Nerve Growth Factor and Artemin Are Paracrine Mediators of Pancreatic Neuropathy in Pancreatic Adenocarcinoma

@article{Ceyhan2010NerveGF,
  title={Nerve Growth Factor and Artemin Are Paracrine Mediators of Pancreatic Neuropathy in Pancreatic Adenocarcinoma},
  author={G{\"u}ralp O Ceyhan and Karl‐Herbert Sch{\"a}fer and Annika G Kerscher and Ulrich Rauch and Ihsan Ekin Demir and Mustafa Kadihasanoglu and Carolin B{\"o}hm and Michael W. M{\"u}ller and Markus W. B{\"u}chler and Nathalia A. Giese and Mert Erkan and Helmut Friess},
  journal={Annals of Surgery},
  year={2010},
  volume={251},
  pages={923-931}
}
Objective:To further characterize the neurotrophic attributes of pancreatic cancer (PCa). Summary Background Data:PCa is characterized by neuropathic alterations which are resulting in pancreatic pain. To further characterize pancreatic neuropathy, we aimed: to analyze whether neuropathic alterations in PCa are only limited to the tumor-core or whether they are similarly encountered in neural structures in the noncancerous pancreas, to demonstrate whether PCa features neurotrophic attributes… 
The neurotrophic factor neurturin contributes toward an aggressive cancer cell phenotype, neuropathic pain and neuronal plasticity in pancreatic cancer.
TLDR
It is shown that PCC produce the neurotrophic factor NRTN, which reinforces their biological properties, triggers neuroplastic alterations, NI and influences pain sensation via the GFRα-2 receptor in PCa.
Neuroplastic changes in a mouse model of pancreatic ductal adenocarcinoma
TLDR
It is found that although disease time course varied, pancreatic cancer typically developed by 16 weeks of age, however pancreatic neurotrophic factor mRNA expression was up-regulated and pancreatic innervation increased dramatically prior to this time point, which demonstrates that the nervous system participates in all stages of PDAC, including those that precede appearance of cancer.
Systemic Depletion of Nerve Growth Factor Inhibits Disease Progression in a Genetically Engineered Model of Pancreatic Ductal Adenocarcinoma
TLDR
Anti-NGF treatment beginning at 4 weeks may increase inflammation and negatively impact disease, however, treatment starting at 8 weeks (after disease onset), reduces neural inflammation, neural invasion, and metastasis.
Perineural Mast Cells Are Specifically Enriched in Pancreatic Neuritis and Neuropathic Pain in Pancreatic Cancer and Chronic Pancreatitis
TLDR
The specific enrichment of MC around intrapancreatic nerves in neuropathic pain due to PCa and CP suggests the presence of MC-induced visceral hypersensitivity in the pancreas.
Neuronal plasticity in chronic pancreatitis is mediated via the neurturin/GFRα2 axis.
TLDR
The NRTN/GFRα2 axis is activated during the course of CP and represents a major key player in the reactive neural alterations in CP, the first study to provide functional evidence for the contribution of neurotrophic factors to neuroplasticity in CP.
Neural plasticity in pancreatitis and pancreatic cancer
TLDR
Novel possibilities for mechanistically uncovering the role of the nervous system in pancreatic disease progression are discussed, as demonstrated by tissue and neural damage inducing neuropathic pain, and activated neurons releasing mediators that modulate inflammation and cancer growth.
Title: Neuroplastic changes occur early in the development of pancreatic ductal adenocarcinoma
TLDR
The results demonstrate that the nervous system participates in all stages of PDAC, including those that precede appearance of cancer, which has been shown to be a precipitating event that can accelerate the transition of precancerous lesions to cancer.
Nerves and Pancreatic Cancer: New Insights into A Dangerous Relationship
TLDR
The main molecules and signaling pathways implicated in PNI are discussed and their roles in the PDAC are discussed.
Neuroplastic changes occur early in the development of pancreatic ductal adenocarcinoma.
TLDR
The results demonstrate that the nervous system participates in all stages of PDAC, including those that precede the appearance of cancer.
Stromal SLIT2 impacts on pancreatic cancer-associated neural remodeling
TLDR
It is reported that the intratumoral microenvironment is a mediator of PDA-associated neural remodeling (PANR), and factors such as ‘SLIT2’ (an axon guidance molecule), which is expressed by cancer-associated fibroblasts (CAFs), that impact on neuroplastic changes in human PDA.
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TLDR
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TLDR
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