CURRICULUM VITAE

THOMAS RUSSELL HUNDLEY

Home Phone : 301-***-****. Email address: acprhm@r.postjobfree.com

SUMMARY

Over 15 years of experience as a scientist in pharmacology,

immunology, experimental anticancer therapeutics, molecular target

identification, molecular biology, biochemistry, nuclear receptor ligand

identification, signal transduction, toxicology, and assay development.

Experience in cell culturing, development of cell proliferation assays,

development of assays for novel nuclear receptors, phospholipid analysis,

the quantitation of various second messengers involved in signal

transduction for the mediation of cancer cell growth, immune responses, and

exocytosis. Presented to clients scientific data on the status of contract

work in progress. Presented oral presentations to corporate partners on

various research projects. Presented lectures on research at national

scientific meetings and published in numerous peer reviewed journals.

Presently, seeking immediate placement as a Research Associate

Scientist or an Assay Development Scientist in a progressive environment

within a government agency or in the pharmaceutical and biotechnology

industries. I enjoy giving presentations to clients, the scientific

community, and to the general public promoting novel medical concepts for

the treatment of diseases. My expertise in pharmacology, molecular biology,

immunology, signal transduction, cancer, and cell biology can be utilized

to support the analysis of protocols for research in immune-regulation,

anti-cancer therapies, and applications for gene regulation in diseases.

Such a position might encompass the review of scientific protocols for the

development of bioassays, novel drug research and drug discovery. My

expertise are quite applicable for assisting junior scientist in searching

scientific literature for the development of research goals and giving

guidance in methodologies that could be employed.

My most recent position was working as a senior scientist in

pharmacology in the Bacteriology Division of United States Army Medical

Research Institute of Infectious Diseases in Frederick, Maryland. Research

involves the development and testing of novel antibiotic drugs against

resistant strains of bacteria. This position was a short term contract

position in February and March of 2015.

Worked as a volunteer Scientific Sales Representative at The McConnell

Group in the SciMed Sales Division (Rockville, Maryland). Collaborations

included working with Dr. Hao Chen (President/CSO at DRI Biosciences

Corporation and former Vice President of Oncology Research and Assay

Development at PerkinElmer, pursuing cancer research involving the

regulation of tumor metastasis by growth factors and cytokines.

As a Pharmacology Assay Development Scientist at PerkinElmer Life

Sciences technologies in Hanover, Maryland my job pursuits were in assay

development and in oncology research. I was involved in assay development

for the screening of client compounds and therapeutic antibodies. I worked

with clients to develop molecular assays and cell based assays to meet the

requirements for preclinical studies of the efficacy of novel drugs and

therapeutic antibodies. My research duties encompassed the development of

in vivo models for breast cancer metastasis and the identification of

target molecules that might be involved in the mediation of malignant cell

metastasis in several cancers.

ACCOMPLISHMENTS:

. Manager Assay Development for the Testing of Therapeutic Antibodies

. Developed a research protocol for an in vivo model of cancer metastasis

and identified target molecules involved in the mediation of malignant

cell metastasis.

. Developed methodologies for proliferation assays to screen client

compounds for interactions with specific growth factor receptors.

. Cancer Cell, Primary Cell, and Animal Tissue Culturing Methods

. Developed method for the isolated human basophils for research centered

upon characterizing the various signal transduction pathways involved

in the mediation of histamine and leukotriene C4 release from human

basophils.

. Development of cell based assays

. Cell proliferation assays.

. 3-D Cell culture development for the study of primary cell cultures

from breast cancer tumors.

. AlphaScreen Assay Developed for high throughput assays for various

"Orphan Nuclear Receptors" including the Farnesoid (FXR), Pregnane

(PXR), Liver (LXR), Thyroid (TR), Androgen (AR) and Retinoic Acid

(RAR).

. AlphaLISA Assays Developed for the quantification of several biological

proteins.

