Researchers discover novel cancer-promoting molecular mechanism

A novel cancer-promoting molecular mechanism has been discovered by Pierluigi Scalia, M.D., Ph.D., with his co-workers at the Sbarro Institute for Cancer Research and Molecular Medicine, Division of Biology, Temple University, the Department of Medical Biotechnologies at University of Siena, Italy and the Italian non-profit research organization ISOPROG, in collaboration with the Center of Biocomputational Sciences, part of the College of Science and Technology in Philadelphia.

The new discovery is described in a study published July 3, 2019 in the journal Oncogene, titled "Identification of a Novel EphB4 Phosphodegron Regulated by the Autocrine IGFII/IRA Axis in Malignant Mesothelioma."

This study identifies a new potential targetable oncogenic mechanism, since it shows how a previously studied tumor self-stimulating signal regulates the function of a molecule known as EphB4, directly involved in malignant cellular behavior such as cancer blood vessels formation, normal tissue invasion and distant site metastasis."

Pierluigi Scalia, M.D., Ph.D,Sbarro Institute for Cancer Research and Molecular Medicine

Scalia continues, "Interestingly, the key components of this newly identified molecular switch appear expressed in all malignant cancer cell lines studied, suggesting that the relevance of this mechanism might extend to many types of solid cancer, beyond mesothelioma."

According to professor Antonio Giordano, M.D., Ph.D., co-author of the study and director of the Sbarro Institute, "this type of discovery is critical for deadly cancers like Malignant Mesothelioma for which the search for new molecular targets is highly invoked in the medical field due to the growing demand for new treatments towards more effective and personalized interventions."

Source:
Journal reference:

Scalia, P. et al. (2019) Identification of a Novel EphB4 Phosphodegron Regulated by the Autocrine IGFII/IRA Axis in Malignant Mesothelioma. Oncogene. doi.org/10.1038/s41388-019-0854-y.

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