Halloween: a “mad scientist”

Amanda K. Ashley, Ph.D.

Assistant Professor

Department of Chemistry and Biochemistry

P.O. Box 30001 MSC 3C

New Mexico State University

Las Cruces, NM


About the Research: Dr. Ashley’s research focuses on replication of genetic information, a fundamental biological process common to all living organisms, and maintenance of its integrity. DNA repair systems protect cells from damage caused by numerous intrinsic and extrinsic sources, thereby helping to maintain genome integrity. The genome is particularly vulnerable during DNA replication, and a growing body of evidence supports a nexus between replication and repair factors that act in complex enzymatic and signaling networks in response to DNA damage-induced replication stress. Various proteins have been identified during the last decade that function to stabilize and restart stalled replication forks, and restart collapsed forks. Many of these proteins have well-defined roles in DNA double-strand break repair, including homologous recombination (HR) repair, nonhomologous end-joining (NHEJ) and/or DNA damage checkpoint signaling. Dr. Ashley’s research centers on understanding perturbations in DNA replication and repair to elucidate cancer etiology and provide novel targets for chemotherapeutic interventions.

Current Research:

Currently, the lab is conducting research on three projects:

  • SENSITIZING TRIPLE NEGATIVE BREAST CANCER TO DOXORUBICIN: The project focuses on researching mechanisms to sensitize triple negative breast cancer (TBNC) cells to doxorubicin. TNBC is a clinical subtype disproportionately fatal to women of African American and Latina descent, in part due to the resistance they develop to the chemotherapeutic agent, doxorubicin. Our goal, in collaboration with Chris Kemp at the Fred Hutchinson Cancer Research Center in Seattle, is to elucidate new targets in this highly fatal breast cancer subtype.
  • EXPLOITING DNA REPAIR DEFICIENCIES FOR BREAST CANCER TREATMENT: This project aims to elucidate how a DNA repair protein involved in nonhomologous end-joining may alter the cellular response to replication stress, specifically stress induced by FDA-approved chemotherapeutic compounds. The hope is that understanding and exploiting cancer cell redundancies and dependencies will provide novel therapeutic strategies.
  • DISCERNING THE INTERPLAY OF DNA-PK AND CTCF IN CANCER: As with the NM-INBRE project, we are assessing how nonhomologous end-joining proteins may affect the cellular response to replication stress, however in this project, we actually focus on a different protein than is the focus of NM-INBRE.