- West Virginia University School of Pharmacy
- Pharmaceutical Sciences
Associate Director of Basic Research
- West Virginia University WVU Cancer Institute
- WVU Cancer Institute Administration
Co-Leader Alexander B. Osborn Hematopoietic Malignancy and Transplantation
Lori's top papers:
Stable and Potent Selenomab-Drug Conjugates.
Li X, Nelson CG, Nair RR, Hazlehurst L, Moroni T, Martinez-Acedo P, Nanna AR, Hymel D, Burke TR Jr, Rader C.
Cell Chem Biol. 2017 Apr 20;24(4):433-442.e6. doi: 10.1016/j.chembiol.2017.02.012. Epub 2017 Mar 16.
MTI-101 (cyclized HYD1) binds a CD44 containing complex and induces necrotic cell death in multiple myeloma.
Gebhard AW, Jain P, Nair RR, Emmons MF, Argilagos RF, Koomen JM, McLaughlin ML, Hazlehurst LA.
Mol Cancer Ther. 2013 Nov;12(11):2446-58. doi: 10.1158/1535-7163.MCT-13-0310. Epub 2013 Sep 18.
A preclinical assay for chemosensitivity in multiple myeloma.
Khin ZP, Ribeiro ML, Jacobson T, Hazlehurst L, Perez L, Baz R, Shain K, Silva AS.
Cancer Res. 2014 Jan 1;74(1):56-67. doi: 10.1158/0008-5472.CAN-13-2397. Epub 2013 Dec 5.
Potentiation of Nilotinib-mediated cell death in the context of the bone marrow microenvironment requires a promiscuous JAK inhibitor in CML.
Nair RR, Tolentino JH, Argilagos RF, Zhang L, Pinilla-Ibarz J, Hazlehurst LA.
Leuk Res. 2012 Jun;36(6):756-63. doi: 10.1016/j.leukres.2011.12.002. Epub 2011 Dec 30.
Acquisition of resistance toward HYD1 correlates with a reduction in cleaved α4 integrin expression and a compromised CAM-DR phenotype.
Emmons MF, Gebhard AW, Nair RR, Baz R, McLaughlin ML, Cress AE, Hazlehurst LA.
Mol Cancer Ther. 2011 Dec;10(12):2257-66. doi: 10.1158/1535-7163.MCT-11-0149. Epub 2011 Oct 6.
HYD1-induced increase in reactive oxygen species leads to autophagy and necrotic cell death in multiple myeloma cells.
Nair RR, Emmons MF, Cress AE, Argilagos RF, Lam K, Kerr WT, Wang HG, Dalton WS, Hazlehurst LA.
Mol Cancer Ther. 2009 Aug;8(8):2441-51. doi: 10.1158/1535-7163.MCT-09-0113. Epub 2009 Aug 11.
Stat3 contributes to resistance toward BCR-ABL inhibitors in a bone marrow microenvironment model of drug resistance.
Bewry NN, Nair RR, Emmons MF, Boulware D, Pinilla-Ibarz J, Hazlehurst LA.
Mol Cancer Ther. 2008 Oct;7(10):3169-75. doi: 10.1158/1535-7163.MCT-08-0314.
Accelerated bottom-up drug design platform enables the discovery of novel stearoyl-CoA desaturase 1 inhibitors for cancer therapy.
von Roemeling CA, Caulfield TR, Marlow L, Bok I, Wen J, Miller JL, Hughes R, Hazlehurst L, Pinkerton AB, Radisky DC, Tun HW, Kim YSB, Lane AL, Copland JA.
Oncotarget. 2017 Oct 6;9(1):3-20. doi: 10.18632/oncotarget.21545. eCollection 2018 Jan 2.
High-content screen using zebrafish (Danio rerio) embryos identifies a novel kinase activator and inhibitor.
Geldenhuys WJ, Bergeron SA, Mullins JE, Aljammal R, Gaasch BL, Chen WC, Yun J, Hazlehurst LA.
Bioorg Med Chem Lett. 2017 May 1;27(9):2029-2037. doi: 10.1016/j.bmcl.2017.02.068. Epub 2017 Feb 28.
1997-1999 NIH NSRA post-doctoral fellowship, “Isolation of A Selected Drug Resistant Gene”
2000-2001 Multiple Myeloma Research Foundation junior fellowship, “The role of CDK2 in fibronectin induced regulation of p27 levels
2011 Educational Session: Emerging Opportunities for Targeting CAM-DR AACR. Orlando, FL
2014 Invited for oral presentation at SBIR investor forum for November 11th , Santa Clara California
2015 Invited platform presentation at the NCI investor forum southeast region, Durham, NC
Post-doctoral Training- University of Arizona and the Moffitt Cancer Center
Graduate Training - Ph.D., Cell and Molecular Biology University of Vermont, 1994
About Lori A Hazlehurst
Dr. Hazlehurst earned her Ph.D. from the Cell and Molecular Biology Program at the University of Vermont. Her post-doctoral studies were performed at the University of Arizona and the Moffitt Cancer Center. Her studies focused on developing strategies for targeting the tumor microenvironment to increase the efficacy of standard of care agents. Her current research focus is to develop strategies for targeting Ca2+ homeostasis in cancer. The laboratory focus is translational with an overall goal of developing novel therapeutic strategies for the treatment of cancer.
1999- 2001 Research Assistant Professor, University of South Florida, College of Medicine Department of Interdisciplinary Oncology
2001- 2002 Research Assistant Professor, University of Arizona
2002- 2007 Assistant Professor, University of South Florida, College of Medicine, Department of Interdisciplinary Oncology
2008-2015 Associate Member Moffitt Cancer Center
2011-Present Modulation Therapeutics Co-Founder
Program 3: Alexander B. Osborn Hematopoietic Malignancy and Transplantation Co-Leader
Dr. Lori Hazlehurst has a strong background in experimental therapeutics. Her research interests are focused on discovering novel therapeutic strategies for the treatment of hematological malignances. To this end herlaboratory is currently investigating the potential of targeting i) integrin mediated pathways ii) the unfolded protein response and iii) identification of novel targets that are appreciated in the context of tumor cell bone marrow microenvironment interactions. She and her research partner propose that the first selection pressure is the tumor microenvironment and second pressure is drug selection. Identification of vulnerabilities that occur during the evolution of tumor progression in this context will enable discovery of new targets for the treatment of drug-resistant cancer.
Her overarching goal is to identify druggable targets and upon validation our laboratory utilizes both HTS strategies and collaborative efforts with chemistry colleagues to define lead compounds that can be utilized to better understand cancer biology and if warranted move towards translational development. She is also co-founder of Modulation Therapeutics which is focused on bridging the valley of death of lead compounds to enable translation to the clinical arena.
Grants and Research
R21 CA191981 Specific skeletal targeting of MMP-2 for the treatment of multiple myeloma
1R01CA195727-01 Targeting CD44-mediated calcium signaling for the treatment of relapsed myeloma