About this document.
This is an educational document. It is written for people who want to understand the endocannabinoid system and the scientific research surrounding it. It is presented in two clearly separated parts, and understanding the difference between them matters.
The research summarised in Part One is drawn from independent scientific literature. The great majority of it is preclinical, meaning it was conducted in laboratory cell cultures and in animals, not in human clinical trials. These findings describe what has been observed in research settings. They are not claims about what any Bonner Natural Health product does, and they do not establish that cannabinoids treat, cure, or prevent cancer in people. Nothing in this document is medical advice. If you are managing a cancer diagnosis or any medical condition, decisions about your care belong with you and your physician or neuro-oncologist.
Understanding the diagnosis, gently and clearly.
A glioblastoma diagnosis is frightening, and if you or someone you love has just received one, that feeling is completely understandable. This short overview is here to help you understand the diagnosis calmly and clearly. It is general information, not a description of your own situation, which only your medical team can give you. Glioblastoma, also called glioblastoma multiforme or GBM, is a serious, fast-growing tumour that begins in the brain's supportive cells, known as glial cells. Because it grows into nearby healthy tissue, it can be hard to remove completely with surgery alone, which is why treatment usually brings together more than one approach.
How It Behaves
Glioblastoma tends to grow quickly and to spread its cells into the surrounding brain rather than staying in one tidy lump. This is why care usually combines surgery, radiation, and medicine working together, and why your team keeps monitoring closely over time. It very rarely spreads outside the brain.
Molecular Markers
Modern diagnosis looks closely at the tumour's molecular features. Two that are often discussed are MGMT, a gene whose switching-off (called methylation) tends to predict a better response to chemotherapy, and IDH status, which helps classify the tumour. These markers help your medical team choose the treatment most likely to help you.
Standard of Care
The established treatment, often called the Stupp protocol, combines safe surgical removal of as much of the tumour as possible with radiation therapy and the chemotherapy drug temozolomide, followed by further cycles of temozolomide. A wearable device delivering tumour-treating fields is used in some cases too. This is powerful, well-established care, and it is the foundation that everything else builds on.
Why the Research Continues
Glioblastoma is a challenging disease, and that is exactly why research around the world is so active. That effort includes a growing body of work on the endocannabinoid system, which the rest of this document explores, and it is part of why many people and their families choose to add supportive, holistic approaches alongside their medical treatment. Whatever the road ahead looks like for you, you deserve clear information and good support at every step.
Conventional treatment is delivered by a neurosurgical and neuro-oncology team. It is powerful and necessary, and it is the standard of care. Nothing in this document is intended to replace it, and every decision about your care belongs with you and your doctors.
The body's master regulatory system.
The Endocannabinoid System, or ECS, is described in the scientific literature as one of the body's central regulatory systems. Woven into virtually every tissue, it is involved in homeostasis, the state of internal balance in which the body functions well, and it participates in the regulation of inflammation, immune activity, pain signalling, cell turnover, mood, sleep, and metabolic balance. It was first identified by science in the late 1980s and early 1990s, and many practising physicians received little formal training in it.
The system operates through three components: endocannabinoids, the messenger molecules the body makes naturally, principally anandamide and 2-arachidonoylglycerol (2-AG); cannabinoid receptors, chiefly CB1 and CB2, found on cells throughout the body; and the enzymes that build and break down these signals. The ECS also interacts with TRP channels (TRPV1, TRPV2, TRPM8, TRPA1), GPR55, PPAR receptors, and serotonin (5-HT) receptors.
A defining feature of the system is timing. Endocannabinoids are not stored in advance; the body makes them on demand, exactly where and when they are needed, and then clears them within minutes. They also work in reverse, released by the receiving nerve cell and travelling backward across the synapse to quieten the cell signalling to it. This on-demand, retrograde design is how the ECS makes precise, moment-to-moment adjustments rather than blunt, system-wide ones.
Although the ECS reaches every organ, it is especially concentrated in the brain and nervous system. CB1 is the most abundant receptor of its kind in the brain, concentrated in regions that govern mood, memory, stress, appetite, and pain, and it is also present in fat, liver, pancreas, muscle, bone, skin, heart, and reproductive tissue. CB2 sits mainly on immune cells and in the spleen, with a presence in bone, liver, and the brain's own immune cells. Because the receptors are almost everywhere, the system touches an unusually wide range of functions: mood, memory, stress and anxiety, sleep, appetite, body temperature, immune balance, pain, neuroprotection, bone health, and metabolism.
