The word cancer is derived from the Latin word for crab because cancers are often very irregularly shaped, and because, like a crab, they “grab on and don’t let go.” The term cancer specifically refers to a new growth which has the ability to invade surrounding tissues, metastasize (spread to other organs) and which may eventually lead to the patient’s death if untreated. The terms tumor and cancer are sometimes used interchangeably which can be misleading. A tumor is not necessarily a cancer. The word tumor simply refers to a mass. For example, a collection of fluid would meet the definition of a tumor. A cancer is a particularly threatening type of tumor. It is helpful to keep these distinctions clear when discussing a possible cancer diagnosis.
Neoplasm– A neoplasm is an abnormal new growth of cells. The cells in a neoplasm usually grow more rapidly than normal cells and will continue to grow if not treated. As they grow, neoplasms can impinge upon and damage adjacent structures. The term neoplasm can refer to benign (usually curable) or malignant (cancerous) growths.
Tumor– A tumor is a commonly used, but non-specific, term for a neoplasm. The word tumor simply refers to a mass. This is a general term that can refer to benign (generally harmless) or malignant (cancerous) growths.
Benign tumor– Benign tumors are non-malignant/non-cancerous tumor. A benign tumor is usually localized, and does not spread to other parts of the body. Most benign tumors respond well to treatment. However, if left untreated, some benign tumors can grow large and lead to serious disease because of their size. Benign tumors can also mimic malignant tumors, and so for this reason are sometimes treated.
Malignant tumor– Malignant tumors are cancerous growths. They are often resistant to treatment, may spread to other parts of the body and they sometimes recur after they were removed.
Cancer– A cancer is another word for a malignant tumor (a malignant neoplasm).
I use ResearchGate for Research like this just because you do not have to pay to read their papers if they are the ones hosting it. Sometime they will redirect you to other Research Journals,but any paper they host is free. Most of the cures are based on the findings of FAAH Inhibitors, and the actions of Fatty Acids in the brain, and Fatty Acid is the FA in FAAH. The H in FAAH is Hydroxylase, FAAH is an enzyme that messes with the Hydrogen atoms hanging off of Fatty Acids. And an FAAH Inhibitor inhibits that action, allowing the Hydrogen to go unscathed. The cures are not themselves FAAH Inhibitors, but have come along within the scope of the same research as FAAH Inhibitors. The reason Fatty Acids are important is because they create new molecules in your brain that attach to receptors like the CB1 and CB2 receptors, and the CB2 receptor is the receptor that most effectively helps cure or prevent Tumors and Cancer.
“Changes in lipid metabolism are intimately related to cancer. Several classes of bioactive lipids play roles in the regulation of signaling pathways involved in neoplastic transformation and tumor growth and progression. The endocannabinoid system, comprising lipid-derived endocannabinoids, their G-protein-coupled receptors (GPCRs), and the enzymes for their metabolism, is emerging as a promising therapeutic target in cancer… A significant number of studies have been performed to clarify the biological role of the ECS, its regulatory functions in health and disease, and the potential of its pharmacological exploitation. The ECS comprises two GPCRs, CB1 and CB2”
“Saturated fatty acids can be used to: boost the immune system, for weight management, as antimicrobials, to support the structure of gut mucosa, and as dietary adjuncts in cases of chronic degenerative disease, such as cardiovascular disease, liver disease and cancer.”
“Similarities between effects of cannabinoids-endocannabinoids, omega-3 LCPUFA and CLAs/CLnAs as anti-inflammatory, antiangiogenic, anti-invasive anti-cancer agents indicate common signalling pathways. Evidence in vivo and in vitro shows EPA and DHA can form endocannabinoids that: (i) are ligands for CB(1/2) receptors and possibly TRPV-1, (ii) have non-receptor mediated bioactivity, (iii) induce cell cycle arrest, (iii) increase autophagy and apoptosis, and (iv) augment chemotherapeutic actions in vitro.”
https://www.researchgate.net/publication/51924103_Cannabidiol_inhibits_lung_cancer_cell_invasion_and_metastasis_via_intercellular_adhesion_molecule-1 “This study investigates the role of intercellular adhesion molecule-1 (ICAM-1) within this action. In the lung cancer cell lines A549, H358, and H460, cannabidiol (CBD; 0.001-3 μM) elicited concentration-dependent ICAM-1 up-regulation compared to vehicle via cannabinoid receptors, transient receptor potential vanilloid 1, and p42/44 mitogen-activated protein kinase. Up-regulation of ICAM-1 mRNA by CBD in A549 was 4-fold at 3 μM, with significant effects already evident at 0.01 μM. ICAM-1 induction became significant after 2 h, whereas significant TIMP-1 mRNA increases were observed only after 48 h. Inhibition of ICAM-1 by antibody or siRNA approaches reversed the anti-invasive and TIMP-1-upregulating action of CBD and the likewise ICAM-1-inducing cannabinoids Δ(9)-tetrahydrocannabinol and R(+)-methanandamide when compared to isotype or nonsilencing siRNA controls. ICAM-1-dependent anti-invasive cannabinoid effects were confirmed in primary tumor cells from a lung cancer patient. In athymic nude mice, CBD elicited a 2.6- and 3.0-fold increase of ICAM-1 and TIMP-1 protein in A549 xenografts, as compared to vehicle-treated animals, and an antimetastatic effect that was fully reversed by a neutralizing antibody against ICAM-1 [% metastatic lung nodules vs. isotype control (100%): 47.7% for CBD + isotype antibody and 106.6% for CBD + ICAM-1 antibody]. Overall, our data indicate that cannabinoids induce ICAM-1, thereby conferring TIMP-1 induction and subsequent decreased cancer cell invasiveness.”
https://www.researchgate.net/publication/5892365_Cannabinoids_and_Gliomas “…inhibit the growth of different types of tumor cells, including glioma cells, in laboratory animals. They do so by modulating key cell signaling pathways, mostly the endoplasmic reticulum stress response, thereby inducing antitumoral actions such as the apoptotic death of tumor cells and the inhibition of tumor angiogenesis.”
Melanoma (Skin Cancer)
https://www.researchgate.net/publication/221975902_Revisiting_CB1_Receptor_as_Drug_Target_in_Human_Melanoma “Previous studies have indicated the antitumoral effect of human melanocytes, human melanoma cell lines expressing CB1 receptor (CB1), and of the peritumoral administration of endocannabinoids. In the present study, we systematically screened several human melanoma cell lines for the expression of CNR1 and demonstrated transcription of the authentic gene. The product of CNR1, the CB1 protein, was found localized to the cell membrane as well as to the cytoskeleton. Further, the studied human melanoma cell lines expressed functional CB1 since physiological and synthetic ligands, anandamide (AEA), Met-F-AEA, ACEA and AM251 showed a wide range of biological effects in vitro, for example anti-proliferative, proapoptotic and anti-migratory. More importantly, our studies revealed that systemic administration of a stable CB1 agonist, ACEA, into SCID mice specifically inhibited liver colonization of human melanoma cells. Since therapeutic options for melanoma patients are still very limited, the endocannabinoid-CB1 receptor system may offer a novel target.”
“Two major enzymes have been cloned and investigated thoroughly: fatty acid amide hydrolase (FAAH) and monoacylglycerol lipase (MAGL). Inhibitors of these enzymes have demonstrated therapeutic benefit in animal models of several disorders, including neuropathic pain, anxiety and inflammatory bowel diseases, as well as against the proliferation and migration of cancer cells. This review describes the major biochemical properties of FAAH and MAGL, and the design and pharmacological properties of inhibitors of these enzymes.”