocarcinoma (PDAC) is a highly aggressive malignancy with a 5-year survival rate of only 10%. One hallmark of PDAC’s tumor microenvironment is dense desmoplasia, due to abnormal accumulation of extracellular matrix and proliferative fibroblasts. During tumorigenesis, pancreatic stellate cells (PSCs) obtain myofibroblast-like signatures and contribute to the fibrotic environment of PDAC. Desmoplasia-induced hypovascularity severely limits oxygen and nutrient delivery. Our laboratory revealed that hypoxia is prominent even at the pancreatic intraepithelial neoplasia

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Ganbold, Munkhzul, Pakavarin Louphrasitthiphol, Yoshihiro Miyazaki, Tatsuya Oda, Kenichi Tominaga, and Hiroko Isoda. "Abstract C068: Isorhamnetin restricts cancer-associated fibroblasts (CAFs) phenotypic plasticity, poising them towards tumor-restraining myCAFs: Potential use of isorhamnetin as neoadjuvant in pancreatic ductal adenocarcinoma (PDAC)." Cancer Research 82, no. 22_Supplement (2022): C068. http://dx.doi.org/10.1158/1538-7445.panca22-c068.

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Abstract Pancreatic ductal adenocarcinoma (PDAC) is the deadliest cancer due lack of early diagnosis and inherent refractory to traditional chemo- and even novel immune-therapies. PDAC is marked by its extensive desmoplastic stroma containing extracellular matrix (ECM), vasculature and most importantly cancer-associated fibroblasts (CAFs). CAFs that exist in heterogenous subtypes are responsible for shaping PDAC tumor microenvironment being the main source of: ECM deposition leading up to desmoplasia that hampers the efficacy of various therapeutics, as well as diverse cytokines and growth fac

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Damiani, Verena, Maria Concetta Cufaro, Maurine Fucito, et al. "Proteomics Approach Highlights Early Changes in Human Fibroblasts-Pancreatic Ductal Adenocarcinoma Cells Crosstalk." Cells 11, no. 7 (2022): 1160. http://dx.doi.org/10.3390/cells11071160.

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Pancreatic ductal adenocarcinoma (PDAC) is a leading cause of cancer mortality worldwide. Non-specific symptoms, lack of biomarkers in the early stages, and drug resistance due to the presence of a dense fibrous stroma all contribute to the poor outcome of this disease. The extracellular matrix secreted by activated fibroblasts contributes to the desmoplastic tumor microenvironment formation. Given the importance of fibroblast activation in PDAC pathology, it is critical to recognize the mechanisms involved in the transformation of normal fibroblasts in the early stages of tumorigenesis. To th

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Kittrell, Caroline G., Jade Macdonald, Blake Sells, et al. "Abstract 2581: Establishing a multi-omic spatial ECM proteome and N-glycome of pancreatic ductal adenocarcinoma tissues." Cancer Research 85, no. 8_Supplement_1 (2025): 2581. https://doi.org/10.1158/1538-7445.am2025-2581.

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Abstract Pancreatic Ductal Adenocarcinoma (PDAC), one of the leading causes of cancer related mortality nationwide, is characterized by an extensive desmoplastic stromal reaction and an altered N-glycome. Stromal collagens serve to modulate the immune microenvironment, limit nutrient and oxygen diffusion, influence chemotherapy resistance, and promote tumor progression and metastasis. Dysregulated cancer cell N-glycosylation also promotes immune evasion and neoplastic spread. Despite their important roles in cancer pathogenesis, little is known about the spatial localization and organization o

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Buchholz, Soeren M., Robert G. Goetze, Shiv K. Singh, et al. "Depletion of Macrophages Improves Therapeutic Response to Gemcitabine in Murine Pancreas Cancer." Cancers 12, no. 7 (2020): 1978. http://dx.doi.org/10.3390/cancers12071978.

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Background: The tumor microenvironment (TME) is composed of fibro-inflammatory cells and extracellular matrix (ECM) components. However, the exact contribution of the various TME compartments towards therapeutic response is unknown. Here, we aim to dissect the specific contribution of tumor-associated macrophages (TAMs) towards drug delivery and response in pancreatic ductal adenocarcinoma (PDAC). Methods: The effect of gemcitabine was assessed in human and murine macrophages, human pancreatic stellate cells (hPSCs), and tumor cells (L3.6pl, BxPC3 and KPC) in vitro. The drug metabolism of gemc

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Carvalho, Tiago M. A., Daria Di Molfetta, Maria Raffaella Greco, et al. "Tumor Microenvironment Features and Chemoresistance in Pancreatic Ductal Adenocarcinoma: Insights into Targeting Physicochemical Barriers and Metabolism as Therapeutic Approaches." Cancers 13, no. 23 (2021): 6135. http://dx.doi.org/10.3390/cancers13236135.

