C-B-D Enhances Chemo for Pancreatic Cancer

KPC mice treated with a combination of the GPR55 antagonist Cannabidiol (CBD) and gemcitabine (GEM, one of the most used drugs to treat Pancreatic Cancer), survived nearly three times longer compared to mice treated with vehicle or GEM alone…

Cannabinoid use is not a silver bullet for pancreatic cancer (PC) patients. However, as a long-term cancer survivor myself, I see both complementary and integrative therapies as a possible improvement over the conventional oncology “standard-of-care” therapy plan.

The studies linked and excerpted below offer an integrative therapy for pancreatic cancer patients and survivors. This integrative approach offers a treatment that may increase the overall survival of a cancer that has not experienced improvements in decades.

If you have been diagnosed with pancreatic cancer your first and most important step is to get an accurate diagnosis. A small number of patients discover their cancers early enough to surgically remove their tumors (Whipple Procedure).

Those PC patients with more advanced cancer must learn about and consider conventional (FDA approved) and integrative therapies like the combining of CBD oil and gemcitabine chemotherapy.

I am a long term survivor of a blood cancer called multiple myeloma. So why am I blogging about CBD enhancing gemcitabine? Because CBD enhances a common myeloma chemotherapy called Velcade. Like pancreatic cancer, my blood cancer, multiple myeloma treatment can benefit from both complementary and integrative therapies.

Both cancers bring dismal five year survival rates. Yet there are dozens of evidence-based non-conventional therapies as well as integrative therapies that are not taken into account in those dismal five year survival rates.

Have you been diagnosed with pancreatic cancer? What is your therapy plan? Scroll down the page, post a question or comment and I will reply to you ASAP.

Thank you,

David Emerson

Cancer Survivor
Cancer Coach
Director PeopleBeatingCancer

Gemcitabine/cannabinoid combination triggers autophagy in pancreatic cancer cells through a ROS-mediated mechanism

“Gemcitabine (GEM, 2′,2′-difluorodeoxycytidine) is currently used in advanced pancreatic adenocarcinoma, with a response rate of < 20%. The purpose of our work was to improve GEM activity by addition of cannabinoids.

Here, we show that GEM induces both cannabinoid receptor-1 (CB1) and cannabinoid receptor-2 (CB2) receptors by an NF-κB-dependent mechanism and that its association with cannabinoids synergistically inhibits pancreatic adenocarcinoma cell growth and increases reactive oxygen species (ROS) induced by single treatments.

The antiproliferative synergism is prevented by the radical scavenger N-acetyl-L-cysteine and by the specific NF-κB inhibitor BAY 11-7085, demonstrating that the induction of ROS by GEM/cannabinoids and of NF-κB by GEM is required for this effect.

In addition, we report that neither apoptotic nor cytostatic mechanisms are responsible for the synergistic cell growth inhibition, which is strictly associated with the enhancement of endoplasmic reticulum stress and autophagic cell death.

Noteworthy, the antiproliferative synergism is stronger in GEM-resistant pancreatic cancer cell lines compared with GEM-sensitive pancreatic cancer cell lines. The combined treatment strongly inhibits growth of human pancreatic tumor cells xenografted in nude mice without apparent toxic effects. These findings support a key role of the ROS-dependent activation of an autophagic program in the synergistic growth inhibition induced by GEM/cannabinoid combination in human pancreatic cancer cells.

GPR55 signalling promotes proliferation of pancreatic cancer cells and tumour growth in mice, and its inhibition increases effects of gemcitabine

“The life expectancy for pancreatic cancer patients has seen no substantial changes in the last 40 years as very few and mostly just palliative treatments are available. As the five years survival rate remains around 5%, the identification of novel pharmacological targets and development of new therapeutic strategies are urgently needed.

Here we demonstrate that inhibition of the G protein-coupled receptor GPR55, using genetic and pharmacological approaches, reduces pancreatic cancer cell growth in vitro and in vivo and we propose that this may represent a novel strategy to inhibit pancreatic ductal adenocarcinoma (PDAC) progression.

Specifically, we show that genetic ablation of Gpr55 in the KRAS mouse model of PDAC significantly prolonged survival. Importantly, KPC mice treated with a combination of the GPR55 antagonist Cannabidiol (CBD) and gemcitabine (GEM, one of the most used drugs to treat PDAC), survived nearly three times longer compared to mice treated with vehicle or GEM alone…

Combination of CBD and GEM inhibited tumour cell proliferation in KPC mice and it opposed mechanisms involved in development of resistance to GEM in vitro and in vivo.

Finally, we demonstrate that the tumour suppressor p53 regulates GPR55 protein expression through modulation of the microRNA miR34b-3p.

Our results demonstrate the important role played by GPR55 downstream of p53 in PDAC progression. Moreover our data indicate that combination of CBD and GEM, both currently approved for medical use, might be tested in clinical trials as a novel promising treatment to improve PDAC patients’ outcome.”

Diagnosed with Cancer? Your two greatest challenges are understanding cancer and understanding possible side effects from chemo and radiation. Knowledge is Power!

C-B-D Enhances Chemo for Pancreatic Cancer

KPC mice treated with a combination of the GPR55 antagonist Cannabidiol (CBD) and gemcitabine (GEM, one of the most used drugs to treat Pancreatic Cancer), survived nearly three times longer compared to mice treated with vehicle or GEM alone…

Recommended Reading:

Gemcitabine/cannabinoid combination triggers autophagy in pancreatic cancer cells through a ROS-mediated mechanism

GPR55 signalling promotes proliferation of pancreatic cancer cells and tumour growth in mice, and its inhibition increases effects of gemcitabine

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