The brain and nervous system are especially rich in ECS components. CB1 is the most abundant receptor of its kind in the brain, and CB2 is carried by the brain's own immune cells, the microglia. Here the ECS helps regulate neuronal signalling and excitability, neuroinflammation, and the survival and turnover of cells. This is why researchers have taken a close interest in the ECS in neurological conditions and, as this document describes, in brain tumours.
Why the system runs strong in some people and low in others.
Every person has a baseline level of endocannabinoid activity, often called endocannabinoid tone. It reflects how much anandamide and 2-AG you make, how many receptors you carry, and how quickly your enzymes clear these signals away. Tone is not fixed. It rises and falls with how you live.
Clinical Endocannabinoid Deficiency
Researchers led by Dr. Ethan Russo have proposed that some people carry a chronically low endocannabinoid tone, a concept named Clinical Endocannabinoid Deficiency. The strongest research support is in migraine, fibromyalgia, and irritable bowel syndrome, conditions that share heightened pain sensitivity and central sensitisation. This remains a scientific hypothesis under active investigation, not an established diagnosis.
What Lowers Tone, and What Supports It
In research settings, chronic stress and diets low in essential fats are associated with reduced endocannabinoid signalling. On the other side, moderate aerobic exercise raises anandamide, the molecule now thought to underlie the "runner's high," and omega-3 fats supply the raw materials the body uses to build its own endocannabinoids. Lifestyle, in other words, is one of the main levers on this system.
Phytocannabinoids as Exogenous Support
Plant phytocannabinoids such as CBD and CBG are shaped much like the endocannabinoids the body makes, so they can act on the same receptors and pathways. In the scientific literature they are described as cannabimimetic, meaning they mimic or support the activity of the endocannabinoid system from the outside. This is the basis of the research interest in hemp-derived phytocannabinoids as a way to support endocannabinoid tone, particularly where that tone may be running low.
Clinical Endocannabinoid Deficiency is a research hypothesis, and supporting endocannabinoid tone is a wellness concept, not a treatment for any named disease. Nothing here should be read as a claim that phytocannabinoids, or any product, diagnose, treat, cure, or prevent migraine, fibromyalgia, irritable bowel syndrome, cancer, or any other condition.
The compounds, and what the science describes.
Hemp produces more than a hundred distinct cannabinoids, alongside terpenes that also interact with the endocannabinoid system. The summaries below describe what published research reports about each compound found in our broad-spectrum profile. This is educational information about the compounds themselves. As with the rest of Part One, much of this research is preclinical, and it is not a statement about the effects of any product.
Major Cannabinoids
CBD (Cannabidiol). The most studied cannabinoid, and non-intoxicating. Rather than binding the CB1 receptor directly, it acts as a negative allosteric modulator of CB1 and raises the body's own anandamide by inhibiting the FAAH enzyme. It also activates TRPV1 (pain and temperature), 5-HT1A serotonin receptors (mood and nausea), and PPAR-gamma (metabolism and inflammation), and blocks GPR55. The purified-CBD medicine Epidiolex is FDA-approved for certain rare epilepsies, and CBD is widely researched for inflammation, anxiety, and pain.
CBDa (Cannabidiolic acid). The raw, acidic form of CBD as it exists in the living plant. It is a selective inhibitor of the COX-2 inflammatory enzyme and a potent activator of 5-HT1A serotonin receptors, which is why it has been studied for nausea and mood. It is often absorbed more readily than CBD itself.
CBG (Cannabigerol). Non-intoxicating. A partial agonist at both CB1 and CB2 receptors, an alpha-2 adrenoceptor agonist, a 5-HT1A antagonist, and a modulator of TRP channels. It is noted in research for antibacterial activity, including against drug-resistant bacteria, and for appetite and neuroprotection.
CBGa (Cannabigerolic acid). The "mother cannabinoid," the acidic precursor from which the plant builds CBD, THC, and CBC. Beyond that structural role, it activates PPAR receptors involved in metabolism and has been studied for metabolic and lipid effects.
Minor Cannabinoids
CBC (Cannabichromene). Non-intoxicating. It binds the classic cannabinoid receptors only weakly, but is a potent activator of TRPA1 channels and slows the reuptake of anandamide, which raises endocannabinoid tone. Research has examined its anti-inflammatory effects and its support of neural stem and progenitor cells.
