West Texas A&M University

Assistant Professor of Biology

As an Assistant Professor of Biology Dr. Lockman was responsible for instructing over 160 students per semester in Basic and Contemporary Biology for science majors, Cell Biology, Human Pharmacology, and Introduction to Biology for non-science majors. Additionally, she was active in research activities in the areas of neuropharmacology and cancer pharmacology. She oversees Master's-seeking thesis students as well as undergraduates interested in research. She was advisor to all pre-dental, pre-chiropractic, and some pre-pharmacy students. She served as co-faculty advisor to the Beta Beta Beta National Biological Honor Society. She has also served on the Institutional Review Board, Developmental Education Committee, and other Departmental committees.

Texas Tech University Health Sciences Center

Graduate Student/Research Assistant, Pharmaceutical Sciences

During graduate school I had three primary research mentors, J. Suzanne Lindsey, David D. Allen, and C.J. (Neels) Van der Schyf. My work with Dr. Lindsey involved investigation of differential gene expression related to osteoclast differentiation and migration. My work with Dr. Allen and Dr. Van der Schyf led to discovery of an alternate (non-traditional) route of iron entry into brain cells (various types) in conditions of iron overload. I also evaluated the differential effects of iron overload on specific brain cell types and evaluated a potential neuroprotective agent in this model.

Texas Tech University Health Sciences Center

Postdoctoral Research Assoc

Dr. Lockman worked in the lab of Dr. Quentin Smith at the Texas Tech Health Sciences Center, Department of Pharmaceutical Sciences. She was integral in establishing the culturing and preparation of human breast cancer cells used in a model of brain metastasis of breast cancer within the Smith lab. She was also responsible for training graduate students in cell culture techniques and various other experimental methods. She co-administered the Pharmacotherapeutics Case Studies course for P-2 students at the School of Pharmacy, serving as case writer, group facilitator, facilitator trainer, etc.

West Virginia University

Director of Faculty Affairs- Health Sciences

Julie worked at West Virginia University as a Director of Faculty Affairs- Health Sciences

West Virginia University

Adjunct Associate Professor

I participate in the Biochemical Pharmacology course for 1st year pharmacy students. Topics: Pharmacodynamics, CNS-agents, Antibacterial agents, translational pharmacology

West Virginia University

Academic Leadership Fellow

Academic Leadership Fellows have part-time administrative appointments during the academic year that allow them to work closely with University administration on major academic initiatives. Dr. Lockman is working on Health Sciences Academic Affairs under the guidance of Dr. Louise Veselicky, Associate Vice-President for Academic Affairs.

West Virginia University

Teaching Associate Professor

I am part of the Pharmacology Teaching team at WVU Health Sciences Center currently teaching in the Medical Pharmacology course for second year medical students. Topics: Drug Discovery and Development, Human Subjects Research, Antibacterials, Anticholinergics, Translational Pharmacology.

I previously served in this role as an Adjunct Faculty member from January 2014 until June 2016.

West Virginia University

Director of Investigator Development/Research Pathfinder and Director of Professional Development

As research pathfinder, I oversee investigator development, service integration, and product development tracking for WVCTSI-funded investigators. I also serve as the point person to support investigators as they navigate the research process providing consultations to advise investigators on available WVCTSI services and resources, identify and assist in development of collaborative research teams, and support the WVCTSI research mentoring initiatives.

“The WVCTSI staff and leadership are passionate about our role in supporting the growth of clinical and translational sciences across the state with the ultimate goal of improving health outcomes,” Dr. Lockman shared. “I am grateful to be a part of such an important initiative working alongside such an experienced and committed team.”

Differential effect of nimodipine in attenuating iron-induced toxicity in brain- and blood-brain barrier-associated cell types.

Neurochemical Research

Differential effect of nimodipine in attenuating iron-induced toxicity in brain- and blood-brain barrier-associated cell types.

Neurochemical Research

Heterogeneous blood-tumor barrier permeability determines drug efficacy in experimental brain metastases of breast cancer.

Clin Cancer Res

Differential effect of nimodipine in attenuating iron-induced toxicity in brain- and blood-brain barrier-associated cell types.

Neurochemical Research

Heterogeneous blood-tumor barrier permeability determines drug efficacy in experimental brain metastases of breast cancer.

Clin Cancer Res

NGP1-01, a multi-targeted polycyclic cage amine, attenuates brain endothelial cell death in iron overload conditions.