. Developed methodologies for the evaluation of receptor kinase

inhibitors and inhibitors of signal transduction pathways utilizing

Luminex multiplex platforms.

. Developed Enzyme Linked Immunosorbent Assays (ELISA) for small

molecules targets for cancer therapeutics.

. DELFIA (Dissociation-Enhanced Lanthanide Fluorescent Immunoassay) Assay

development for the quantification of several biological proteins.

. Conducted research to test drug combinations directed at targeting

growth factor receptors.

. Submitted and awarded grants for the National Institutes of Health for

Cancer Research.

. Researched and identified the antiproliferative mechanism of action for

a novel class of non-steroidal anti-inflammatory drugs that inhibit

cancerous cell growth by utilizing RNA silencing (siRNA) directed at a

cell cycle regulating protein identified as p21. Discovered that these

compounds act by stimulating several mitogen activated protein kinase

pathways (MAPK) for signaling the induction of cell cycle arrest and

thus the inhibition of cell proliferation.

. Researched the MAP kinase pathways involved in the mediation of

degranulation and eicosanoid production in a mast cell line.

. Developed monoclonal antibodies directed at cellular membrane proteins.

. Trained laboratory personnel, medical residents, medical students, and

undergraduate students in biomedical technology methods. I have trained

laboratory personnel and university students in cell and tissue culture

methods at the BSL2 and BSL3 levels.

SKILLS and LEARNED METHODOLOGIES:

. AlphaScreen Assay Development

. AlphaLISA Assay Development

. DEFIA Assay Development

. ELISA Assay Development

. Diverse scientific knowledge from pursuits in research and industry

encompassing the areas of cancer, pharmacology, immunology, molecular

biology, biochemistry, cell biology, and developmental biology

. Acquired expertise in cell culturing

. Cell proliferation assay development for cancer and immunology

therapeutics

. Conducted cell culturing at the BSL2 and BSL3 levels

. Cancer Cell Culturing

. Primary Cell Culturing

. Animal Tissue Culturing

. Development of cell based assays

. Cell proliferation assays.

. 3-D Cell culture development for the study of primary cell cultures

from breast cancer tumors.

. Development of in vivo models for studying cancer cell metastasis

. Luminex multiplex platforms

. TR-FRET assay development

. Quantitation of various second messengers involved in signal

transduction for the mediation of cancer cell growth, immune

responses, and exocytosis

. Development of assays for the analysis of enzymatic activities

. PCR(Polymerase Chain Reaction)

. Stable cellular transfections,

. siRNA (Small Interfering RNA)

. Electric Mobility Shift Assays (EMSAs)

. Gas chromatography-negative ion chemical ionization mass spectrometry

(GCMS) for the quantitation of eicosanoids, arachidonic acid and

diacylglycerols

. Proper handling of and applications using radioactive isotopes

. Production of monoclonal antibodies

. Ultracentrifugation

. Chromatography of proteins and small molecules

. Protein Purification and Isolation

. Spectrophotometry

. Western Blotting

. Enzyme and Binding Assays utilizing Radioisotopes

EDUCATION:

Ph.D. in Pharmacology

September, 1989 to June, 1993

Department of Pharmacology and Therapeutics

State University of New York at Buffalo

Doctoral thesis centered upon determining the mechanisms that stimulate

lipid hydrolysis during agonist-stimulated secretion and the role of lipid

hydrolysis in the mediation of exocytosis. The triacylglycerol lipid pool

was examined as a source of free arachidonic acid and diacylglycerols

generated during agonist-stimulation.

September, 1989: Department of Pharmacology and Toxicology Medical College

of Virginia,

Virginia Commonwealth University, started instruction for a Ph.D. in

pharmacology and transferred to accompany my advisor (Dr. Ronald P. Rubin)

when he took over the Chairmanship in the Department of Pharmacology and

Therapeutics at the State University of New York at Buffalo.

