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cbd oil non hodgkin’s lymphoma

Non-Hodgkin lymphoma can begin in B lymphocytes, T lymphocytes, or natural killer cells. Lymphocytes can also be found in the blood and also collect in the lymph nodes, spleen, and thymus. — National Cancer Institute

Non-Hodgkin lymphoma is a type of cancer that forms in the lymph system, which is part of the body’s immune system. The immune system protects the body from foreign substances, infection, and diseases. The lymph system is made up of the following lymphocytes: B lymphocytes, T lymphocytes, and Natural Killer Cells.

Prospective Analysis of Safety and Efficacy of Medical Cannabis in Large Unselected Population of Patients with Cancer

Below is a Library of Cannabis Research Study for Non-Hodgkin’s Lymphoma.

Over 1000 studies covering over 130 topics compiled for easy browsing.

When part of the lymph system, a section of the immune system, is attacked by cancer lymphoma is contracted. There are two types of lymphoma: Hodgkin, non-Hodgkin. Cancer.net reports as of January 2020, approximately 4,690 men and 3,790 women in the U.S. will contract Hodgkin lymphoma. Treatment for the cancer is harsh, including blood-forming stem cell transplants, bone marrow transplants, and heavy medications, according to MedlinePlus, the clinical periodical for the U.S. Library of Medicine .

The Mayo Clinic points out the several causes and symptoms of lymphoma, both Hodgkin and non-Hodgkin. The cause is complicated, with clinic admitting doctors remain unsure of lymphoma’s origin. What they do know “it begins when a disease-fighting white blood cell called a lymphocyte develops a genetic mutation,” eventually causing “too many diseased and ineffective lymphocytes in your lymph nodes and causes the lymph nodes, spleen and liver to swell.”

Lymphoma Causes, Symptoms & Treatments

“It was the first dispensary in Texas to provide medical cannabis to a patient under the newly expanded conditions—an Austin woman being treated for non-Hodgkin’s lymphoma—and legislation is paving the way for their growth,” reports D. Magazine .

Several risk factors can bring on the gene mutation that causes fatal inflammation and chronic pain , and include gender, with more men contracting cancer, age, impaired immune system, certain infections. Signs of lymphoma are painless swelling of lymph nodes, constant tiredness, fever, shortness of breath, night sweats, itchy skin, and sudden weight loss. As noted, treatments for both Hodgkin and non-Hodgkin are harsh and include chemotherapy and radiation treatments, bone marrow transplants, and immunotherapy medications.

Lymphoma News Today cites the National Cancer Institute , to point out how several studies including a 1996 National Toxicology Program trial , proved that rats given delta (9)-tetrahydrocannabinol (THC) had decreased benign polyps and adenomas, and fewer cases of cancer in the mammary gland , uterus , pituitary , testis , and pancreas .

CBD treatment concomitantly upregulated the tissue inhibitor of matrix metalloproteinases-1 (TIMP-1) and the CBD-elicited decrease in tumour cell invasiveness was reversed by knocking down TIMP-1 expression through a siRNA approach. These results suggest a causal link between TIMP-1 upregulation and CBD anti-invasive action. CBD was also shown to induce p38 and ERK phosphorylation as upstream mechanisms for TIMP-1 induction and subsequent decreased invasiveness. Interestingly all these cellular events were blocked by cannabinoids or TRPV1 receptor antagonists.

It is worth noting that CBD decreased invasiveness in a range of therapeutically relevant concentrations (0.01 to 0.05 µ m ), since the peak plasma concentrations of CBD in healthy volunteers following administration of Sativex™ (1:1 ratio of Δ 9 -THC and CBD) was reported to be between 0.01 µ m to 0.05 µ m [54].

Thyroid cancer is the most common endocrine malignancy and Ligresti et al. [30] demonstrated that CBD exerted anti-proliferative effects on rat thyroid KiMol cells, transformed with the v-K-ras oncogene. This effect of CBD was associated with a cell cycle block at the G1/S phase transition, as well as the induction of apoptosis.

CBD and endocrine tumours

In 2006 Ligresti et al. [30] demonstrated for the first time that CBD potently and selectively inhibited the growth of different breast tumour cell lines (MCF7, MDA-MB-231), with an IC50 of about 6 µ m , and exhibited significantly lower potency in non-cancer cells. CBD and CBD-rich extracts (containing approximately 70% CBD together with lesser amounts of other cannabinoids) also inhibited the growth of xenografts, obtained by s.c. injection into athymic mice of human MDA-MB-231 cells, and reduced infiltration of lung metastases derived from intrapaw injection of breast carcinoma cells. Among the possible cellular and molecular mechanisms underlying these effects, CBD seemed to involve direct TRPV1 activation and/or CB2 indirect activation (via FAAH), as well as induction of oxidative stress. Later on, McAllister’s group [31] demonstrated that, besides proliferation, CBD also interfered with two other crucial steps of breast cancer cell progression, invasion and metastasization. Among the three different groups of cannabinoid compounds tested (phytocannabinoids with affinity for CB1 and CB2 receptors, phytocannabinoids with no appreciable affinity for CB1 and CB2 receptors and synthetic compounds with affinity for CB1 and CB2 receptors), CBD was shown to be one of the most effective inhibitors of human breast cancer cell proliferation, being equipotent to Δ 9 -THC and CP55940 in inhibiting, respectively, MDA-MB-231 and MDA-MB-436 cell growth, and being the most potent inhibitor of the MDA-MB-231 cell migration. Interestingly, CBD regulated the expression of key genes involved in the control of cell proliferation and invasion through the downregulation of Id-1 expression, an inhibitor of basic helix-loop-helix transcription factors, whose overexpression in breast cancer cells is responsible for proliferation, migration and invasion. Therefore, the ability of CBD to decrease significantly Id-1 expression in breast cancer cells was associated with its efficacy in reducing tumour aggressiveness.

Angiogenesis consists of the formation of new blood vessels from pre-existing ones and represents another promising therapeutic target for cancer therapy. Collectively, cannabinoids have been demonstrated to act as anti-angiogenic factors by disposing tumour cells to decrease the production of pro-angiogenic factors and/or by direct modulation of endothelial cells [27].

However, the clinical use of Δ 9 -THC and additional synthetic agonists is often limited by their unwanted psychoactive side effects, and for this reason interest in non-psychoactive phytocannabinoids, such as CBD, has substantially increased in recent years. Interestingly CBD has no psychotropic activity and, although it has very low affinity for both CB1 and CB2 receptors, it has been recently reported to act with unexpectedly high potency in vitro as antagonist of CB1 receptors in the mouse vas deferens [28] and brain [29] tissues. Additionally, CBD displays inverse agonism at human CB2 receptors [29]. Moreover, other putative molecular targets of CBD are TRPV, 5-HT1A, GPR55 and PPARγ receptors (see Figure 2 ). Besides its beneficial effects in the treatment of pain and spasticity and other CNS pathologies, several reports demonstrated that CBD possesses antiproliferative, pro-apoptotic effects and inhibits cancer cell migration, adhesion and invasion.

Physiological or pathological stimuli induce synthesis and release of endocannabinoids, which can subsequently activate cannabinoid receptors. Therefore eCBs are synthesized and released ‘on demand’ through the cleavage of membrane phospholipid precursors.