Groundbreaking study in the field of chemotherapy neuropathy

Development of new drugs aimed at targeting enzymes responsible for the accumulation of tubulin D2 in sensory neurons in order to reduce neuropathic damage.

Paving the way is the groundbreaking study in the field of peripheral neuropathies carried out thanks to a research project developed by Maria Elena Pero, a researcher in the Department of Veterinary Medicine and Animal Production at theUniversity of Naples Federico II, and Francesca Bartolini, an associate professor in the Department of Pathology and Cell Biology at Columbia University in New York.

The work has, in fact, shown that Bortezomib -Bort, a chemotherapeutic drug used to treat blood cancers, including multiple myeloma, which also induces peripheral neuropathy, promotes the selective accumulation of delta tubulin 2 (D2) in sensory neurons and that this accumulation causes peripheral nerve degeneration. A key finding that may promote the production of drugs that specifically target delta 2 by reducing its accumulation in sensory neurons in order to decrease neuropathic damage.

The importance of this study is demonstrated by the fact that no drugs exist to combat this condition that can affect 40 percent of patients being treated for multiple myeloma. Understanding the mechanisms underlying the pathogenesis is critical to minimize, in cancer survivors, the side effects caused by chemotherapy treatment.

The study also involved the University of Milan Bicocca, Pennsylvania State University, the Zuckerman Mind Brain Behaviour Institute and the Department of Neurology at Columbia University.

The work was published in the journal PNAS - Proceedings of the National Academy of Sciences through the article "Pathogenic role of D2-tubulin in Bortezomib Induced Peripheral Neuropathy."

Chemotherapy-induced peripheral neuropathy (CIPN) is a debilitating form of neuropathy characterized by degeneration of peripheral nerves observed in cancer patients undergoing chemotherapy, resulting in pain and impaired sensory and motor perception of body extremities. The pathogenetic mechanisms of CIPN are largely unknown, which is why there is no therapeutic strategy that can reduce or prevent these symptoms, due to which there is often a need to discontinue therapy with serious consequences for the patient.