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Currently, the median overall survival of PDAC patients rarely exceeds 1 year and has an overall 5-year survival rate of about 9%. These numbers are anticipated to worsen in the future due to the lack of understanding of the factors involved in its strong chemoresistance. Chemotherapy remains the only treatment option for most PDAC patients; however, the available therapeutic strategies are insufficient. The factors involved in chemoresistance include the development of a desmoplastic stroma which reprograms cellular metabolism, and both contribute to an impaired response to therapy. PDAC stro

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Tavares-Valente, Diana, Stefania Cannone, Maria Raffaella Greco, et al. "Extracellular Matrix Collagen I Differentially Regulates the Metabolic Plasticity of Pancreatic Ductal Adenocarcinoma Parenchymal Cell and Cancer Stem Cell." Cancers 15, no. 15 (2023): 3868. http://dx.doi.org/10.3390/cancers15153868.

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Pancreatic ductal adenocarcinoma (PDAC) has a 5-year survival rate of less than 10 percent largely due to the intense fibrotic desmoplastic reaction, characterized by high levels of extracellular matrix (ECM) collagen I that constitutes a niche for a subset of cancer cells, the cancer stem cells (CSCs). Cancer cells undergo a complex metabolic adaptation characterized by changes in metabolic pathways and biosynthetic processes. The use of the 3D organotypic model in this study allowed us to manipulate the ECM constituents and mimic the progression of PDAC from an early tumor to an ever more ad

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Gao, Mei, Charles J. Bailey, Megan M. Harper, et al. "Abstract A029: Identification of tumor microenvironment components in patient-derived pancreatic ductal adenocarcinoma organoids." Cancer Research 82, no. 10_Supplement (2022): A029. http://dx.doi.org/10.1158/1538-7445.evodyn22-a029.

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Abstract Background: Pancreatic ductal adenocarcinoma (PDAC) is highly drug resistant with no change in therapeutic approach for the last decade. The PDAC tumor microenvironment (TME) is highly desmoplastic and associated with altered treatment response. Our group previously identified 9 distinct cell types in human PDAC tumors using single-cell RNA-sequencing, demonstrating a diverse TME. However, the TME of in vitro organoid PDAC models remains underexplored. We initiated characterization of the TME from PDAC patient derived organoids (PDOs) to establish a working model for accurate drug sen

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Pfeifer, Ester, Joy M. Burchell, Francesco Dazzi, Debashis Sarker, and Richard Beatson. "Apoptosis in the Pancreatic Cancer Tumor Microenvironment—The Double-Edged Sword of Cancer-Associated Fibroblasts." Cells 10, no. 7 (2021): 1653. http://dx.doi.org/10.3390/cells10071653.

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Pancreatic ductal adenocarcinoma (PDAC) is associated with poor prognosis. This is attributed to the disease already being advanced at presentation and having a particularly aggressive tumor biology. The PDAC tumor microenvironment (TME) is characterized by a dense desmoplastic stroma, dominated by cancer-associated fibroblasts (CAF), extracellular matrix (ECM) and immune cells displaying immunosuppressive phenotypes. Due to the advanced stage at diagnosis, the depletion of immune effector cells and lack of actionable genomic targets, the standard treatment is still apoptosis-inducing regimens

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Chen, Jiao, Daphne Weihs, and Fred J. Vermolen. "Computational modeling of therapy on pancreatic cancer in its early stages." Biomechanics and Modeling in Mechanobiology 19, no. 2 (2019): 427–44. http://dx.doi.org/10.1007/s10237-019-01219-0.

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Abstract More than eighty percent of pancreatic cancer involves ductal adenocarcinoma with an abundant desmoplastic extracellular matrix surrounding the solid tumor entity. This aberrant tumor microenvironment facilitates a strong resistance of pancreatic cancer to medication. Although various therapeutic strategies have been reported to be effective in mice with pancreatic cancer, they still need to be tested quantitatively in wider animal-based experiments before being applied as therapies. To aid the design of experiments, we develop a cell-based mathematical model to describe cancer progre

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Ngodup, Tenzin, and Ashley Mello. "Abstract B039: Hypoxia promotes an inflammatory phenotype of fibroblasts in pancreatic cancer." Cancer Research 84, no. 2_Supplement (2024): B039. http://dx.doi.org/10.1158/1538-7445.panca2023-b039.

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Abstract Pancreatic ductal adenocarcinoma (PDAC) is notable for its dense desmoplastic stroma, consisting of extracellular matrix, cancer-associated fibroblasts (CAFs), and immune cells. Another notable feature of the PDAC microenvironment is hypoxia, a condition of insufficient oxygen availability. Although hypoxia leads to adaptive responses in both cancer cells and stromal cells, the effects of hypoxia on the PDAC stroma and tumor-stroma interactions are not fully understood. Cancer-associated fibroblasts (CAFs) are a predominant and heterogeneous stromal cell type in PDAC, and single-cell

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Han, Xu, Michelle Burrows, Celeste Simon, Yanqing Jiang, and Brian Keith. "Abstract PO-025: Investigating lipid homeostasis in pancreatic ductal adenocarcinoma under tumor-like stress." Cancer Research 81, no. 22_Supplement (2021): PO—025—PO—025. http://dx.doi.org/10.1158/1538-7445.panca21-po-025.