WORK EXPERIENCE:

Senior Pharmacology Scientist

February, 2015 to March, 2015 (Clinical Research Management Contractor)

Bacteriology Division

United States Army Medical Research Institute

of Infectious Diseases (USAMRIID)

Frederick, Maryland

Working as a senior scientist in pharmacology in the Bacteriology

Division of United States Army Medical Research Institute of Infectious

Diseases (USAMRIID) in Frederick, Maryland. Research involves the

development and testing of novel antibiotic drugs and therapeutic protocols

against resistant strains of bacteria.

Scientific Sales Representative (Volunteer Worker):

August, 2014 to January, 2015 The McConnell Group

1901 Research Blvd. Suite 502

Rockville, Maryland 20850

Duties include providing scientific expertise for the sale of

scientific equipment. Our company identifies and acquires scientific

equipment and personnel for the completion of government contracts and for

individuals preparing grants. As an experienced scientist in research and

industry my duties encompass finding sources for the acquisition of

specific scientific equipment. My duties also encompass the review of

scientific proposals to determine the expertise, proficiency, knowledge,

and experience of staff required to successfully complete the contracted

work.

Research Scientist in Oncology (Volunteer Worker):

2013 to 2014 DRI Biosciences Corporation

Baltimore, Maryland

Collaboration research work with Dr. Hao Chen (President/CSO at DRI

Biosciences Corporation and former Vice President of Oncology Research and

Assay Development at PerkinElmer, pursuing cancer research involving the

regulation of tumor metastasis by growth factors and cytokines. This

research included the application of novel drugs and drug combinations for

antineoplastic drug therapies.

WORK EXPERIENCE:

Assay Development Scientist:

May, 2007 to October, 2013 PerkinElmer Life Sciences Technologies

(formerly Caliper Discovery Alliances and

Services)

7170 Standard Drive

Hanover, Maryland 21076-1334

As a Pharmacology Scientist at PerkinElmer, my duties encompassed the

development of new assays for client projects. I worked with clients to

develop molecular assays to meet the requirements for preclinical studies.

I enjoyed working with clients engaging in scientific discussions to

determine what services (assays) we could offer them. I would suggest to

clients what protocols I could use so that they would gain the most

information from my work. My duties included giving presentations to

clients on the current status of contract work, giving oral presentations

on the progression of assays that I was developing to the company, and

determining if milestones in contracts had been reached. I additionally

gave presentations on oncology research projects with the purpose of

reviewing my ongoing research, to inform collaborators of the current

status of the projects, to get suggestions on what alternative goals I

might incorporate into my work, to give other scientist ideas on projects

in cancer drug discovery that they might wish to pursue, and to inform the

company on how the data generated by my research could be used to develop

services that could be offered to clients.

Assay development included assays for molecular target identification,

cell based assays, and cell proliferation assays. Independent research

projects involved a study to identify the pathways that are utilized by

breast cancer cells for the development of resistance to hormone therapies.

The experiments conducted in this research were aimed at identify the

signaling cascades that are active in endowing breast cancer cells with

resistance to hormone therapies.

Oncology contract duties were to optimize and conduct cell-based

assays for the testing of growth factor inhibitors, kinase inhibitors, and

possible antineoplastic drugs. Oncology research goals were to develop

novel anti-neoplastic agents and more effective drug combinations of

existing anti-cancer drugs for breast cancer.

Assays for the testing of therapeutic antibodies were developed

utilizing AlphaLISA and ELISA methodologies. Assay development included the

development of Luminex Bead assays for kinase pathway molecules. Novel

therapeutic agents were tested for their effects on kinase pathways using

Luminex Bead assays. Western Blots and protein purification methods were

developed to identify protein targets for clients.