Brain Research

Differential effect of nimodipine in attenuating iron-induced toxicity in brain- and blood-brain barrier-associated cell types.

Neurochemical Research

Heterogeneous blood-tumor barrier permeability determines drug efficacy in experimental brain metastases of breast cancer.

Clin Cancer Res

NGP1-01, a multi-targeted polycyclic cage amine, attenuates brain endothelial cell death in iron overload conditions.

Brain Research

Using WebCt to implement a basic science competency education course.

Am J Pharm Ed

Differential effect of nimodipine in attenuating iron-induced toxicity in brain- and blood-brain barrier-associated cell types.

Neurochemical Research

Heterogeneous blood-tumor barrier permeability determines drug efficacy in experimental brain metastases of breast cancer.

Clin Cancer Res

NGP1-01, a multi-targeted polycyclic cage amine, attenuates brain endothelial cell death in iron overload conditions.

Brain Research

Using WebCt to implement a basic science competency education course.

Am J Pharm Ed

Lapatinib distribution in HER2 overexpressing experimental brain metastases of breast cancer.

Pharmaceutical Research

Results show that lapatinib distribution to brain metastases of breast cancer is restricted and blood-tumor barrier permeability is a key component of lapatinib therapeutic efficacy which varies within and between tumors.

Differential effect of nimodipine in attenuating iron-induced toxicity in brain- and blood-brain barrier-associated cell types.

Neurochemical Research

Heterogeneous blood-tumor barrier permeability determines drug efficacy in experimental brain metastases of breast cancer.

Clin Cancer Res

NGP1-01, a multi-targeted polycyclic cage amine, attenuates brain endothelial cell death in iron overload conditions.

Brain Research

Using WebCt to implement a basic science competency education course.

Am J Pharm Ed

Lapatinib distribution in HER2 overexpressing experimental brain metastases of breast cancer.

Pharmaceutical Research

Results show that lapatinib distribution to brain metastases of breast cancer is restricted and blood-tumor barrier permeability is a key component of lapatinib therapeutic efficacy which varies within and between tumors.

Quantitative Fluorescence Microscopy Measures Vascular Pore Size in Primary and Metastatic Brain Tumors.

Cancer Research

Tumors residing in the central nervous system (CNS) compromise the blood–brain barrier (BBB) via increased vascular permeability, with the magnitude of changes dependent on the tumor type and location. Current studies determine penetrability of a cancer therapeutic by administering progressively larger molecules until cutoff is observed where little to no tumor accumulation occurs. However, decades-old experimental work and mathematical modeling document methods to calculate both the size of the vascular opening (pore) with solute permeability values. In this study, we updated this classic mathematical modeling approach with quantitative fluorescence microscopy in two preclinical tumor models, allowing simultaneous administration of multiple sized tracers to determine vascular permeability at a resolution of nearly one micron. We observed that three molecules ranging from 100 Da to 70 kDa permeated into a preclinical glioblastoma model at rates proportional to their diffusion in water. This suggests the solutes freely diffused from blood to glioma across vascular pores without steric restriction, which calculates to a pore size of >140 nm in diameter. In contrast, the calculated pore size of a brain metastasis of breast cancer was approximately 10-fold smaller than glioma vasculature. This difference explains why antibodies are effective against glioblastoma but generally fail in brain metastases of breast cancer. On the basis of our observations, we hypothesize that trastuzumab most likely fails in the treatment of brain metastases of breast cancer because of poor CNS penetration, while the similar sized antibody bevacizumab is effective in the same tumor type not because it penetrates the CNS degree better, but because it scavenges VEGF in the vascular compartment, which reduces edema and permeation. Cancer Res; 77(2); 238–46. ©2016 AACR.

Differential effect of nimodipine in attenuating iron-induced toxicity in brain- and blood-brain barrier-associated cell types.

Neurochemical Research

Heterogeneous blood-tumor barrier permeability determines drug efficacy in experimental brain metastases of breast cancer.

Clin Cancer Res

NGP1-01, a multi-targeted polycyclic cage amine, attenuates brain endothelial cell death in iron overload conditions.

Brain Research

Using WebCt to implement a basic science competency education course.

Am J Pharm Ed

Lapatinib distribution in HER2 overexpressing experimental brain metastases of breast cancer.

Pharmaceutical Research

Results show that lapatinib distribution to brain metastases of breast cancer is restricted and blood-tumor barrier permeability is a key component of lapatinib therapeutic efficacy which varies within and between tumors.