CBN (Cannabinol). Mildly active at most; it forms naturally as THC ages. It has modest affinity for the CB2 receptor and acts on TRPV2 and TRPA1 channels. It is popularly associated with relaxation and sleep, though robust human sleep data is still limited; preclinical work has looked at appetite and anti-inflammatory effects.
CBNa (Cannabinolic acid). The acidic precursor of CBN, present in small amounts. Dedicated research is sparse, and it is included as a natural part of the full-spectrum profile.
CBDV (Cannabidivarin). A non-intoxicating relative of CBD with a shorter molecular chain. It activates TRPA1, TRPV1, and TRPV2 channels and blocks TRPM8. Its best-studied property is anticonvulsant activity in animal models, and it has been investigated for neurodevelopmental conditions.
THCV (Tetrahydrocannabivarin). A relative of THC. At the low levels found in hemp it behaves as a CB1 antagonist, a property researched in connection with appetite regulation and glucose and metabolic control; at higher doses its behaviour changes. It is non-intoxicating at typical hemp levels.
Rare and Trace Cannabinoids
CBE (Cannabielsoin). An oxidation product and natural metabolite of CBD, meaning the body itself converts some CBD into CBE. Recent laboratory work characterises it as a "biased" CB1 agonist. Research remains early and limited.
CBL (Cannabicyclol). A stable compound that forms when CBC is exposed to light over time. It is well described chemically, but its pharmacology is largely uncharacterised; it is present as a natural component of mature, full-spectrum hemp.
CBT (Cannabicitran). A rare, non-intoxicating cannabinoid that occurs naturally in the plant. Published research is minimal; the main documented finding is a reduction of intraocular (eye) pressure in animal studies.
Trace Delta-9 THC. Present only in the small, federally limited amounts (below 0.3%) characteristic of broad-spectrum hemp. Delta-9 THC is the main activator of the CB1 receptor; at these trace levels it contributes to the entourage effect without intoxication.
Delta-8 THC. Used as a purified isolate in certain formulations only. A milder relative of delta-9 THC that partially activates CB1, studied historically for nausea and appetite. Its legal status varies by state, which is worth confirming market by market.
A Dietary Terpene That Acts Like a Cannabinoid
Beta-Caryophyllene. Not a classical cannabinoid but a dietary terpene found in black pepper, cloves, and hemp. Uniquely among common terpenes, it is a selective full agonist of the CB2 receptor, and also activates PPAR, which is why it is often called a "dietary cannabinoid." It is well researched for anti-inflammatory and pain-related effects mediated specifically through CB2, and is recognised as safe for use as a food flavouring.
What independent researchers have reported.
Glioblastoma is one of the most extensively studied cancers in cannabinoid research, and one of the few in which cannabinoids have reached human clinical testing. The findings below are drawn from peer-reviewed publications, and each describes what researchers observed in their study. Most of this work is preclinical, conducted in cell lines and animals; the human studies so far are small and early. None of it describes a Bonner Natural Health product.
The First Human Study
Guzman and colleagues, in the British Journal of Cancer in 2006, carried out the first human study of a cannabinoid's antitumour action, delivering THC directly into the tumours of nine patients with recurrent glioblastoma who had exhausted standard treatment. The main finding was that THC could be given safely, without significant psychoactive harm or acceleration of the disease, alongside laboratory signs the authors interpreted as reduced tumour cell growth.
Cell Death Through Autophagy
Salazar and colleagues, in the Journal of Clinical Investigation in 2009, reported that THC drove human glioma cells to die through autophagy, a self-digesting form of programmed cell death, by triggering a build-up of ceramide and stress in the cell's endoplasmic reticulum. This described a clear molecular pathway by which a cannabinoid could kill glioma cells.
Cannabidiol Against Glioma Cells
Massi and colleagues, in the Journal of Pharmacology and Experimental Therapeutics in 2004, reported that cannabidiol, the non-intoxicating cannabinoid, slowed the growth of human glioma cells and triggered apoptosis both in culture and in animals, with the effect linked to CB2 receptors and oxidative stress.
Combining Cannabinoids With Temozolomide
Torres and colleagues, in Molecular Cancer Therapeutics in 2011, reported that combining THC with the standard chemotherapy drug temozolomide produced a strong antitumour effect in glioma models, including in tumours resistant to temozolomide, and that adding cannabidiol strengthened the effect. Separately, Nabissi and colleagues, in Carcinogenesis in 2013, reported that cannabidiol, acting through the TRPV2 channel, made glioblastoma cells more sensitive to temozolomide and other chemotherapy agents while sparing normal brain cells.
