Dawn S Chandler, PhD

College

College of Medicine

Department/Division

Pediatrics

Academic Title

Assoc Professor

Research Program

Molecular Biology and Cancer Genetics

Research Interest

Cancer, Muscular Atrophy, Spinal, Rhabdomyosarcoma, DNA Damage, Breast Cancer, Loss of Heterozygosity, Anoxia, Carcinoma, Renal Cell, von Hippel-Lindau Disease, Myopathies, Structural, Congenital

Dawn Chandler, PhD, is a member of the Molecular Biology and Cancer Genetics Program at the OSUCCC – James, where her work focuses on the regulation of pre-mRNA splicing and how its disruption can lead to pediatric diseases such as cancer.

In one recent study, her team’s research identified for the first time a clear mechanism for regulating damage-induced oncogene MDM2 splicing. The work offers potential strategies for manipulating MDM2 expression via splicing modulation.

Dr. Chandler has co-authored numerous articles in well-respected publications, including Human Molecular Genetics, Nucleic Acids Research and the Journal of Biological Chemistry.

Education and Background

Office Location

WA5023 Columbus Children's Research Institute

700 Children's Drive, Columbus, OH 43205

614-722-5302

614-722-5895

Dawn.Chandler@nationwidechildrens.org;chandler.135@osu.edu

Publications

A novel mouse model of rhabdomyosarcoma underscores the dichotomy of MDM2-ALT1 function in vivo.

Sanford BL, Bebee TW, Chandler DS, Boyaka P, Goodwin AK, Comiskey DF Jr, La Perle K, Tapia-Santos AS, Montes M, Matsa E, Jacob AG, Steiner H, Grieves J

Oncogene 37 95-106 01/04/2018
SMN regulation in SMA and in response to stress: new paradigms and therapeutic possibilities.

Dominguez CE, Cunningham D, Chandler DS

Hum Genet in press 08/29/2017
Splicing factor SRSF1 negatively regulates alternative splicing of MDM2 under damage.

Comiskey DF Jr, Jacob AG, Singh RK, Tapia-Santos AS, Chandler DS

Nucleic Acids Res 43 4202-18 04/30/2015
The splicing factor FUBP1 is required for the efficient splicing of oncogene MDM2 pre-mRNA.

Jacob AG, Singh RK, Mohammad F, Bebee TW, Chandler DS

J Biol Chem 289 17350-64 06/20/2014
Stress-induced alternative splice forms of MDM2 and MDMX modulate the p53-pathway in distinct ways.

Jacob AG, Singh RK, Comiskey DF Jr, Rouhier MF, Mohammad F, Bebee TW, Chandler DS

PLoS One 9 e104444 01/01/2014
DEAR1 is a chromosome 1p35 tumor suppressor and master regulator of TGF-ß-driven epithelial-mesenchymal transition.

Lokken E, Chen J, Frazier ML, Sahin AA, Wistuba II, Sen S, Lott ST, Killary AM, Chen N, Balasenthil S, Reuther J, Frayna A, Wang Y, Chandler DS, Abruzzo LV, Rashid A, Rodriguez J, Lozano G, Cao Y

Cancer Discov 3 1172-89 10/01/2013
Stress-induced isoforms of MDM2 and MDM4 correlate with high-grade disease and an altered splicing network in pediatric rhabdomyosarcoma.

Jacob AG, O'Brien D, Singh RK, Comiskey DF Jr, Littleton RM, Mohammad F, Gladman JT, Widmann MC, Jeyaraj SC, Bolinger C, Anderson JR, Barkauskas DA, Boris-Lawrie K, Chandler DS

Neoplasia 15 1049-63 09/01/2013
miR-29 acts as a decoy in sarcomas to protect the tumor suppressor A20 mRNA from degradation by HuR.

Balkhi MY, Iwenofu OH, Bakkar N, Ladner KJ, Chandler DS, Houghton PJ, London CA, Kraybill W, Perrotti D, Croce CM, Keller C, Guttridge DC

Sci Signal 6 ra63 07/30/2013

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Dawn S Chandler, PhD

College

Department/Division

Academic Title

Research Program

Research Interest

Education and Background

Office Location

Publications

A novel mouse model of rhabdomyosarcoma underscores the dichotomy of MDM2-ALT1 function in vivo.

SMN regulation in SMA and in response to stress: new paradigms and therapeutic possibilities.

Splicing factor SRSF1 negatively regulates alternative splicing of MDM2 under damage.

The splicing factor FUBP1 is required for the efficient splicing of oncogene MDM2 pre-mRNA.

Stress-induced alternative splice forms of MDM2 and MDMX modulate the p53-pathway in distinct ways.

DEAR1 is a chromosome 1p35 tumor suppressor and master regulator of TGF-ß-driven epithelial-mesenchymal transition.

Stress-induced isoforms of MDM2 and MDM4 correlate with high-grade disease and an altered splicing network in pediatric rhabdomyosarcoma.

miR-29 acts as a decoy in sarcomas to protect the tumor suppressor A20 mRNA from degradation by HuR.

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Dawn S Chandler, PhD

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