Quantitative Fluorescence Microscopy Measures Vascular Pore Size in Primary and Metastatic Brain Tumors.

Cancer Research

Tumors residing in the central nervous system (CNS) compromise the blood–brain barrier (BBB) via increased vascular permeability, with the magnitude of changes dependent on the tumor type and location. Current studies determine penetrability of a cancer therapeutic by administering progressively larger molecules until cutoff is observed where little to no tumor accumulation occurs. However, decades-old experimental work and mathematical modeling document methods to calculate both the size of the vascular opening (pore) with solute permeability values. In this study, we updated this classic mathematical modeling approach with quantitative fluorescence microscopy in two preclinical tumor models, allowing simultaneous administration of multiple sized tracers to determine vascular permeability at a resolution of nearly one micron. We observed that three molecules ranging from 100 Da to 70 kDa permeated into a preclinical glioblastoma model at rates proportional to their diffusion in water. This suggests the solutes freely diffused from blood to glioma across vascular pores without steric restriction, which calculates to a pore size of >140 nm in diameter. In contrast, the calculated pore size of a brain metastasis of breast cancer was approximately 10-fold smaller than glioma vasculature. This difference explains why antibodies are effective against glioblastoma but generally fail in brain metastases of breast cancer. On the basis of our observations, we hypothesize that trastuzumab most likely fails in the treatment of brain metastases of breast cancer because of poor CNS penetration, while the similar sized antibody bevacizumab is effective in the same tumor type not because it penetrates the CNS degree better, but because it scavenges VEGF in the vascular compartment, which reduces edema and permeation. Cancer Res; 77(2); 238–46. ©2016 AACR.

Vorinostat inhibits brain metastatic colonization in a model of triple-negative breast cancer and induces DNA double-strand breaks.

Clin Cancer Res

Differential effect of nimodipine in attenuating iron-induced toxicity in brain- and blood-brain barrier-associated cell types.

Neurochemical Research

Heterogeneous blood-tumor barrier permeability determines drug efficacy in experimental brain metastases of breast cancer.

Clin Cancer Res

NGP1-01, a multi-targeted polycyclic cage amine, attenuates brain endothelial cell death in iron overload conditions.

Brain Research

Using WebCt to implement a basic science competency education course.

Am J Pharm Ed

Lapatinib distribution in HER2 overexpressing experimental brain metastases of breast cancer.

Pharmaceutical Research

Results show that lapatinib distribution to brain metastases of breast cancer is restricted and blood-tumor barrier permeability is a key component of lapatinib therapeutic efficacy which varies within and between tumors.

Quantitative Fluorescence Microscopy Measures Vascular Pore Size in Primary and Metastatic Brain Tumors.

Cancer Research

Tumors residing in the central nervous system (CNS) compromise the blood–brain barrier (BBB) via increased vascular permeability, with the magnitude of changes dependent on the tumor type and location. Current studies determine penetrability of a cancer therapeutic by administering progressively larger molecules until cutoff is observed where little to no tumor accumulation occurs. However, decades-old experimental work and mathematical modeling document methods to calculate both the size of the vascular opening (pore) with solute permeability values. In this study, we updated this classic mathematical modeling approach with quantitative fluorescence microscopy in two preclinical tumor models, allowing simultaneous administration of multiple sized tracers to determine vascular permeability at a resolution of nearly one micron. We observed that three molecules ranging from 100 Da to 70 kDa permeated into a preclinical glioblastoma model at rates proportional to their diffusion in water. This suggests the solutes freely diffused from blood to glioma across vascular pores without steric restriction, which calculates to a pore size of >140 nm in diameter. In contrast, the calculated pore size of a brain metastasis of breast cancer was approximately 10-fold smaller than glioma vasculature. This difference explains why antibodies are effective against glioblastoma but generally fail in brain metastases of breast cancer. On the basis of our observations, we hypothesize that trastuzumab most likely fails in the treatment of brain metastases of breast cancer because of poor CNS penetration, while the similar sized antibody bevacizumab is effective in the same tumor type not because it penetrates the CNS degree better, but because it scavenges VEGF in the vascular compartment, which reduces edema and permeation. Cancer Res; 77(2); 238–46. ©2016 AACR.

Vorinostat inhibits brain metastatic colonization in a model of triple-negative breast cancer and induces DNA double-strand breaks.

Clin Cancer Res

Uptake of ANG1005, a novel paclitaxel derivative, through the blood-brain barrier into brain and experimental brain metastases of breast cancer.

