Pancreatic Cancer

Pancreatic cancer occurs in the tissues of the pancreas which is an organ in the abdomen involved in releasing enzymes that help with digestion and production of hormones.

  • What is Pancreatic Cancer?
  • Pancreatic Cancer & cannabinoids
  • Text references, literature discussion
    & clinical trials

What is Pancreatic Cancer?

Pancreatic Cancer occurs in the tissues of the pancreas which is an organ in the abdomen involved in releasing enzymes that help with digestion and production of hormones.1

There is a lack of symptoms in the early stages of the disease and cancer often spreads to other parts of the body before it is detected. However, common symptoms may include:1

  • Back pain
  • Unintended weight loss
  • Loss of appetite
  • Jaundice, yellowing of the skin
  • Pale colored feces
  • Dark-colored urine
  • Itchy skin
  • Blood clots
  • Fatigue
  • Aggravation of diabetes or detected new diagnosis of diabetes

Currently, the exact cause of Pancreatic Cancer is not clear. Factors that may increase the risk of this cancer are smoking and certain genetic mutations. As other types of cancer, Pancreatic Cancer involves the growth of abnormal cells that contain mutations leading to uncontrollable cell division and growth. Similarly, it can spread and damage/destroy normal tissue.
The most common types of pancreatic cancer form in the cells lining the ducts of the pancreas and is referred to as pancreatic adenocarcinoma or pancreatic exocrine cancer. Cancer can also begin in the hormone-producing cells and/or neuroendocrine cells in the pancreas. These types of cancer are less common and are known as pancreatic neuroendocrine tumors, islet cell tumors, or pancreatic endocrine cancer.1

  • Cannabinoids
  • Cannabinoid receptors
  • Endocannabinoids

  • THC

  • CB1
  • CB2

Plant Cannabinoids

  • Terpenes
  • Strains
  • Enzymes
  • Metabolites



  • FAAH
  • MAGL


The connection between Pancreatic Cancer
& cannabinoids

Pancreatic Cancer Xray

Preclinical evidence proposes that the endocannabinoid system may play a role in the development of pancreatic cancer and that cannabinoids like THC may exhibit anti-tumoral properties. In addition, cannabinoids may be beneficial in treatments supplementing chemotherapy as cannabinoids appear to enhance the effect of the treatment.2

It was shown that endogenous cannabinoids play a role in reducing tumor invasion and growth, promoting tumor cell death, and suppressing tumor angiogenesis. through cannabinoid receptor or receptor-independent pathways.3

Note: If you have any further information relevant to the connection between Pancreatic Cancer and cannabinoids, or find any of the information inaccurate, outdated, or incomplete please contact us here.

Text references, literature discussion
& clinical trials

  • Text references
  • Literature discussion
  • Clinical trials

In one study, it was shown that pancreatic cancer cells (MiaPaCa2, Panc1, Capan2, and BxPc3 cell lines) can effectively be killed by THC (2 μM and higher concentrations) (Carracedo et al., 2006).

Furthermore, the authors found that both cannabinoid receptors CB1 and CB2 are expressed by the pancreatic tumor biopsies and cell lines. In mice, the growth of pancreatic tumor cells can be decreased by THC (15 mg/kg/d). Also, THC was seen to induce apoptosis of pancreatic cells (Carracedo et al., 2006).

In human pancreatic cancer cells (MIA PaCa-2), it was shown that cell death can be triggered by various agonists and antagonists via a receptor-independent mechanism (Fogli et al., 2006).

In human patients, decreased survival was connected to high expression of CB1 in pancreatic cancer cells. Similarly, decreased survival was connected to low levels of endocannabinoid-degrading enzyme FAAH and MAGL. Furthermore, levels of Anandamide and 2AG were found to be unaffected in pancreatic cancer. Finally, increased survival and strong pain symptoms were found to be connected to low CB1 receptor levels in nerves (Michalski et al., 2008). More research is needed to elucidate the mechanistic value of these correlations.

AMP-kinase and ROS-dependent autophagy of cancer cells can be triggered by cannabinoids specific for the CB1 (ACPA) and CB2 (GW) receptors in Panc1 cells (Dando et al., 2013).

Combination of CB1 and CB2 agonists with the anti-cancer drug Gemcitabine synergistically suppressed pancreatic adenocarcinoma cell proliferation and enhanced intracellular ROS production (Donadelli et al., 2011).

Clinical trials

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