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Molecular and Cellular Biosciences at Wake Forest University

Wake Forest University Graduate School » Molecular and Cellular Biosciences

Elizabeth Alli, PhD

Elizabeth Alli, PhD
Education & Training 
B.S., Exercise Science (major) /Chemistry (minor)
University of Southern California, 1995
M.S., Molecular and Cellular Pharmacology
Rutgers University-Biomedical and Health Sciences, 2002
Ph.D., Molecular and Cellular Pharmacology
Rutgers University-Biomedical and Health Sciences, 2006
Postdoctoral Fellow, Medicine-Oncology
Stanford University-School of Medicine, 2011
Professional Affiliations
American Association for Cancer Research
American Association for the Advancement of Science
AACR-Women in Cancer Research
AACR- Chemistry in Cancer Research Working Group
American Society of Clinical Oncology


Oxidative DNA damage, which is generated endogenously by normal biological processes, is typically repaired by the DNA base-excision repair (BER) pathway.  Cells with defective BER tend to accumulate excessive oxidative DNA damage, which leads to mutagenesis, genetic instability, and ultimately, tumorigenesis.  My lab investigates and manipulates such tumorigenic mechanisms for purposes of cancer chemoprevention and targeted therapy.

alliOur main focus is on triple-negative breast cancers which are named for their lack of expression of estrogen receptor, progesterone receptor, and HER2/NEU.  They often encompass hereditary breast cancers due to germline mutations in the Breast Cancer Susceptibility Gene 1 (BRCA1).  Collectively, triple-negative breast cancers associate with an aggressive clinical course and are relatively insensitive to existing drugs available via precision medicine, and thus, are in need of more effective anti-cancer strategies.

Tumorigenic Mechanisms

Triple-negative breast cancer cells have been shown to exhibit a defective BER phenotype that results in elevated levels of oxidative DNA damage.  We are working to specify the molecular defects that produce this phenotype as well as identifying other malignancies that display it.  The purpose of this project is to gain a better understanding of tumorigenic mechanisms and to identify potential targets for new anti-cancer drugs.

Cancer Chemoprevention

BRCA1 is gaining attention for its role in repair of oxidative DNA damage by BER, and when mutated or deficient, produces a defective-BER phenotype.  Given that mutations in BRCA1 significantly lead to the development of breast, ovarian, and other cancers, it seems feasible to circumvent defective BER to prevent tumorigenesis.  We are currently developing a new class of drugs termed “DNA-repair activating agents” that reduce levels of oxidative DNA damage and impede tumorigenesis by enhancing base-excision repair.  These drugs are anticipated to be the first chemoprevention agents that target BRCA1-mutated cancers.

Targeted Therapy

Agents that lend to excessive amounts of DNA damage may overwhelm defective DNA repair systems in cancer cells and force death pathways.  We are in the process of discovering novel therapeutic agents that inhibit the BER pathway or that increase levels of oxidative DNA damage beyond a viable threshold for selective targeting of cancers with a defective-BER phenotype.  Our current efforts focus on treatment regimens that are better-targeted for triple-negative breast cancers.


Alli E and Ford JM.  BRCA1: Beyond double-strand break repair.  DNA Repair 2015 Aug;32:165-71.
Alli E and Ford JM.  A movement toward cancer prevention.  Molecular & Cellular Oncology 2015, 2:3, e979685. []
Alli E, Solow-Cordero DE, Casey SC, Ford JM.  Therapeutic targeting of BRCA1-mutated breast cancers with agents that activate DNA Repair.  Cancer Res 2014 Nov 1;74(21):6205-15.
Vinayak S, Schwartz E, Jensen K, Lipson J, Alli E, McPherson L, Sharma VB, Sanderso AS, Mills MA, Schackmann EA, Telli ML, Kardashian A, Ford JM, and Kurian AW.  A clinical trial of lovastatin for modification of biomarkers associated with breast cancer risk.  Breast Cancer Res Treat 2013 Nov;142(2):389-98.
Alli E and Ford JM. Breast cancers with compromised DNA repair exhibit selective sensitivity to elesclomol. DNA Repair 2012 May 1;11(5):522-4.
Alli E, Sharma VB, Hartman AR, Lin PS, and Ford JM.  Enhanced sensitivity to cisplatin and gemcitabine in Brca1-deficient murine mammary epithelial cells.  BMC Pharmacology 2011 July 19; 11(7): 1-12
Hastak K, Alli E, and Ford JM.  Synergistic chemosensitivity of triple-negative breast cancer cell lines to poly(ADP-Ribose) polymerase inhibition, gemcitabine, and cisplatin.  Cancer Res 2010 Oct; 70(20):7970-80.
Alli E, Sharma VB, Sunderesakumar P, and Ford JM.  Defective repair of oxidative DNA damage in triple-negative breast cancer confers sensitivity to inhibition of poly(ADP-ribose) polymerase.  Cancer Res 2009 April; 69(8): 3589-96.
Alli E, Yang J-M, Ford JM, and Hait WN.  Reversal of stathmin-mediated resistance to paclitaxel and vinblastine in human breast carcinoma cells.  Mol Pharmacol 2007 May; 71(5): 1233-40.
Hait WN, Rubin E, Alli E, and Goodin S.  Tubulin targeting agents.  Update Cancer Ther 2007 March; 2(1): 1-18.
Alli E, Yang J-M, and Hait WN.  Silencing of stathmin induces tumor-suppressor function in breast cancer cell lines harboring mutant p53.   Oncogene 2007 Feb 15; 26(7): 1003-12.
Alli E, Bash-Babula J, Yang J-M, and Hait WN.  Effect of stathmin on the sensitivity to antimicrotubule drugs in human breast cancer.  Cancer Res 2002 Dec 1; 62(23): 6864-9.
Bash-Babula J, Toppmeyer D, Labassi M, Reidy J, Orlick M, Senzon, R, Alli E, Kearney T, August D, Shih W, Yang J-M, and Hait WN.  A phase I/pilot study of sequential doxorubicin/vinorelbine: effects on p53 and microtubule-associated protein 4.  Clin Cancer Res 2002 May; 8(5): 1057-64.
BIS(Thiohydrazide Amide) Compounds for Treating Cancers.  U.S. Patent Application PCT/US2013/020257, filed January 2013.
Modulation of Cellular DNA Repair Activity to Intercept Malignancy.  U.S. Patent Application PCT/US2014/23351.  U.S. Serial No. 14/774,623, filed March 2014; Israel Serial No. 241401, filed March 2014; European Serial No. 14778577.8, filed March 2014