Researchers at the Garvan institute have published findings revealing a promising new therapeutic target to slow down or inhibit metastasis in pancreatic cancer. The study identified a metabolic signaling molecule involved in facilitating the spread of the disease to other locations within the body.
Pancreatic cancer ranks among the most lethal forms of cancer, with an average five-year survival rate of only 13%. Typically, the disease is diagnosed at an advanced stage, rendering surgical treatment unfeasible as the cancer has spread to other organs in the body, in most cases, to the liver. Understanding of the mechanisms involved in metastasis has the potential to lead to novel therapeutic strategies.
Metabolic molecule involved in the spread of Pancreatic Cancer
The research describes the pivotal role of NPY in the progression of pancreatic cancer. The NPY molecule is known to be involved in regulating metabolism, evidence also links the molecule to tumour progression in other types of cancer, including breast, prostate and neuroblastoma. However, the role of the molecule in pancreatic cancer metastasis has not been previously investigated.
The study, published this month in Sciences Advances, utilised genetically engineered mouse models along with tissue sourced from donors and the APGI pancreatic cancer biobank. The study showed that, NPY expression is increased in pancreatic cancer compared with normal tissue, particularly in pancreatic ductal adenocarcinoma (PDAC), which accounts for over 90% of pancreatic cancers. Further investigation showed that the NPY molecule is a key factor in driving metastasis.
Furthermore, chemical inhibition of NPY in mouse models has shown a significant decrease in liver metastasis. First author, Dr Cecelia Chambers states, “By blocking this molecule, we could slow down pancreatic cancer cell movement and metastatic outgrowth in the liver thereby limiting the spread of the cancer.” The process of metastasis significantly contributes to the disease’s morbidity, therefore, discovering new pathways to inhibit the spread of pancreatic cancer is crucial for enhancing therapeutic approaches and improving patient outcomes.
An interesting finding of the research is the potential dual benefit whereby the inhibition of NPY reduces muscle and fat loss in pancreatic cancer patients, known as cachexia. The addition of retaining muscle and fat could be advantageous in tolerating treatment for cancer patients.
The progress in understanding of the role of NYP in pancreatic cancer led the team to develop an antibody aimed at blocking the molecules effect, currently being tested in models.
Future Clinical Trials
The research has provided preliminary evidence for the effects of NPY in pancreatic cancer. The results are promising, and the team are investigating how NPY inhibition could be combined with standard of care treatments and understanding when inhibition of NPY would be more effective in the treatment schedule. This information is key to translating the findings into clinical trials that have the potential to improve the clinical management of pancreatic cancer patients.
Further information can be found here: Garvan News: A metabolism switch that could help stop the spread of pancreatic cancer