ROCKVILLE, MD - A trio of papers co-authored by four National Foundation for Cancer Research (NFCR) scientists has been published this week in highly-cited and respected journals. Each acknowledges NFCR support as having helped make the works possible.
Rakesh K. Jain, Ph.D., and colleagues detail new knowledge on the interaction of brain cancers, blood vessels and tumor microenvironments, specifically a mechanism by which gliomas resist anti-angiogenesis drugs. The discoveries offer additional insight into why glioblastoma multiforme (GBM), the deadliest form of brain cancer, has to-date remained so notoriously difficult to treat, while too potentially paving the way for future therapeutic approaches that account for these findings.
"I had presented some exciting data on vessel cooption in glioblastoma multiforme at the NFCR scientific symposium in August 2017," stated Jain, an NFCR fellow. "Our paper based on that work--supported by the Foundation--has now been published in Cancer Cell."
The article appears in the journal's issue dated May 14th--Monday.
Another paper specific to gliomas, both of whose corresponding authors, Webster K. Cavenee, Ph.D., and Paul B. Fisher, M.P.H., Ph.D., are closely associated with NFCR, too was published on Monday. Availed online in the Proceedings of the National Academy of Sciences, it identifies a connection between various cellular mechanisms associated with cancer and MDA-9/Syntenin, a gene previously discovered by Dr. Fisher, an NFCR fellow.
These findings are explicitly pertinent to better understanding and combating GBM, a cancer on which Dr. Cavenee, NFCR's scientific advisory board chairman, is an authority.
"We have effectively identified a potential Achilles' heel of glioblastoma multiforme that may allow exploitation to uncover enhanced therapies with improved prognosis," summarized Fisher. "In these contexts, MDA-9/Syntenin may provide a viable and effective therapeutic strategy for GBM."
Lastly, Paul Schimmel, Ph.D., co-authored a paper published online today in Nature which advances understanding of mistranslation--errors in the interpretation of genetic information. Dr. Schimmel, an NFCR fellow, is one of the world's leading experts in the field. The mouse model findings outlined in the article, while pertinent well beyond only cancer research, offer new insight into somatic mutations. These, according to the National Cancer Institute's dictionary of cancer terms, are described as such:
an alteration in DNA that occurs after conception. Somatic mutations can occur in any of the cells of the body except the germ cells (sperm and egg) and therefore are not passed on to children. These alterations can (but do not always) cause cancer or other diseases.
"Although a cancer investigation was not pursued in this paper," noted Schimmel, speaking of the Nature piece, "I believe mistranslation can be a course of somatic mutations that lead to cancers."