This is not a comprehensive list, simply some articles I have found along the way.

Not only does excess glutamate (dietary sources, immune activation, inflammation, etc) contribute to cancer development, but it is a primary cause of cancer growth and metastasis. Glutamate is utilized by cancer cells as a sort of “food/energy source” to allow cancer growth. Additionally, cancer cells secrete high levels of glutamate (excitotoxic), which excites nearby cells until they die off, allowing room for cancer cells to grow and proliferate. This recent study indicates that cancer cells are essentially scavenging for additional glutamate and a newly discovered reservoir of glutamate may actually contribute to the feeding cancer cells. By blocking this reservoir of glutamate, cancer growth may slow.  A simple google search of “______ cancer & glutamate” will often result in several published research articles confirming the connection

“A growing number of researchers are finding that stimulating these glutamate receptors can cause cancer cells to grow much faster and become more invasive — and therefore more deadly. This mechanism was first found in brain tumors, but now is known to affect many other types of cancer. Some of these cancers actually secrete high concentrations of glutamate themselves, which in turn stimulates their cells to grow and invade even more aggressively.” “Of particular concern is the finding that stimulating certain glutamate receptors can convert normal cells into cancer cells.” “If a person already has a cancer, the glutamate additives in food will make the cancer much more aggressive and more likely to kill.”
http://www.newsmax.com/…/Dr-B…/article/2012/06/07/id/482880/

“Chronic inflammation appears to be a major initiating mechanism in most human cancers, involving cell-signaling pathways, which are responsible for cell cycling, cancer cell migration, invasion, tumor aggressiveness, and angiogenesis. It is less well appreciated that glutamate receptors also play a significant role in both proliferation and especially glioma invasion. There is some evidence that sustained elevations in glutamate may play a role in initiating certain cancers and new studies demonstrate an interaction between inflammation and glutamate receptors that may enhance tumor invasion and metastasis by affecting a number of cell- signaling mechanisms.” http://www.talkingaboutthescience.com/stud…/Blaylock2012.pdf

“Research into the role of Glu signaling in cancer development and progression is still in its infancy; however, important progress has been made in recent years. Considerable evidence exists and indicates that glutamate plays an important role in tumor development, acting as a growth factor and a signal mediator in neural as well as non-neuronal tumors tissues, in both autocrine and paracrine fashions. It has been proven that its actions involve mainly a family of receptors consisting of metabotropic glutamate receptors and ionotropic glutamate receptors whose presence has been proven in a variety of benign and malignant lesions throughout the body.” https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4133641/

“They noted that targeting both GCPII and glutaminase, the enzyme that converts glutamine to glutamate, resulted in a more substantial tumor reduction in patient-derived pancreatic cancer tumors implanted in pancreas of mice, since it attacked the production of glutamate from both glutamine and from NAAG.  Seven years ago, we found that glutamine was a big deal in cancer metabolism, and inhibiting the conversion of glutamine to glutamate was the right target to curb cancer growth,” Le says. “It turns out, that’s correct. But it’s not enough, because cancer cells have another way to make glutamate through this hidden reservoir. Targeting both pathways could improve cancer treatments,” she adds.” https://www.eurekalert.org/pub_releases/2019-04/jhm-hri042319.php

“Glutamate dehydrogenase (GDH) is a key enzyme that catalyzes the final reaction of the glutamine metabolic pathway, and has been reported implicated in tumor growth and metastasis.” https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4490642/

“Cancer cells can occur in various tissues throughout the body and involves abnormal metabolic activity with the ability to invade other cells. Aberrant glutamatergic signaling (signaling involving glutamate) can lead to tumorigenesis and is likely the mechanism leading to many cancers[i],[ii],[iii] With a release of excess glutamate from cancer cells, nearby cells will either die or be transformed to participate in increased glutamatergic signaling through its increase in glutamate receptor expression. In this way, cancer cells invade normal tissues and transform normal cell signaling.[iv] Inflammation is mediated in part through glutamatergic signaling. At elevated levels, glutamate can initiate inflammation through activation of glial cells, a type of nerve cell.[v] The glial cells then participate in cascading this glutamate stress signal throughout the body, particularly the brain, leading to chronic inflammation if glutamate levels remain elevated. Chronic inflammation leads to increased risk of cancer[vi] and a major under appreciated link is the role glutamate plays in these pathways. https://unblindmymind.org/2015/01/cancer-and-glutamate/

“Although these mechanisms are still being investigated, the inhibition of the mitogen-activated protein kinase pathway was shown to play a key role in the antiproliferative activity of iGluR antagonists. Importantly, MK-801, a NMDAR channel blocker, was effective and well tolerated in animal models of melanoma, lung, and breast cancers, suggesting that the blockade of iGluR signaling may represent a new strategy for cancer treatment. In this review, we focus on the significance of NMDA and AMPA receptor expression in tumor cells, as well as possible therapeutic strategies targeting these receptors.” https://www.ncbi.nlm.nih.gov/pubmed/27586965

“Cancer cell lines release glutamate into the extracellular environment”
https://link.springer.com/article/10.1007/s10585-009-9277-4

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