Pharm Res

Differential effect of nimodipine in attenuating iron-induced toxicity in brain- and blood-brain barrier-associated cell types.

Neurochemical Research

Heterogeneous blood-tumor barrier permeability determines drug efficacy in experimental brain metastases of breast cancer.

Clin Cancer Res

NGP1-01, a multi-targeted polycyclic cage amine, attenuates brain endothelial cell death in iron overload conditions.

Brain Research

Using WebCt to implement a basic science competency education course.

Am J Pharm Ed

Lapatinib distribution in HER2 overexpressing experimental brain metastases of breast cancer.

Pharmaceutical Research

Results show that lapatinib distribution to brain metastases of breast cancer is restricted and blood-tumor barrier permeability is a key component of lapatinib therapeutic efficacy which varies within and between tumors.

Quantitative Fluorescence Microscopy Measures Vascular Pore Size in Primary and Metastatic Brain Tumors.

Cancer Research

Tumors residing in the central nervous system (CNS) compromise the blood–brain barrier (BBB) via increased vascular permeability, with the magnitude of changes dependent on the tumor type and location. Current studies determine penetrability of a cancer therapeutic by administering progressively larger molecules until cutoff is observed where little to no tumor accumulation occurs. However, decades-old experimental work and mathematical modeling document methods to calculate both the size of the vascular opening (pore) with solute permeability values. In this study, we updated this classic mathematical modeling approach with quantitative fluorescence microscopy in two preclinical tumor models, allowing simultaneous administration of multiple sized tracers to determine vascular permeability at a resolution of nearly one micron. We observed that three molecules ranging from 100 Da to 70 kDa permeated into a preclinical glioblastoma model at rates proportional to their diffusion in water. This suggests the solutes freely diffused from blood to glioma across vascular pores without steric restriction, which calculates to a pore size of >140 nm in diameter. In contrast, the calculated pore size of a brain metastasis of breast cancer was approximately 10-fold smaller than glioma vasculature. This difference explains why antibodies are effective against glioblastoma but generally fail in brain metastases of breast cancer. On the basis of our observations, we hypothesize that trastuzumab most likely fails in the treatment of brain metastases of breast cancer because of poor CNS penetration, while the similar sized antibody bevacizumab is effective in the same tumor type not because it penetrates the CNS degree better, but because it scavenges VEGF in the vascular compartment, which reduces edema and permeation. Cancer Res; 77(2); 238–46. ©2016 AACR.

Vorinostat inhibits brain metastatic colonization in a model of triple-negative breast cancer and induces DNA double-strand breaks.

Clin Cancer Res

Uptake of ANG1005, a novel paclitaxel derivative, through the blood-brain barrier into brain and experimental brain metastases of breast cancer.

Pharm Res

P-glycoprotein mediated efflux limits substrate and drug uptake in a preclinical brain metastases of breast

Frontiers in Pharmacology

The blood–brain barrier (BBB) is a specialized vascular interface that restricts the entry of many compounds into brain. This is accomplished through the sealing of vascular endothelial cells together with tight junction proteins to prevent paracellular diffusion. In addition, the BBB has a high degree of expression of numerous efflux transporters which actively extrude compounds back into blood. However, when a metastatic lesion develops in brain the vasculature is typically compromised with increases in passive permeability (blood-tumor barrier; BTB). What is not well documented is to what degree active efflux retains function at the BTB despite the changes observed in passive permeability. In addition, there have been previous reports documenting both increased and decreased expression of P-glycoprotein (P-gp) in lesion vasculature. Herein, we simultaneously administer a passive diffusion marker (14C-AIB) and a tracer subject to P-gp efflux (rhodamine 123) into a murine preclinical model of brain metastases of breast cancer. We observed that the metastatic lesions had similar expression (p > 0.05; n = 756–1214 vessels evaluated) at the BBB and the BTB. Moreover, tissue distribution of R123 was not significantly (p > 0.05) different between normal brain and the metastatic lesion. It is possible that the similar expression of P-gp on the BBB and the BTB contribute to this phenomenon. Additionally we observed P-gp expression at the metastatic cancer cells adjacent to the vasculature which may also contribute to reduced R123 uptake into the lesion. The data suggest that despite the disrupted integrity of the BTB, efflux mechanisms appear to be intact, and may be functionally comparable to the normal BBB. The BTB is a significant hurdle to delivering drugs to brain metastasis.

