Research Topics
Species | Lori A HazlehurstSummaryAffiliation: H. Lee Moffitt Cancer Center and Research Institute Country: USA Publications
Research Grants
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Detail Information
Publications
Signaling networks associated with BCR-ABL-dependent transformationLori A Hazlehurst
Molecular Oncology Program, H Lee Moffitt Cancer Center and Research Institute, Tampa, Florida 33612, USA
Cancer Control 16:100-7. 2009..The fusion protein BCR-ABL results in constitutive tyrosine kinase activity. It also affects downstream targets as well as the subcellular location of the normally tightly regulated Abl tyrosine kinase...- Cell adhesion to fibronectin (CAM-DR) influences acquired mitoxantrone resistance in U937 cellsLori A Hazlehurst
Department of Interdisciplinary Oncology and Experimental Therapeutics Program, H. Lee Moffitt Cancer Center and Research Institute at the University of South Florida, Tampa, Florida 33613, USA
Cancer Res 66:2338-45. 2006..Taken together, our results suggest that the development of drug resistance models must consider interactions with the microenvironment to identify clinically relevant targets and mechanisms associated with acquired drug resistance... 
Potentiation of Nilotinib-mediated cell death in the context of the bone marrow microenvironment requires a promiscuous JAK inhibitor in CMLRajesh R Nair
Molecular Oncology Program, H Lee Moffitt Cancer Center, Tampa, FL, USA
Leuk Res 36:756-63. 2012..Finally, we demonstrate that in patient-derived primitive leukemic cells, co-cultured with BM stromal cells, inhibition of BCR-ABL and JAK activity was a successful strategy to potentiate their elimination...- Acquisition of resistance toward HYD1 correlates with a reduction in cleaved α4 integrin expression and a compromised CAM-DR phenotypeMichael F Emmons
Molecular Oncology Program, H Lee Moffitt Cancer Center Tampa, FL, USA
Mol Cancer Ther 10:2257-66. 2011..Moreover, our data provide further rationale for continued preclinical development of HYD1 and analogues of HYD1 for the treatment of multiple myeloma and potentially other tumors that home and/or metastasize to the bone... - The FA/BRCA pathway is involved in melphalan-induced DNA interstrand cross-link repair and accounts for melphalan resistance in multiple myeloma cellsQing Chen
Department of Interdisciplinary Oncology and Experimental Therapeutics Program, Biostatistics Core Facility, H. Lee Moffitt Cancer Center and Research Institute at University of South Florida, 12902 Magnolia Dr, Tampa, FL 33612, USA
Blood 106:698-705. 2005..These data show that enhanced DNA repair via the Fanconi anemia/BRCA pathway is involved in acquired melphalan resistance. Our findings provide for a new target to enhance response to DNA cross-linking agents in cancer treatment... 
Targeting the Fanconi anemia/BRCA pathway circumvents drug resistance in multiple myelomaDanielle N Yarde
Cancer Biology Ph D Program, University of South Florida, Tampa, Florida 33612, USA
Cancer Res 69:9367-75. 2009....- Beta1 integrin adhesion enhances IL-6-mediated STAT3 signaling in myeloma cells: implications for microenvironment influence on tumor survival and proliferationKenneth H Shain
Experimental Therapeutics and Oncologic Sciences Program, H Lee Moffitt Cancer Center and Research Institute, Tampa, Florida 33612, USA
Cancer Res 69:1009-15. 2009..Taken together, these results suggest a mechanism by which collaborative signaling by beta1 integrin and gp130 confers an increased survival advantage to MM cells... - HYD1-induced increase in reactive oxygen species leads to autophagy and necrotic cell death in multiple myeloma cellsRajesh R Nair
Moffitt Cancer Center, Tampa, Florida 33613, USA
Mol Cancer Ther 8:2441-51. 2009..Taken together, our data describe an important role of ROS in HYD1-induced necrotic cell death in MM cells... - The bone marrow microenvironment as a tumor sanctuary and contributor to drug resistanceMark B Meads
Department of Experimental Therapeutics, H Lee Moffitt Cancer Center and Research Institute, Tampa, Florida 33612, USA
Clin Cancer Res 14:2519-26. 2008..This protection allows tumor cells to survive the insult of chemotherapy, leading to minimal residual disease, and thereby increases the probability for the development of acquired drug resistance... - Genotypic and phenotypic comparisons of de novo and acquired melphalan resistance in an isogenic multiple myeloma cell line modelLori A Hazlehurst
