Charles Hemenway, MD, PhD
Ronald McDonald House Charities
Endowed Professor in Pediatric
Gene Regulation and Epigenetics
Dr. Hemenway received his medical degree from the University of Massachusetts Medical School. He completed a combined residency in Internal Medicine and Pediatrics at the University of Florida in Gainesville after which he began fellowship training in Pediatric Hematology/Oncology at Duke University. During the course of fellowship training, he developed an active interest in basic research and remained at Duke for five years where he received a Ph.D. in Genetics.
In 1996, he joined the Department of Pediatrics at Tulane University in New Orleans. There, he established a research laboratory while participating actively in clinical care and medical education. He focused his research on acute leukemias characterized by rearrangements of the MLL gene with a specific interest in developing small molecule inhibitors of abnormal MLL gene products.
In 2007, he moved to Loyola University where he was named the Ronald McDonald Charities Professor of Pediatric Hematology/Oncology. His work in the Oncology Institute of the Cardinal Bernardin Cancer Center continues to center on the rational design of inhibitors of MLL leukemias.
- Hemenway, C.S., de Erkenez, A.C., Gould, C.G.D.: The Polycomb protein MPc3 interacts with AF9, an MLL fusion partner in t(9;11)(p22;q23) acute leukemias. Oncogene 20:3798-3805, 2001.
- Srinivasan, R.S., de Erkenez, A.C., Hemenway, C.S.: The Mixed Lineage Leukemia fusion partner AF9 binds specific isoforms of the BCL-6 corepressor. Oncogene 22:3395-3406, 2003.
- Erfurth, F., Hemenway, C.S., de Erkenez, A.C., Domer, P.H.: MLL fusion partners AF4 and AF9 interact at subnuclear foci. Leukemia 18:92-102, 2004.
- Srinivasan, R.S., Nesbit, J.B., Marrero, L., Erfurth, F., LaRussa V.F., Hemenway, C.S.: The synthetic peptide PFWT disrupts AF4-AF9 protein complexes and induces apoptosis in t(4;11) leukemia cells. Leukemia 18:1364-1372, 2004.
- Zhang, W., Xia, X., Reisenauer, M.R., Hemenway, C.S., Kone, B.C.: DOT1a-AF9 complex mediates histone H3 K79 hypermethylation and repression of ENaCalpha in an aldosterone-sensitive manner. J Biol Chem 281:18059-18068, 2006
- Palermo, C.M., Bennett, C.A., Winters, A.C., Hemenway, C.S.: The AF4-mimetic peptide, PFWT, induces necrotic cell death in MV4-11 leukemia cells. Leukemia Res 32:633-642, 2008
- Bennett, C.A., Winters, A.C., Barretto, N.N., Hemenway, C.S.: Molecular targeting of MLL-rearranged leukemia cell lines with the synthetic peptide PFWT synergistically enhances the cytotoxic effect of established chemotherapeutic agents (E-pub ahead of print, Leukemia Res, 2009 doi:10.1016/j.leukres.2009.01.018)
- Lin, J.J., Hemenway, C.S.: Hsp90 directly modulates the spatial distribution of AF9/MLLT3 and affects
target gene expression. J Biol Chem 285:11966-11973, 2010. PMID: 20159978
- Chang, M-J., Wu, H., Achille, N.J., Reisenauer, M.R., Chou, C-W., Zeleznik-Le, N.J. , Hemenway, C.S.*,
Zhang, W.*: The Histone H3 Lysine 79 Methyltransferase Dot1 is Required for Immortalization by MLL Oncogenes. (*Co-corresponding authors) Cancer Res 70:10324-10242, 2010.