As an assay development scientist, my duties involved the application

of AlpaSreen and AlphaLISA technologies for the identification and for the

development of new therapeutic drugs. As part of two Environmental

Protection Agency (EPA) contracts I have developed ligand-binding assays

for various "Orphan Nuclear Receptors" including the Farnesoid (FXR),

Pregnane (PXR), Liver (LXR), Thyroid (TR), Androgen (AR) and Retinoic Acid

(RAR). These receptors are possible targets for several synthetic

environmental contaminants. The effects of synthetic reagents on these

nuclear receptors may possibly lead to several metabolic disorders such as

"Lipid-X-Syndrome", heart disease, obesity, and diabetes.

WORK EXPERIENCE:

Research Scientist with a Joint Appointment in Cancer Prevention:

May, 2004 to July, 2006 Department of Medicine,

Cancer Prevention Section

State University of New York at Stony Brook

May, 2002 to May 2004 New York Medical College and the

Institute for Cancer Prevention (American Health

Foundation) Valhalla, New York

(Laboratory moved to State University of New York at Stony

Brook in 2004)

In the Cancer Prevention Section of the Department of Medicine at

SUNY at Stony Brook, I worked as a Research Scientist investigating the

mechanism(s) by which a novel class of nonsteroidal anti-inflammatory drugs

(NSAIDs) inhibits cancerous cell growth. The compounds under study are two

novel aspirin like drugs that are coupled to nitric oxide and are in

preclinical trials. I discovered that these compounds act by stimulating

several mitogen activated protein kinase pathways (MAPK) for signaling the

induction of cell cycle arrest and thus the inhibition of cell

proliferation. Utilizing RNA silencing (siRNA) I demonstrated that MAPK

activation is required and that the inhibitory protein p21 is the induced

mediator of the antiproliferative effect of these novel compounds. This

research also involved the study of nitric oxide and cyclooxygenase in

cancer.

Research focus was on the clinical use of non-steroidal anti-

inflammatory drugs containing a nitric oxide moiety, with the hope that

these novel compounds can be used prophylactic for the prevention of colon

cancer. The goal of my initial project is to identify molecular pathways by

which these drugs can act to prevent the growth of cancerous cells. The

molecular pathways investigated the mitogen activated kinase (MAP kinases)

pathways, inducible nitric oxide synthase (iNOS) and novel pathways that

may mediate selective death of cancer cells. Other molecular targets

studied for these drugs were the generation of free radicals and the

cyclooxygenase pathways.

Postdoctoral Fellow and Research Scientist:

June, 1996 to May, 2002 Laboratory of Molecular Immunology

National Heart, Lung, and Blood Institute

National Institutes of Health

Bethesda, Maryland

Research pursuits center upon determining the components of the MAP

kinase pathway that are involved in the mediation of degranulation and

eicosanoid production in a mast cell line. The major focus my

investigations were to characterize the roles of cytosolic phospholipase

A2, secretory phospholipase A2 and cyclooxygenase 2 (COX-2) in the

mediation of eicosanoid synthesis in mast cells. Later investigations were

to determine how the induction of cyclooxygenase is regulated by various

MAP kinases and to identify how the induction of COX-2 can be inhibited.

These investigations also encompass the study of COX-2 inhibitors that may

be used to inhibit the growth of cancer cells. Research collaborations

involved the development of a human mast cell line for the study of mast

cell activation by antigen stimulation.

WORK EXPERIENCE:

Postdoctoral Fellow:

July, 1993 to May, 1996 Johns Hopkins University

Asthma and Allergy Center

Baltimore, Maryland

Working in the laboratory of Dr. Donald W. MacGlashan, Jr. research

centered upon characterizing the various signal transduction pathways

involved in the mediation of histamine and leukotriene C4 release from

human basophils. Human basophils were obtained by a combination of

elutriation-centrifugation and Percoll gradient separation. The goals of

these investigations were to identify pathways that are common and points

of divergence in the pathways for the release of inflammatory mediators

stimulated by various stimuli. Also the second messengers that mediate

signal transduction were identified. Stimuli used in these investigations

were anti-IgE, formyl-methionyl-leucyl-phenylalanine, C5a, and calcium

ionophores. The major second messengers observed in these studies were

arachidonic acid and diacylglycerol. A major finding from these studies was

the identification of a secretory type phospholipase A2 as the source of

arachidonic acid for the synthesis of leukotriene C4.

