Critical information about the size and growth speed of gliomas
- Date:
- October 7, 2022
- Source:
- Mayo Clinic
- Summary:
- An important new clue for preventing and treating brain tumors known as gliomas has been identified. The study provides a rare window into the biological changes behind glioma development.
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An important new clue for preventing and treating brain tumors known as gliomas has been identified in research led by the Lunenfeld-Tannenbaum Research Institute (LTRI) at Mount Sinai Hospital in Toronto and Mayo Clinic Comprehensive Cancer Center and Mayo Clinic Center for Individualized Medicine. The study, published in the journal Science, provides a rare window into the biological changes behind glioma development.
Researchers found that animal models who carry a change in DNA known as germline alteration rs55705857 developed gliomas much more frequently -- and in half the time -- compared to animal models without the alteration. In addition to brain tumors, the findings are relevant to other cancers and diseases.
"While we understand much of the biologic function of germline alterations within genes that code for proteins, we know very little about the biologic function of germline alterations outside of genes that code for proteins. In some way, these germline alterations interact with other mutations in cells to accelerate tumor formation," says co-lead author Robert Jenkins, M.D., Ph.D., a genetics researcher at Mayo Clinic in Rochester. "Based on this new understanding of its mechanism of action, future research may lead to novel and specific therapies that target the rs55705857 alteration."
The study offers new knowledge that may help clinicians determine, pre-surgery, whether a patient has a glioma.
"We expected that rs55705857 would accelerate low-grade glioma development, but we were surprised by the magnitude of that acceleration," says co-lead author Daniel Schramek, Ph.D., a researcher at Lunenfeld-Tannenbaum Research Institute.
There are many alterations, likely thousands, outside of genes associated with the development of cancer and other diseases, but the mechanism of action is only understood for very few, Dr. Schramek says.
This study demonstrates that, with the tools of modern molecular/cell biology, it is possible to decipher much of the mechanism of action of such alterations.
Dr. Jenkins is a Ting Tsung and Wei Fong Chao Professor in Individualized Medicine Research and researcher in Mayo Clinic's Department of Laboratory Medicine and Pathology.
Dr. Schramek is a senior investigator and holds a Kierans & Janigan Research Chair at the LTRI and is an associate professor, Department of Molecular Genetics, Faculty of Medicine, University of Toronto.
Story Source:
Materials provided by Mayo Clinic. Original written by Kelley Luckstein. Note: Content may be edited for style and length.
Journal Reference:
- Connor Yanchus, Kristen L. Drucker, Thomas M. Kollmeyer, Ricky Tsai, Warren Winick-Ng, Minggao Liang, Ahmad Malik, Judy Pawling, Silvana B. De Lorenzo, Asma Ali, Paul A. Decker, Matt L. Kosel, Arijit Panda, Khalid N. Al-Zahrani, Lingyan Jiang, Jared W. L. Browning, Chris Lowden, Michael Geuenich, J. Javier Hernandez, Jessica T. Gosio, Musaddeque Ahmed, Sampath Kumar Loganathan, Jacob Berman, Daniel Trcka, Kulandaimanuvel Antony Michealraj, Jerome Fortin, Brittany Carson, Ethan W. Hollingsworth, Sandra Jacinto, Parisa Mazrooei, Lily Zhou, Andrew Elia, Mathieu Lupien, Housheng Hansen He, Daniel J. Murphy, Liguo Wang, Alexej Abyzov, James W. Dennis, Philipp G. Maass, Kieran Campbell, Michael D. Wilson, Daniel H. Lachance, Margaret Wrensch, John Wiencke, Tak Mak, Len A. Pennacchio, Diane E. Dickel, Axel Visel, Jeffrey Wrana, Michael D. Taylor, Gelareh Zadeh, Peter Dirks, Jeanette E. Eckel-Passow, Liliana Attisano, Ana Pombo, Cristiane M. Ida, Evgeny Z. Kvon, Robert B. Jenkins, Daniel Schramek. A noncoding single-nucleotide polymorphism at 8q24 drives IDH1 -mutant glioma formation. Science, 2022; 378 (6615): 68 DOI: 10.1126/science.abj2890
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