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Abstract Pancreatic ductal adenocarcinoma (PDAC) is a highly aggressive malignancy with a 5-year survival rate of only 10%. Nearly 95% of PDAC harbor oncogenic KRAS, which has been largely “undruggable” in the past. One hallmark of PDAC tumor microenvironment is dense desmoplasia, as a result of abnormal accumulation of extracellular matrix and proliferative fibroblasts. During tumorigenesis, pancreatic stellate cells (PSCs) become activated to a myofibroblast-like phenotype and contribute to the fibrotic environment of PDAC. Desmoplasia-induced hypovascularity severely limits the delivery of

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Ijichi, Hideaki. "Multiphasic Heterogeneity of Fibroblasts in the Microenvironment of Pancreatic Ductal Adenocarcinoma: Dissection and the Sum of the Dynamics." Cancers 14, no. 19 (2022): 4880. http://dx.doi.org/10.3390/cancers14194880.

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Pancreatic cancer is still the most intractable cancer, with a 5-year survival of around 10%. To conquer the most common type, pancreatic ductal adenocarcinoma (PDAC), we need to understand its pathobiology, especially the tumor microenvironment (TME) that characteristically contains abundant stromal components, with marked fibrosis. In this Special Issue, “Tumor Microenvironment and Pancreatic Cancer,” various aspects of TME were discussed, most frequently including articles related to cancer-associated fibroblasts (CAFs) and the extracellular matrix (ECM). CAFs and ECM have been considered i

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Ngodup, Tenzin, Ashley Mello, and Katelyn Donahue. "Abstract A037: Role of hypoxia in fibroblast reprogramming in pancreatic cancer." Cancer Research 84, no. 17_Supplement_2 (2024): A037. http://dx.doi.org/10.1158/1538-7445.pancreatic24-a037.

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Abstract Pancreatic ductal adenocarcinoma (PDAC) is characterized by a dense desmoplastic stroma, comprised of extracellular matrix, cancer-associated fibroblasts (CAFs), and immune cells. Due to the rapid tumor growth and the unusually low blood vessel density of PDAC, both tumor cells and stromal cells experience hypoxia, or the low availability of oxygen. Although hypoxia is a crucial feature of the tumor milieu and predicts poor clinical outcome, the effects of hypoxia on the PDAC stromal cells, as well as the interplay between tumor and stroma, is not well understood. Cancer-associated fi

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Rabe, Brian, Anna Lyubetskaya, Andrew Kavran, et al. "Abstract B081: In situ multi-modal characterization of pancreatic ductal adenocarcinoma reveals tumor cell identity as a defining factor of the surrounding microenvironment." Cancer Research 84, no. 17_Supplement_2 (2024): B081. http://dx.doi.org/10.1158/1538-7445.pancreatic24-b081.

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Abstract Pancreatic Ductal Adenocarcinoma (PDAC) is heterogeneous with low tumor purity, prominent microenvironment and complex architecture, which preclude identification of shared tumor intrinsic biology within and across patients. We overcame these challenges by applying complementary spatial omics approaches – providing necessary resolution and context – to primary untreated PDAC tumors from 39 patients capturing 341,949 low-bulk and 531,718 single-cell spatial transcriptomes. Of these, 59,403 low-bulk profiles and 205,665 single-cells represented tumor cells. We leveraged this data to bui

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Finan, Jennifer M., Yifei Guo, Kevin MacPherson, et al. "Abstract A037: Unraveling the importance of pancreatic cancer extracellular signaling to endothelial cells within the tumor microenvironment." Cancer Research 84, no. 2_Supplement (2024): A037. http://dx.doi.org/10.1158/1538-7445.panca2023-a037.

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Abstract In many solid tumors, including pancreatic ductal adenocarcinoma (PDAC), the secretion of extracellular vesicles (EVs) has been shown to support tumor progression, chemotherapeutic resistance, and metastasis. Importantly, PDAC tumors are composed of up to 80% non-tumor cells and an extracellular matrix, yet no studies have been performed to determine whether PDAC EVs are preferentially imported by specific cells within the tumor microenvironment. Further, the RNA-binding protein HuR plays an important role in PDAC cells, supporting the stability and translation of transcripts that aid

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Kim, Sumin, Yeongmin Choi, Jihye Baek, et al. "Abstract 1328: Building a 3D co-culture model for metastatic pancreatic ductal cancer using Curiochips microphysiological system." Cancer Research 83, no. 7_Supplement (2023): 1328. http://dx.doi.org/10.1158/1538-7445.am2023-1328.

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Abstract Despite the use of multi-agent conventional chemotherapy regimens, metastatic pancreatic ductal adenocarcinoma (PDAC) remains one of the most lethal solid tumors with a 5-year survival of 9%. PDAC is characterized by a complex tumor microenvironment with multilayered interplay between neoplastic and stromal cells and the natural extracellular matrix (ECM). To date, models that recapitulate the complexity of these features are only partially reproduced ex vivo and lack the capacity to recreate PDAC tumor microenvironment physiology, fluid flow and the ECM architecture. To address these

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