A Randomised Clinical Trial
Twelves and colleagues, in the British Journal of Cancer in 2021, reported a small phase 1b randomised, placebo-controlled trial that added nabiximols, a standardised THC and CBD oromucosal spray, to temozolomide in patients with recurrent glioblastoma. The combination was generally tolerated, and among the small numbers studied, one-year survival was higher in the cannabinoid group than in the placebo group. The authors stressed that the trial was small and designed mainly to assess safety, so the survival signal needs confirmation in larger studies.
These are independent findings from laboratory, animal, and small early human studies. They show that glioblastoma is an active and serious area of cannabinoid research. They do not establish that cannabinoids, or any product, treat or cure glioblastoma, and they are not statements about Bonner Natural Health formulations. Larger clinical trials, including the ongoing ARISTOCRAT study, are needed before any firm conclusions can be drawn.
Why cannabinoids are of interest for a brain tumour.
A central challenge in treating any brain disease is the blood-brain barrier, a tight lining of blood vessels that keeps most substances in the bloodstream out of the brain. Many drugs simply cannot get through it. This section describes general pharmacology; it is educational and does not describe the use of any product for any disease.
Crossing the Blood-Brain Barrier
THC and CBD are highly lipophilic, meaning they dissolve readily in fats. Because the blood-brain barrier is itself built from fatty membranes, lipophilic molecules like these cross it comparatively easily and reach the brain. This is one reason cannabinoids have drawn research interest in neurological conditions and brain tumours. The endocannabinoid system is also unusually concentrated in the brain, so the machinery these compounds act on is already present in the affected tissue.
Delivery Formats
Because cannabinoids are fat-soluble and are heavily broken down when swallowed and processed by the liver, the delivery route affects how much reaches the bloodstream. Oral and sublingual (under-the-tongue) formats are common, and suppository delivery bypasses first-pass liver metabolism to reach high systemic bioavailability. The human glioblastoma trials to date have used an oromucosal spray absorbed through the lining of the mouth.
The published studies referenced above.
The research described in Part One is drawn from the peer-reviewed publications below, listed with their source and identifier so that you and your medical team can review them directly.
First Human Study of THC in Glioblastoma
Guzman M, et al. "A pilot clinical study of Delta-9-tetrahydrocannabinol in patients with recurrent glioblastoma multiforme." British Journal of Cancer. 2006;95(2):197 to 203. PMID: 16804518.
Autophagy-Mediated Glioma Cell Death
Salazar M, et al. "Cannabinoid action induces autophagy-mediated cell death through stimulation of ER stress in human glioma cells." Journal of Clinical Investigation. 2009;119(5):1359 to 1372. PMID: 19425170.
Cannabidiol and Human Glioma Cells
Massi P, et al. "Antitumor effects of cannabidiol, a nonpsychoactive cannabinoid, on human glioma cell lines." Journal of Pharmacology and Experimental Therapeutics. 2004;308(3):838 to 845. PMID: 14617682.
Cannabinoids Combined With Temozolomide
Torres S, et al. "A combined preclinical therapy of cannabinoids and temozolomide against glioma." Molecular Cancer Therapeutics. 2011;10(1):90 to 103. PMID: 21220494.
Cannabidiol and Chemosensitisation via TRPV2
Nabissi M, et al. "Triggering of the TRPV2 channel by cannabidiol sensitizes glioblastoma cells to cytotoxic chemotherapeutic agents." Carcinogenesis. 2013. PMID: 23079154.
Randomised Clinical Trial of Nabiximols
Twelves C, et al. "A phase 1b randomised, placebo-controlled trial of nabiximols cannabinoid oromucosal spray with temozolomide in patients with recurrent glioblastoma." British Journal of Cancer. 2021;124(8):1379 to 1387. PMID: 33623076.
Standard of Care Reference
Stupp R, et al. "Radiotherapy plus concomitant and adjuvant temozolomide for glioblastoma." New England Journal of Medicine. 2005;352(10):987 to 996. PMID: 15758009.
Everything above is a summary of independent scientific research. What follows is a description of Bonner Natural Health's own formulations. These are wellness products designed to support the body's endocannabinoid system. They are not the subject of the research above, and the following statements have not been evaluated by the Food and Drug Administration. These products are not intended to diagnose, treat, cure, or prevent any disease.
Broad-spectrum phytocannabinoid formulations to support your endocannabinoid system.
