Sarcosine (from Glycine metabolism), Arginine and Citrulline are endogenous compounds produced by muscle tissue/ meat, and they are also used as supplements. However, it would appear these compounds may promote cancer growth, especially in combination. A summary will be provided addressing these findings towards the end of the post.

https://pubmed.ncbi.nlm.nih.gov/11358107/

Because sarcosine can be nitrosated to form N-nitrososarcosine, a known animal carcinogen, these ingredients should not be used in cosmetic products in which N-nitroso compounds may be formed.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10023554/

NO itself is a non-effective nitrosating agent.

...NO can be activated by iodine to yield nitrosyl iodide.

...nitrosyl iodide, nitrosyl halides and nitrosonium salts are the most common commercially available reagents as nitrosating agents.

Alkyl nitrites are very powerful nitrosating agents...

Nitrosating agents, including sodium nitrite, nitrous acid, nitrous anhydride, and nitrosyl halides...

It seems the mixture of Iodine, Sarcosine and a NO-increasing compound (such as a PDE5I like Viagra/ Cialis, or Arginine/ Citrulline), can hypothetically generate carcinogenic N-nitrososarcosine. Iodine, like Sarcosine, Arginine, and Citrulline, is a common endogenous nutrient.

https://onlinelibrary.wiley.com/doi/10.1002/pros.23450

We identified that irrespective of the cell type, sarcosine stimulates up-regulation of distinct sets of genes involved in cell cycle and mitosis, while down-regulates expression of genes driving apoptosis. Moreover, it was found that in all cell types, sarcosine had pronounced stimulatory effects on clonogenicity.

Our comparative study brings evidence that sarcosine affects not only metastatic PCa cells, but also their malignant and non-malignant counterparts and induces very similar changes in cells behavior, but via distinct cell-type specific targets.

https://pubmed.ncbi.nlm.nih.gov/31050554/

Elevated sarcosine levels are associated with Alzheimer's, dementia, prostate cancer, colorectal cancer, stomach cancer and sarcosinemia.

https://www.mdpi.com/1422-0067/24/22/16367

N-methyl-glycine (sarcosine) is known to promote metastatic potential in some cancers; however, its effects on bladder cancer are unclear. T24 cells derived from invasive cancer highly expressed GNMT, and S-adenosyl methionine (SAM) treatment increased sarcosine production, promoting proliferation, invasion, anti-apoptotic survival, sphere formation, and drug resistance.

Immunostaining of 86 human bladder cancer cases showed that GNMT expression was higher in cases with muscle invasion and metastasis.

https://pubmed.ncbi.nlm.nih.gov/19212411/

Sarcosine, an N-methyl derivative of the amino acid glycine, was identified as a differential metabolite that was highly increased during prostate cancer progression to metastasis and can be detected non-invasively in urine. Sarcosine levels were also increased in invasive prostate cancer cell lines relative to benign prostate epithelial cells. Knockdown of glycine-N-methyl transferase, the enzyme that generates sarcosine from glycine, attenuated prostate cancer invasion. Addition of exogenous sarcosine or knockdown of the enzyme that leads to sarcosine degradation, sarcosine dehydrogenase, induced an invasive phenotype in benign prostate epithelial cells.

Due to the above, it's possible that the addition of sarcosine is not recommended for those at risk of cancer.

https://www.mdpi.com/2072-6694/13/14/3541

As a semi-essential amino acid, arginine deprivation based on biologicals which metabolize arginine has been a staple of starvation therapies for years. While the safety profiles for both arginine depletion remedies are generally excellent, as a monotherapy agent, it has not reached the intended potency.

It would appear as though arginine starvation has been utilized with moderate benefit in the treatment of cancer, though it's too weak as monotherapy and requires adjunct use of other drugs. The reasoning for this is multifaceted, as cancer relies on Arginine more than non-cancerous cells, Arginine promotes mTOR signaling, and as mentioned, Arginine's production of nitric oxide may promote carcinogenesis via multiple mechanisms, one of which being the nitrosation of sarcosine and other compounds.

https://pubmed.ncbi.nlm.nih.gov/38770826/

The proliferation, migration, invasion, glycolysis, and EMT processes of LC (lung cancer) cells were substantially enhanced after citrulline treatment.

In addition, animal experiments disclosed that citrulline promoted tumor growth in mice. Citrulline accelerated the glycolysis and activated the IL6/STAT3 pathway through the RAB3C protein, consequently facilitating the development of LC.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9637975/

L-citrulline showed its toxicity on HeLa (human cervix adenocarcinoma) cells in a dose-dependent manner.

L-citrulline also showed a migration inhibitory effect.

While L-Citrulline, appears to offer circumstantial benefit to human cervix adenocarcinoma cells, it promoted lung cancer and tumorigenesis in a different study. It may have other cancer-promoting effects, through its facilitation of Arginine and nitric oxide. L-Citrulline is better tolerated than L-Arginine.

https://sci-hub.se/https://link.springer.com/article/10.1007/BF01461047

The fact that a number of antioxidants can act as strong inhibitors of nitrosation in a variety of circumstances suggests that nitrosamine synthesis includes a free-radical intermediate. Some of the compounds involved, such as the gallates, are oxidisable phenols, which have been reported to stimulate nitrosation [12], probably through the intermediate formation of nitric oxide or nitrogen dioxide as effective nitrosating agents. This process could account for the stimulatory action of ascorbic acid that has been sometimes observed, since its interaction with nitrite has led to the production of oxides of nitrogen.

Using this technique, a number of antioxidants of both classes at a concentration of 2 mmol have inhibited strongly the formation of N-nitrosarcosine from 25 mmol-sarcosine and 25 mmol-nitrite.

Occasionally, the inhibitory effect of low levels of ascorbic acid on nitrosamine formation was converted into a stimulatory action at higher concentrations [7].

Nitrosation is effectively inhibited by various antioxidants, which indicates the process relies heavily on the presence of free radicals.

Summary

Sarcosine, Arginine, and to a lesser extent Citrulline can play a carcinogenic role under the right conditions, and that other dietary nutrients can influence this risk. The process of nitrosation leading to the formation of N-nitrososarcosine, seems possible when supplementing Sarcosine, and the co-application of Arginine, Citrulline, Vitamin C, or a PDE5 inhibitor should worsen this, in addition to facilitating endogenous N-nitrosodimethylamine (another extremely toxic carcinogen). Processed meat, which often contains nitrites and nitrates already, is well established to promote cancer. Antioxidants can inhibit nitrosation, which was shown with Vitamin C, although there was a bell curve observed wherein higher amounts of Vitamin C promoted nitrosation. This may relate to purported benefits of Vitamin C supplementation regarding cancer.

Sarcosine, Arginine, and to a lesser extent Citrulline may promote cancer through proliferation, however in the context of nitrosation, they may also contribute towards carcinogenesis and other maladies. Sarcosine aside, concern is warranted when using Arginine, Citrulline, and various PDE5 inhibitors without adjunct usage of an antioxidant (such as Carnosic Acid and Idebenone among others), given the process nitrosation with relevance to nitric oxide relies heavily on presence of free radicals.