Abstract
| Original language | English |
|---|---|
| Pages (from-to) | 1292-1312 |
| Number of pages | 21 |
| Journal | Cancers |
| Volume | 7 |
| Issue number | 3 |
| DOIs | |
| Publication status | Published - 2015 |
Keywords
- Beta-adrenergic
- Beta-blockers
- Metastasis
- Neural
- Pancreatic cancer
- Stress
Cite this
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Neural regulation of pancreatic cancer: a novel target for intervention. / Chang, Aeson; Kim-Fuchs, Corina; Le, Caroline P; Hollande, Frederic; Sloan, Erica K.
In: Cancers, Vol. 7, No. 3, 2015, p. 1292-1312.Research output: Contribution to journal › Article › Research › peer-review
TY - JOUR
T1 - Neural regulation of pancreatic cancer: a novel target for intervention
AU - Chang, Aeson
AU - Kim-Fuchs, Corina
AU - Le, Caroline P
AU - Hollande, Frederic
AU - Sloan, Erica K
PY - 2015
Y1 - 2015
N2 - The tumor microenvironment is known to play a pivotal role in driving cancer progression and governing response to therapy. This is of significance in pancreatic cancer where the unique pancreatic tumor microenvironment, characterized by its pronounced desmoplasia and fibrosis, drives early stages of tumor progression and dissemination, and contributes to its associated low survival rates. Several molecular factors that regulate interactions between pancreatic tumors and their surrounding stroma are beginning to be identified. Yet broader physiological factors that influence these interactions remain unclear. Here, we discuss a series of preclinical and mechanistic studies that highlight the important role chronic stress plays as a physiological regulator of neural-tumor interactions in driving the progression of pancreatic cancer. These studies propose several approaches to target stress signaling via the β-adrenergic signaling pathway in order to slow pancreatic tumor growth and metastasis. They also provide evidence to support the use of β-blockers as a novel therapeutic intervention to complement current clinical strategies to improve cancer outcome in patients with pancreatic cancer.
AB - The tumor microenvironment is known to play a pivotal role in driving cancer progression and governing response to therapy. This is of significance in pancreatic cancer where the unique pancreatic tumor microenvironment, characterized by its pronounced desmoplasia and fibrosis, drives early stages of tumor progression and dissemination, and contributes to its associated low survival rates. Several molecular factors that regulate interactions between pancreatic tumors and their surrounding stroma are beginning to be identified. Yet broader physiological factors that influence these interactions remain unclear. Here, we discuss a series of preclinical and mechanistic studies that highlight the important role chronic stress plays as a physiological regulator of neural-tumor interactions in driving the progression of pancreatic cancer. These studies propose several approaches to target stress signaling via the β-adrenergic signaling pathway in order to slow pancreatic tumor growth and metastasis. They also provide evidence to support the use of β-blockers as a novel therapeutic intervention to complement current clinical strategies to improve cancer outcome in patients with pancreatic cancer.
KW - Beta-adrenergic
KW - Beta-blockers
KW - Metastasis
KW - Neural
KW - Pancreatic cancer
KW - Stress
UR - http://search.proquest.com.ezproxy.lib.monash.edu.au/docview/1721938292/fulltextPDF/CDD897198F1A46A3PQ/11?accountid=12528
U2 - 10.3390/cancers7030838
DO - 10.3390/cancers7030838
M3 - Article
VL - 7
SP - 1292
EP - 1312
JO - Cancers
JF - Cancers
SN - 2072-6694
IS - 3
ER -