Bonner Natural Health produces broad-spectrum phytocannabinoid formulations made from industrial hemp, together with purified single-cannabinoid isolates used in certain products. Our broad-spectrum extracts contain the full range of naturally occurring hemp cannabinoids, including only trace THC below the 0.3% federal hemp limit; our isolate-based products are formulated without THC. All are designed to support the body's own endocannabinoid system and its role in maintaining balance and overall wellbeing, using a broad spectrum of compounds working together, an approach often described as the entourage effect.
Transdermal Oil
A hemp seed oil based topical formulation, applied to the skin, designed to support the endocannabinoid system.
Sublingual Tincture
An MCT oil based tincture taken under the tongue, designed for everyday support of the endocannabinoid system.
Suppository
A suppository format that bypasses first-pass liver metabolism to reach high systemic bioavailability, one of several delivery routes discussed in Part One.
Our formulations draw on the compounds described in Section 05, including the cannabinoids CBD, CBDa, CBG, CBGa, CBC, CBN, CBNa, CBDV, and THCV; the rare, naturally occurring cannabinoids CBE, CBL, and CBT; and the dietary CB2-active terpene beta-caryophyllene. We also use purified isolates of CBD, CBG, CBN, CBGa, CBDa, and, in certain cases, Delta-8. A full scientific overview of what each compound does is set out in Section 05.
Ingredients
- Broad-spectrum cannabinoids, U.S. grown from the hemp plant
- Cocoa butter
- MCT oil
- Apricot seed oil
Personalised wellness support, alongside your medical care.
Bonner Natural Health offers a personalised wellness program delivered by telehealth. We work with people who want to support their general wellbeing and their endocannabinoid system as part of a healthy lifestyle. Our program is designed to complement, never to replace, the care of your physician and medical team.
- We do not diagnose, treat, or cure disease, and we do not provide medical advice
- We never advise anyone to stop or change prescribed medical treatment; those decisions rest with you and your doctors
- We encourage you to keep your physician and, where relevant, your neuro-oncology team fully informed about any wellness product you use
- Our support focuses on nutrition, lifestyle, and general endocannabinoid system wellbeing
- Any product you use should be discussed with your medical team first, especially alongside chemotherapy, radiation, or anti-seizure medication
We believe in offering hope. Not false promises, but the honest hope that comes from understanding your body, caring for it well, and being supported as a whole person alongside your medical treatment. Given good nutrition, a healthy lifestyle, and support for its own regulatory systems, the body has a remarkable capacity to seek its own balance.
Bonner Natural HealthLearn more about the endocannabinoid system.
Reach out to Barry directly to learn more about the science of the endocannabinoid system and our wellness formulations. There is no obligation, just an honest conversation.
A plain-English glossary.
This glossary explains the technical words used in this document in everyday language, grouped by theme. It is provided to make the science easier to follow and is not a substitute for advice from your medical team.
The Endocannabinoid System
Endocannabinoid system (ECS). The body's built-in regulatory network that helps keep internal systems in balance, made up of messengers, receptors, and enzymes.
Homeostasis. The body's state of internal balance, where things like temperature, mood, and inflammation are held within a healthy range.
Endocannabinoids. Signalling molecules the body makes itself, mainly anandamide and 2-AG, that act on the ECS.
Anandamide. One of the body's main endocannabinoids, sometimes called the bliss molecule, involved in mood, pain, and the runner's high.
2-AG (2-arachidonoylglycerol). The body's other main endocannabinoid, widely involved in ECS signalling.
Endocannabinoid tone. The overall level of activity in your ECS, which can run higher or lower from person to person and day to day.
Clinical Endocannabinoid Deficiency (CECD). A research idea that some people have a chronically low endocannabinoid tone, studied in migraine, fibromyalgia, and irritable bowel syndrome.
Retrograde signalling. The ECS's unusual way of working, where the receiving nerve cell sends a signal backward to quieten the cell that is signalling to it.
CB1 and CB2 receptors. Docking points on cells that cannabinoids attach to. CB1 is common in the brain and nerves; CB2 is common on immune cells.
TRP channels (TRPV1, TRPV2, TRPM8, TRPA1). A family of cell sensors involved in pain, temperature, and other signals that cannabinoids can act on.
GPR55, GPR18, PPAR, 5-HT receptors. Additional receptors that form part of the wider endocannabinoid system, involved in inflammation, metabolism, and mood.
