Affiliation:
1. Department of Medical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02215, USA.
2. The Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA.
Abstract
Tumors put in a vulnerable position
Cancer cells often display alterations in metabolism that help fuel their growth. Such metabolic “rewiring” may also work against the cancer cells, however, by creating new vulnerabilities that can be exploited therapeutically. A variety of human tumors show changes in methionine metabolism caused by loss of the gene coding for 5-methylthioadenosine phosphorylase (MTAP). Mavrakis
et al.
and Kryukov
et al.
found that the loss of MTAP renders cancer cell lines sensitive to growth inhibition by compounds that suppress the activity of a specific arginine methyltransferase called PRMT5. Conceivably, drugs that inhibit PRMT5 activity could be developed into a tailored therapy for MTAP-deficient tumors.
Science
, this issue pp.
1208
and
1214
Funder
Novartis Institutes for BioMedical Research
Dr. Miriam and Sheldon G. Adelson Medical Research Foundation
Melanoma Research Alliance
NIH PO1 Research Program
Integrative Cancer Biology Program
Conquer Cancer Foundation
2014 AACR-Bristol-Myers Squibb Oncology Fellowship in Clinical Cancer Research
arin Grunebaum Cancer Research Foundation
National Center for Research Resources
National Center for Advancing Translational Sciences
NIH
Publisher
American Association for the Advancement of Science (AAAS)
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