Department of Interdisciplinary Oncology, H. Lee Moffitt Cancer Center and Research Institute, at the University of South Florida, 12902 Magnolia Drive, Tampa, FL 33612, USA
Cancer Res 63:7900-6. 2003.... - Human multiple myeloma cells are sensitized to topoisomerase II inhibitors by CRM1 inhibitionJoel G Turner
Experimental Therapeutics Program and Department of Blood and Marrow Transplantation, H Lee Moffitt Cancer Center and Research Institute, Tampa, Florida 33612, USA
Cancer Res 69:6899-905. 2009..These results suggest that blocking topo IIalpha nuclear export sensitizes myeloma cells to topo II inhibitors. This method of sensitizing myeloma cells suggests a new therapeutic approach to multiple myeloma... - Stat3 contributes to resistance toward BCR-ABL inhibitors in a bone marrow microenvironment model of drug resistanceNadine N Bewry
Molecular Oncology Program, H Lee Moffitt Cancer Center and Research Institute, Tampa, FL 33613, USA
Mol Cancer Ther 7:3169-75. 2008.... - Emerging strategies for targeting cell adhesion in multiple myelomaRajesh R Nair
Molecular Oncology Program, H Lee Moffitt Cancer Center, Tampa, FL, USA
Adv Pharmacol 65:143-89. 2012..Ultimately, the goal is to use these therapies in combination with the existing antimyeloma agents in order to further reduce or abolish minimal residual disease and improve patient outcomes... - Cell adhesion induces p27Kip1-associated cell-cycle arrest through down-regulation of the SCFSkp2 ubiquitin ligase pathway in mantle-cell and other non-Hodgkin B-cell lymphomasTint Lwin
Department of Interdisciplinary Oncology and Experimental Therapeutics Program, H Lee Moffitt Cancer Center and Research Institute at the University of South Florida, Tampa, FL 33613, USA
Blood 110:1631-8. 2007..The understanding of this novel molecular pathway may prove valuable in designing new therapeutic approaches for modifying tumor cell growth and response to therapy... - The bone marrow microenvironment as a sanctuary for minimal residual disease in CMLRajesh R Nair
Molecular Oncology Program, H Lee Moffitt Cancer Center, Tampa, FL 33612, United States
Biochem Pharmacol 80:602-12. 2010.... - Detection of DNA damage induced by topoisomerase II inhibitors, gamma radiation and crosslinking agents using the comet assayLori A Hazlehurst
Department of Interdisciplinary Oncology, Experimental Therapeutics and Drug Discovery Programs, H Lee Moffitt Cancer Center and Research Institute, Tampa, FL, USA
Methods Mol Biol 523:169-76. 2009..In this chapter we will outline the comet assay for the detection of DNA damage induced by topoisomerase II inhibitors, cross-linking agents and gamma radiation... - Proteomic contributions to personalized cancer careJohn M Koomen
H Lee Moffitt Cancer Center and Research Institute, University of South Florida, Tampa, Florida 33612, USA
Mol Cell Proteomics 7:1780-94. 2008.... - Role of STAT3 in Transformation and Drug Resistance in CMLRajesh R Nair
Molecular Oncology Program, H Lee Moffitt Cancer Center Tampa, FL, USA
Front Oncol 2:30. 2012.... - Tipifarnib-induced apoptosis in acute myeloid leukemia and multiple myeloma cells depends on Ca2+ influx through plasma membrane Ca2+ channelsNiranjan Yanamandra
Department of Interdisciplinary Oncology, H Lee Moffitt Cancer Center and Research Institute, Tampa, Florida, USA
J Pharmacol Exp Ther 337:636-43. 2011..Our results indicate tipifarnib causes cell death via a novel mechanism involving activation of a plasma membrane Ca(2+) channel and intracellular Ca(2+) overload... - Role of the tumor microenvironment in mediating de novo resistance to drugs and physiological mediators of cell deathLori A Hazlehurst
Clinical Investigations Program at H Lee Moffitt Cancer Center, University of South Florida, 12902 Magnolia Drive, Tampa, FL 33612, USA
Oncogene 22:7396-402. 2003..This review will focus on the bone marrow microenvironment and its role in conferring resistance to cytotoxics and physiological mediators of cell death...
Research Grants
- Role of Bim in mediating CAM-DR in hematopoietic tumorsLori A Hazlehurst; Fiscal Year: 2010..In this proposal we will test whether disrupting beta 1 integrin mediated signaling increases the potency of standard chemotherapy in the bone marrow microenvironment. ..