Differential effect of nimodipine in attenuating iron-induced toxicity in brain- and blood-brain barrier-associated cell types.

Neurochemical Research

Heterogeneous blood-tumor barrier permeability determines drug efficacy in experimental brain metastases of breast cancer.

Clin Cancer Res

NGP1-01, a multi-targeted polycyclic cage amine, attenuates brain endothelial cell death in iron overload conditions.

Brain Research

Using WebCt to implement a basic science competency education course.

Am J Pharm Ed

Lapatinib distribution in HER2 overexpressing experimental brain metastases of breast cancer.

Pharmaceutical Research

Results show that lapatinib distribution to brain metastases of breast cancer is restricted and blood-tumor barrier permeability is a key component of lapatinib therapeutic efficacy which varies within and between tumors.

Quantitative Fluorescence Microscopy Measures Vascular Pore Size in Primary and Metastatic Brain Tumors.

Cancer Research

Tumors residing in the central nervous system (CNS) compromise the blood–brain barrier (BBB) via increased vascular permeability, with the magnitude of changes dependent on the tumor type and location. Current studies determine penetrability of a cancer therapeutic by administering progressively larger molecules until cutoff is observed where little to no tumor accumulation occurs. However, decades-old experimental work and mathematical modeling document methods to calculate both the size of the vascular opening (pore) with solute permeability values. In this study, we updated this classic mathematical modeling approach with quantitative fluorescence microscopy in two preclinical tumor models, allowing simultaneous administration of multiple sized tracers to determine vascular permeability at a resolution of nearly one micron. We observed that three molecules ranging from 100 Da to 70 kDa permeated into a preclinical glioblastoma model at rates proportional to their diffusion in water. This suggests the solutes freely diffused from blood to glioma across vascular pores without steric restriction, which calculates to a pore size of >140 nm in diameter. In contrast, the calculated pore size of a brain metastasis of breast cancer was approximately 10-fold smaller than glioma vasculature. This difference explains why antibodies are effective against glioblastoma but generally fail in brain metastases of breast cancer. On the basis of our observations, we hypothesize that trastuzumab most likely fails in the treatment of brain metastases of breast cancer because of poor CNS penetration, while the similar sized antibody bevacizumab is effective in the same tumor type not because it penetrates the CNS degree better, but because it scavenges VEGF in the vascular compartment, which reduces edema and permeation. Cancer Res; 77(2); 238–46. ©2016 AACR.

Vorinostat inhibits brain metastatic colonization in a model of triple-negative breast cancer and induces DNA double-strand breaks.

Clin Cancer Res

Uptake of ANG1005, a novel paclitaxel derivative, through the blood-brain barrier into brain and experimental brain metastases of breast cancer.

Pharm Res

P-glycoprotein mediated efflux limits substrate and drug uptake in a preclinical brain metastases of breast

Frontiers in Pharmacology

The blood–brain barrier (BBB) is a specialized vascular interface that restricts the entry of many compounds into brain. This is accomplished through the sealing of vascular endothelial cells together with tight junction proteins to prevent paracellular diffusion. In addition, the BBB has a high degree of expression of numerous efflux transporters which actively extrude compounds back into blood. However, when a metastatic lesion develops in brain the vasculature is typically compromised with increases in passive permeability (blood-tumor barrier; BTB). What is not well documented is to what degree active efflux retains function at the BTB despite the changes observed in passive permeability. In addition, there have been previous reports documenting both increased and decreased expression of P-glycoprotein (P-gp) in lesion vasculature. Herein, we simultaneously administer a passive diffusion marker (14C-AIB) and a tracer subject to P-gp efflux (rhodamine 123) into a murine preclinical model of brain metastases of breast cancer. We observed that the metastatic lesions had similar expression (p > 0.05; n = 756–1214 vessels evaluated) at the BBB and the BTB. Moreover, tissue distribution of R123 was not significantly (p > 0.05) different between normal brain and the metastatic lesion. It is possible that the similar expression of P-gp on the BBB and the BTB contribute to this phenomenon. Additionally we observed P-gp expression at the metastatic cancer cells adjacent to the vasculature which may also contribute to reduced R123 uptake into the lesion. The data suggest that despite the disrupted integrity of the BTB, efflux mechanisms appear to be intact, and may be functionally comparable to the normal BBB. The BTB is a significant hurdle to delivering drugs to brain metastasis.

Voltage-gated calcium channels provide an alternate route for iron uptake in neuronal cell cultures.

Neurochemical Research