scholarly journals Interleukin 1α Sustains the Expression of Inflammatory Factors in Human Pancreatic Cancer Microenvironment by Targeting Cancer-Associated Fibroblasts

Neoplasia ◽  
2011 ◽  
Vol 13 (8) ◽  
pp. 664-IN3 ◽  
Author(s):  
Vegard Tjomsland ◽  
Anna Spångeus ◽  
Johanna Välilä ◽  
Per Sandström ◽  
Kurt Borch ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Human Pancreatic Cancer ◽  
Inflammatory Factors ◽  
Cancer Microenvironment ◽  
Cancer Associated Fibroblasts ◽  
Interleukin 1Α

scholarly journals Nanoparticle-based delivery systems modulate the tumor microenvironment in pancreatic cancer for enhanced therapy

2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Ming Jia ◽  
Dan Zhang ◽  
Chunxiang Zhang ◽  
Chunhong Li
Keyword(s):  
Pancreatic Cancer ◽  
Tumor Microenvironment ◽  
Immune Cells ◽  
Malignant Tumors ◽  
Treatment Strategies ◽  
Delivery Systems ◽  
Cancer Microenvironment ◽  
Cancer Associated Fibroblasts ◽  
Hypoxic Environment ◽  
Promising Therapeutic Approach

AbstractPancreatic cancer is one of the most lethal malignant tumors with a low survival rate, partly because the tumor microenvironment (TME), which consists of extracellular matrix (ECM), cancer-associated fibroblasts (CAFs), immune cells, and vascular systems, prevents effective drug delivery and chemoradiotherapy. Thus, modulating the microenvironment of pancreatic cancer is considered a promising therapeutic approach. Since nanoparticles are one of the most effective cancer treatment strategies, several nano-delivery platforms have been developed to regulate the TME and enhance treatment. Here, we summarize the latest advances in nano-delivery systems that alter the TME in pancreatic cancer by depleting ECM, inhibiting CAFs, reversing immunosuppression, promoting angiogenesis, or improving the hypoxic environment. We also discuss promising new targets for such systems. This review is expected to improve our understanding of how to modulate the pancreatic cancer microenvironment and guide the development of new therapies. Graphical Abstract

Interleukin-1α Enhances Integrin α6β1 Expression and Metastatic Capability of Human Pancreatic Cancer

Oncology ◽  
2003 ◽  
Vol 65 (2) ◽  
pp. 167-173 ◽  
Author(s):  
Hirozumi Sawai ◽  
Hitoshi Funahashi ◽  
Minoru Yamamoto ◽  
Yuji Okada ◽  
Tetsushi Hayakawa ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Human Pancreatic Cancer ◽  
Interleukin 1Α

Alteration of Integrins by Interleukin-1α in Human Pancreatic Cancer Cells

Pancreas ◽  
2001 ◽  
Vol 23 (4) ◽  
pp. 399-405 ◽  
Author(s):  
Hirozumi Sawai ◽  
Minoru Yamamoto ◽  
Yuji Okada ◽  
Mikinori Sato ◽  
Yoshimi Akamo ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Cancer Cells ◽  
Human Pancreatic Cancer ◽  
Pancreatic Cancer Cells ◽  
Interleukin 1Α

scholarly journals Lactate-mediated epigenetic reprogramming regulates formation of human pancreatic cancer-associated fibroblasts

eLife ◽  
2019 ◽  
Vol 8 ◽  
Author(s):  
Tushar D Bhagat ◽  
Dagny Von Ahrens ◽  
Meelad Dawlaty ◽  
Yiyu Zou ◽  
Joelle Baddour ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Cytosine Methylation ◽  
De Novo ◽  
Human Pancreatic Cancer ◽  
Ductal Adenocarcinoma ◽  
Molecular Pathways ◽  
Cancer Associated Fibroblasts ◽  
Neoplastic Cells ◽  
Epigenomic Reprogramming

Even though pancreatic ductal adenocarcinoma (PDAC) is associated with fibrotic stroma, the molecular pathways regulating the formation of cancer associated fibroblasts (CAFs) are not well elucidated. An epigenomic analysis of patient-derived and de-novo generated CAFs demonstrated widespread loss of cytosine methylation that was associated with overexpression of various inflammatory transcripts including CXCR4. Co-culture of neoplastic cells with CAFs led to increased invasiveness that was abrogated by inhibition of CXCR4. Metabolite tracing revealed that lactate produced by neoplastic cells leads to increased production of alpha-ketoglutarate (aKG) within mesenchymal stem cells (MSCs). In turn, aKG mediated activation of the demethylase TET enzyme led to decreased cytosine methylation and increased hydroxymethylation during de novo differentiation of MSCs to CAF. Co-injection of neoplastic cells with TET-deficient MSCs inhibited tumor growth in vivo. Thus, in PDAC, a tumor-mediated lactate flux is associated with widespread epigenomic reprogramming that is seen during CAF formation.

Epigenetic reprogramming of cancer-associated fibroblasts suppresses human pancreatic cancer progression

Pancreatology ◽  
2016 ◽  
Vol 16 (4) ◽  
pp. S63
Author(s):  
Keisuke Yamamoto ◽  
Keisuke Tateishi ◽  
Mayumi Hoshikawa ◽  
Mariko Tanaka ◽  
Koji Miyabayashi ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Cancer Progression ◽  
Epigenetic Reprogramming ◽  
Human Pancreatic Cancer ◽  
Cancer Associated Fibroblasts
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