NAPE-PLD, DAGL, FAAH, MAGL. Enzymes that build the endocannabinoids (NAPE-PLD and DAGL) and break them down again (FAAH and MAGL).
Microglia. The brain's own immune cells, which carry CB2 receptors.
Cannabinoids and Compounds
Cannabinoid. A compound that acts on the endocannabinoid system, whether made by the body or found in a plant.
Phytocannabinoid. A cannabinoid made by a plant, such as CBD or THC. Phyto means plant.
CBD (cannabidiol). The most studied non-intoxicating hemp cannabinoid.
THC (tetrahydrocannabinol). The main intoxicating cannabinoid in cannabis, present only in trace amounts in broad-spectrum hemp.
Delta-9 and Delta-8 THC. Two closely related forms of THC; delta-8 is milder.
Cannabimimetic. Something that mimics or supports the activity of the endocannabinoid system.
Broad-spectrum. A hemp extract containing the full range of natural cannabinoids together, rather than a single isolated one.
Isolate. A single, purified cannabinoid on its own.
Entourage effect. The idea that cannabinoids and related plant compounds work better together than any one does alone.
Beta-caryophyllene. A dietary terpene, found in black pepper and cloves, that acts on the CB2 receptor.
How Cannabinoids Reach the Body
Bioavailability. The proportion of a dose that actually reaches the bloodstream and can have an effect.
First-pass metabolism. The way the liver breaks down much of a swallowed substance before it reaches the rest of the body.
Lipophilic. Fat-loving; a substance that dissolves easily in fats and can cross fatty barriers such as cell membranes.
Blood-brain barrier. A tight lining around the brain's blood vessels that blocks most substances from entering the brain.
Sublingual. Taken under the tongue for absorption.
Oromucosal. Absorbed through the lining of the mouth, for example a mouth spray.
Transdermal. Applied to and absorbed through the skin.
Suppository. A dose inserted rectally, which bypasses the liver and can reach high bioavailability.
Inside the Cell
Apoptosis. Programmed cell death, the body's orderly way of removing damaged or unwanted cells.
Autophagy. A cell's self-cleaning and recycling process, which in some cases can also lead to cell death.
Mitochondria. The energy factories inside cells. The ECS can act on them through mtCB1 receptors.
Oxidative stress and reactive oxygen species (ROS). Damage caused by reactive oxygen molecules; too much can harm cells.
Cell proliferation. The multiplication of cells. Uncontrolled proliferation is a hallmark of cancer.
Ceramide. A fatty molecule inside cells that can trigger cell death when it builds up.
Endoplasmic reticulum (ER) stress. Strain on a cell's protein-processing system that can push the cell toward death.
Neuroprotection. Protecting nerve cells from damage.
Neuroinflammation. Inflammation within the brain and nervous system.
Neurons, glial cells, and astrocytes. Neurons are the brain's signalling cells; glial cells, including astrocytes, support them. Glioblastoma arises from glial cells.
Glioblastoma and Its Treatment
Glioblastoma (GBM). The most common and fast-growing primary brain tumour in adults.
Glioma. A broader family of brain tumours arising from glial cells; glioblastoma is the most severe type.
Grade 4. The highest severity grade a tumour can be given.
Recurrent. A cancer that has come back after treatment.
MGMT and methylation. MGMT is a gene whose switching-off, called methylation, predicts a better response to chemotherapy.
IDH status. A molecular feature used to classify gliomas and help estimate prognosis.
Temozolomide. The standard chemotherapy drug for glioblastoma.
Stupp protocol. The standard treatment combining surgery, radiation, and temozolomide.
Tumour-treating fields. A wearable device that uses electric fields to slow tumour growth.
Nabiximols (Sativex). A pharmaceutical mouth spray with a standardised, roughly equal mix of THC and CBD.
Chemosensitisation. Making cancer cells more responsive to chemotherapy.
Understanding the Research
Preclinical. Research done in cells or animals, before human testing.
In vitro and in vivo. In vitro means in a dish (cells); in vivo means in a living body (animals or people).
Cell line. Cancer cells grown in the laboratory for study.
Xenograft. A human tumour grown in an animal for research.
Randomised. Patients assigned to treatment or comparison groups by chance, to keep the comparison fair.
Placebo-controlled. Compared against a dummy treatment, so real effects can be told apart from expectation.
Phase 1b. An early-stage clinical trial whose main job is to test safety.
Peer-reviewed. Checked by independent experts before publication.
PMID. A unique ID number for a study in the PubMed medical database, so you can look it up directly.