scholarly journals Cancer-associated fibroblasts promote M2 polarization of macrophages in pancreatic ductal adenocarcinoma

2017 ◽  
Vol 6 (2) ◽  
pp. 463-470 ◽  
Author(s):  
Aibin Zhang ◽  
Yigang Qian ◽  
Zhou Ye ◽  
Haiyong Chen ◽  
Haiyang Xie ◽  
...  
2020 ◽  
Vol 34 (7) ◽  
pp. 9405-9418 ◽  
Author(s):  
Mohammad Awaji ◽  
Sugandha Saxena ◽  
Lingyun Wu ◽  
Dipakkumar R. Prajapati ◽  
Abhilasha Purohit ◽  
...  

Cancers ◽  
2019 ◽  
Vol 11 (3) ◽  
pp. 290 ◽  
Author(s):  
Mohammad Awaji ◽  
Rakesh Singh

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 paracrine factors. Attempts to resolve desmoplasia by targeting CAFs can render an adverse outcome, which is likely due to CAFs heterogeneity. Recent reports describe subsets of CAFs that assume more secretory functions, in addition to the typical myofibroblast phenotype. Here, we review the literature and describe the relationship between CAFs and inflammation and the role of the secretory-CAFs in PDAC.


2019 ◽  
Vol 9 (8) ◽  
pp. 1102-1123 ◽  
Author(s):  
Ela Elyada ◽  
Mohan Bolisetty ◽  
Pasquale Laise ◽  
William F. Flynn ◽  
Elise T. Courtois ◽  
...  

2021 ◽  
Vol 22 (24) ◽  
pp. 13408
Author(s):  
Utpreksha Vaish ◽  
Tejeshwar Jain ◽  
Abhi C. Are ◽  
Vikas Dudeja

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 respect to their origins, spatial distribution, and functional phenotypes within the PDAC tumor microenvironment. Therefore, it is imperative to understand and delineate this heterogeneity prior to targeting CAFs for PDAC therapy.


Tumor Biology ◽  
2017 ◽  
Vol 39 (10) ◽  
pp. 101042831771840 ◽  
Author(s):  
Hyunjin Park ◽  
Yangkyu Lee ◽  
Hyejung Lee ◽  
Jin-Won Kim ◽  
Jin-Hyeok Hwang ◽  
...  

Cancers ◽  
2021 ◽  
Vol 13 (4) ◽  
pp. 799 ◽  
Author(s):  
Cédric Leroux ◽  
Georgia Konstantinidou

Cytotoxic chemotherapy remains the only treatment option for most pancreatic ductal adenocarcinoma patients. Currently, the median overall survival of patients with advanced disease rarely exceeds 1 year. The complex network of pancreatic cancer composed of immune cells, endothelial cells, and cancer-associated fibroblasts confers intratumoral and intertumoral heterogeneity with distinct proliferative and metastatic propensity. This heterogeneity can explain why tumors do not behave uniformly and are able to escape therapy. The advance in technology of whole-genome sequencing has now provided the possibility of identifying every somatic mutation, copy-number change, and structural variant in a given cancer, giving rise to personalized targeted therapies. In this review, we provide an overview of the current and emerging treatment strategies in pancreatic cancer. By highlighting new paradigms in pancreatic ductal adenocarcinoma treatment, we hope to stimulate new thoughts for clinical trials aimed at improving patient outcomes.


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