Evil serotonin (5-HT) strikes again. This time by being exposed as a potent tumor growth promoter. Cortisol is another one, contrary to what medicine says and practices in regards to cortisol, and considering cortisol and serotonin promote each other’s synthesis it is little surprise to see evidence of serotonin promoting tumor growth. While the study focused on only one tumor type, the authors explain that the mechanism of serotonylation is very generic and seen in most other tumor types, so the findings likely apply to all cancers. In corroboration, there have been quite a few recent publications demonstrating beneficial effects of the serotonin antagonist cyproheptadine in a wide variety of both solid and hematological malignancies. There is even a case study of terminal metastatic liver cancer in a human patient being completely cured by cyproheptadine in just 2 weeks. All in all, a damning verdict for serotonin and its promoters in Big Pharma, medical organizations, and public health agencies.
https://www.nature.com/articles/s41586-024-07751-z
https://www.bcm.edu/news/serotonin-producing-neurons-regulate-malignancy-in-ependymoma-brain-tumors
https://d.newswise.com/articles/serotonin-uptake-regulates-ependymoma-tumor-growth
“…Do neurons play a role in brain tumor growth and development? Scientists at St. Jude Children’s Research Hospital and Baylor College of Medicine have evidence showing that, for childhood ependymomas, they do. There are no targeted therapies available to treat ependymoma due in large part to a lack of understanding of the tumor microenvironment. By leveraging a recently developed murine model, scientists explored the interaction between ependymoma cells and surrounding neurons. They found that hyperactivation of a specific subset of neurons has different effects on tumor cell proliferation. Increased serotonin production in the tumor microenvironment drives tumor growth. The findings were published today in Nature.”
“…This is notably relevant for difficult to treat cancers, such as ependymoma, the third most common type of brain tumor in children. The present study offers fundamental insights into how ependymoma regulation is impacted by the surrounding neuronal environment. Ependymoma is associated with poor survival and neurocognitive outcomes due to a lack of available targeted therapies. A newly developed mouse model successfully mimics an aggressive form of the cancer caused by a gene fusion between ZFTA and RELA, which creates a rogue transcription factor that drives tumor growth. The model has allowed researchers, including Mack, to finally gain insight into the biology of the disease, the lack of which has stymied drug discovery efforts from the outset.”
“…The researchers found that in ependymoma, pathways involved in neuronal function and neurotransmission were enriched, implying not just a tumor neuronal interaction but a dependency. Further analysis of this link steered them towards serotonergic neurons, those responsible for producing the neurotransmitter serotonin. Enrichment of serotonin transporters within tumor cells implied that the tumor cells were foraging serotonin from their environment, but it was not clear why. “We found that serotonin added to histone proteins is a modification critical for ependymoma tumor growth,” added first author Hsiao-Chi Chen, Baylor College of Medicine.”
“…The researchers also demonstrated that the tumor cells can “talk back” to the neurons. “We’ve dissected some of the gene regulatory mechanisms in these tumors and seen how tumor cells secrete factors that modulate normal activity,” Mack said. “You lose control of factors you would normally release to inhibit hyperactivity. It’s a vicious loop where these cells are communicating with each other to drive tumor cell proliferation.” Identifying such a fundamental link between tumor neuronal communication and tumor proliferation may impact cancers beyond ependymoma. “Finding that histone serotonylation regulates tumorigenesis and that it’s being driven by neurons in the microenvironment is remarkable,” said Mack. “It could apply to other tumor types too.”
