scholarly journals Role of lymphangiogenesis and lymphangiogenic factors during pancreatic cancer progression and lymphatic spread

2006 ◽  
Author(s):  
Martin Schneider ◽  
Peter Büchler ◽  
Nathalia Giese ◽  
Thomas Giese ◽  
Jörg Wilting ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Cancer Progression ◽  
Lymphatic Spread

scholarly journals Abstract 2679: Role of TH2 cells in pancreatic cancer progression

2021 ◽  
Author(s):  
Aftab Alam ◽  
Maulasri Bhatta ◽  
Parker Denz ◽  
Eric Levanduski ◽  
Prasenjit Dey
Keyword(s):  
Pancreatic Cancer ◽  
Cancer Progression ◽  
Th2 Cells

Role of the immune system in pancreatic cancer progression and immune modulating treatment strategies

2014 ◽  
Vol 40 (4) ◽  
pp. 513-522 ◽  
Author(s):  
K. Sideras ◽  
H. Braat ◽  
J. Kwekkeboom ◽  
C.H. van Eijck ◽  
M.P. Peppelenbosch ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Immune System ◽  
Cancer Progression ◽  
Treatment Strategies

scholarly journals Advances in Tumor-Stroma Interactions: Emerging Role of Cytokine Network in Colorectal and Pancreatic Cancer

2019 ◽  
Vol 2019 ◽  
pp. 1-12 ◽  
Author(s):  
Chiara Bazzichetto ◽  
Fabiana Conciatori ◽  
Italia Falcone ◽  
Francesco Cognetti ◽  
Michele Milella ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Tumor Progression ◽  
Cancer Progression ◽  
Epidemiological Data ◽  
Tumor Stroma ◽  
Cytokine Network ◽  
Pharmacological Response ◽  
Wide Range ◽  
Clinical Models

Cytokines are a family of soluble factors (Growth Factors (GFs), chemokines, angiogenic factors, and interferons), which regulate a wide range of mechanisms in both physiological and pathological conditions, such as tumor cell growth and progression, angiogenesis, and metastasis. In recent years, the growing interest in developing new cancer targeted therapies has been accompanied by the effort to characterize Tumor Microenvironment (TME) and Tumor-Stroma Interactions (TSI). The connection between tumor and stroma is now well established and, in the last decade, evidence from genetic, pharmacological, and epidemiological data supported the importance of microenvironment in tumor progression. However, several of the mechanisms behind TSI and their implication in tumor progression remain still unclear and it is crucial to establish their potential in determining pharmacological response. Many studies have demonstrated that cytokines network can profoundly affect TME, thus displaying potential therapeutic efficacy in both preclinical and clinical models. The goal of this review is to give an overview of the most relevant cytokines involved in colorectal and pancreatic cancer progression and their implication in drug response.

The Role of Stromal Components in Pancreatic Cancer Progression

2016 ◽  
Vol 16 (9) ◽  
pp. 1117-1124 ◽  
Author(s):  
Mengdan Xu ◽  
Binhua P. Zhou ◽  
Min Tao ◽  
Jingyi Liu ◽  
Wei Li
Keyword(s):  
Pancreatic Cancer ◽  
Cancer Progression

scholarly journals Elucidating the Role of Extracellular Vesicles in Pancreatic Cancer

Cancers ◽  
2021 ◽  
Vol 13 (22) ◽  
pp. 5669
Author(s):  
Akbar Lulu Marzan ◽  
Sarah Elizabeth Stewart
Keyword(s):  
Drug Delivery ◽  
Pancreatic Cancer ◽  
Survival Rate ◽  
Extracellular Vesicles ◽  
Cancer Progression ◽  
Current Knowledge ◽  
Treatment Options ◽  
Metabolic Dysfunction ◽  
Underlying Mechanisms

Pancreatic cancer is one of the deadliest cancers worldwide, with a 5-year survival rate of less than 10%. This dismal survival rate can be attributed to several factors including insufficient diagnostics, rapid metastasis and chemoresistance. To identify new treatment options for improved patient outcomes, it is crucial to investigate the underlying mechanisms that contribute to pancreatic cancer progression. Accumulating evidence suggests that extracellular vesicles, including exosomes and microvesicles, are critical players in pancreatic cancer progression and chemoresistance. In addition, extracellular vesicles also have the potential to serve as promising biomarkers, therapeutic targets and drug delivery tools for the treatment of pancreatic cancer. In this review, we aim to summarise the current knowledge on the role of extracellular vesicles in pancreatic cancer progression, metastasis, immunity, metabolic dysfunction and chemoresistance, and discuss their potential roles as biomarkers for early diagnosis and drug delivery vehicles for treatment of pancreatic cancer.

The role of SPARC expression in pancreatic cancer progression and patient survival

2015 ◽  
Vol 50 (9) ◽  
pp. 1170-1174 ◽  
Author(s):  
Chinmay Gundewar ◽  
Agata Sasor ◽  
Katarzyna Said Hilmersson ◽  
Roland Andersson ◽  
Daniel Ansari
Keyword(s):  
Pancreatic Cancer ◽  
Cancer Progression ◽  
Patient Survival ◽  
Sparc Expression

scholarly journals Role of microenvironmental periostin in pancreatic cancer progression

Oncotarget ◽  
2016 ◽  
Vol 8 (52) ◽  
pp. 89552-89565 ◽  
Author(s):  
Yang Liu ◽  
Fan Li ◽  
Feng Gao ◽  
Lingxi Xing ◽  
Peng Qin ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Cancer Progression

Curcumin Inhibits Pancreatic Cancer Progression via Down-Regulation of miR-21-5p

2020 ◽  
Vol 18 (3) ◽  
pp. 236-240
Author(s):  
Li Junjian ◽  
Xu Qigang ◽  
Tao Chonglin
Keyword(s):  
Pancreatic Cancer ◽  
Cell Proliferation ◽  
B Cell ◽  
Cancer Cells ◽  
Cancer Progression ◽  
Migration And Invasion ◽  
Dependent Manner ◽  
Promote Cell Proliferation ◽  
Pancreatic Cancer Cells

In this study, we investigated the role of curcumin in pancreatic cancer through the regulation of miR-21-5p. We first evaluated the expression of miR-21-5p in pancreatic cancer cells (ASPC-1) treated with different concentrations of curcumin. The results showed that curcumin effectively inhibited the expression of miR-21-5p in ASPC-1 cells in a dose-dependent manner. B cell translocation gene 2 was identified as a target gene of miR-21-5p. MiR-21-5p mimics could promote cell proliferation, migration, and invasion of ASPC-1, as well as decrease the expression of B cell translocation gene 2. Curcumin treatment inhibited cell proliferation, migration and invasion of ASPC-1, as well as increased the expression of B cell translocation gene 2. MiR-21-5p could reverse the inhibitory activities of curcumin on ASPC-1 cell proliferation, migration, and invasion. In conclusion, curcumin is capable of inhibiting the proliferation, migration and invasion of pancreatic cancer cells via down-regulating miR-21-5p-mediated B cell translocation gene 2.

scholarly journals Role of integrin-linked kinase in regulating the protein stability of the MUC1-C oncoprotein in pancreatic cancer cells

Oncogenesis ◽  
2017 ◽  
Vol 6 (7) ◽  
pp. e359-e359 ◽  
Author(s):  
H-L Huang ◽  
H-Y Wu ◽  
P-C Chu ◽  
I-L Lai ◽  
P-H Huang ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Protein Stability ◽  
Cancer Cells ◽  
Cancer Progression ◽  
Ectopic Expression ◽  
Pancreatic Tumors ◽  
Alternative Mechanism ◽  
Pancreatic Cancer Cells ◽  
Integrin Linked Kinase

Abstract MUC1-C overexpression has been associated with the progression of pancreatic tumors by promoting the aggressive and metastatic phenotypes. As MUC1 is a STAT3 target gene, STAT3 plays a major role in regulating MUC1-C expression. In this study, we report an alternative mechanism by which integrin-linked kinase (ILK) post-transcriptionally modulates the expression of MUC1-C by maintaining its protein stability in pancreatic cancer cells. We found that ILK acts in concert with STAT3 to facilitate IL-6-mediated upregulation of MUC1-C; ILK depletion was equally effective as STAT3 depletion in abolishing IL-6-induced MUC1-C overexpression without disturbing the phosphorylation or cellular distribution of STAT3. Conversely, ectopic expression of constitutively active ILK increased MUC1-C expression, though this increase was not noted with kinase-dead ILK. This finding suggests the requirement of the kinase activity of ILK in regulating MUC1-C stability, which was confirmed by using the ILK kinase inhibitor T315. Furthermore, our data suggest the involvement of protein kinase C (PKC)δ in mediating the suppressive effect of ILK inhibition on MUC1-C repression. For example, co-immunoprecipitation analysis indicated that ILK depletion-mediated MUC1-C phosphorylation was accompanied by increased phosphorylation of PKCδ at the activation loop Thr-507 and increased binding of PKCδ to MUC1-C. Conversely, ILK overexpression resulted in decreased PKCδ phosphorylation. From a mechanistic perspective, the present finding, together with our recent report that ILK controls the expression of oncogenic KRAS through a regulatory loop, underscores the pivotal role of ILK in promoting pancreatic cancer progression.

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