HONORS and AWARDS:

National Cancer Institute N.I.H. Supplemental Grant for New Investigators,

2003 - 2006

Asthma and Allergy Award for Underrepresented Minority Investigators, 1993

Johns Hopkins Asthma and Allergy Center

BIBLIOGRAPHY:

ARTICLES:

1) Thomas R. Hundley and Basil Rigas

NO-donating aspirin inhibits colon cancer cell growth via MAP kinase

activation.The Journal of Pharmacology and Experimental Therapeutics Vol.

316:25-34. 2006

2) Adam Spiegel, Thomas R. Hundley, Jie Chen, Jianjun Gao, Nengtai

Ouyang, Xiaoping Liu, Mae F. Go, George J. Tsioulias, Khosrow Kashfi, and

Basil Rigas

No-donating aspirin inhibits both the expression and catalytic activity

of inducible nitric oxide synthase in HT-29 human colon cancer cells.

Biochemical Pharmacology Vol. 70: 993-1000. 2005

3) Thomas R. Hundley, Alasdair M. Gilfillan, Christine Tkaczyk, Marcus

V. Andrade, Dean D. Metcalfe, and Michael A. BeavenKit and Fc{epsilon} RI

Mediate Unique and Convergent Signals for Release of Inflammatory

Mediators from Human Mast Cells.

Blood Vol. 104: 2410-2417. 2004

4) Raymond Yeh, Jie Chen, Jennie L. Williams, Mehdi Baluch, Thomas R.

Hundley, Raphael E. Rosenbaum, Srinivas Kalala, Frank Traganos, Francesca

Benardini, Piero del Soldato, Khosrow Kashfi, and Basil Rigas

NO-donating nonsteroidal anti-inflammatory drugs (NSAIDs) inhibit colon

cancer cell growth more potently than traditional NSAIDs: a general

pharmacological property? Biochemical Pharmacology Vol. 67: 2197-2205.

2004

BIBLIOGRAPHY: ARTICLES

6) Audrey Robinson-White, Thomas R. Hundley, Miriam Shiferaw, Jerome

Bertherat, Fabiano Sandrini, and Constantine A. Stratakis Protein kinase-

A activity in PRKAR1A-mutant cells, and regulation of mitogen-activated

protein kinases ERK1/2.

Human Molecular Genetics Vol. 12(13):1475-1484. 2003

7) Michael A. Beaven and Thomas Hundley. 2003.

Mast cell related diseases: Genetics, signaling pathways, and novel

therapies. In "Signal Transduction and Human Disease" Eds T. Finkel and

J. S. Gutkind. John Wiley & Sons, Hoboken, NJ. pp307-355

8) Thomas R. Hundley, Anjana R. Prasad, and Michael A. BeavenElevated

levels of cyclooxygenase-2 in antigen-stimulated mast cells is associated

with minimal activation of p38 mitogen-activated-protein kinase.

The Journal of Immunology Vol. 167(3):1629-1636. 2001

9) Cristina Chaves-Dias, Thomas R. Hundley, Alasdair M. Gilfillan,

Arnold S. Kirshenbaum, Jose Renan Cunha-Melo, Dean D. Metcalfe, and

Michael A. Beaven

Induction of Telomerase Activity During Development of Human Mast Cells

from Peripheral Blood CD34+ Cells: Comparisons with Tumor Mast-Cell

Lines.

The Journal of Immunology Vol. 166(11): 6647-6656. 2001

10) Michael A. Beaven, David S. Cissel, and Thomas R. Hundley

Suppression of MAP kinase pathways in mast cells by glucocorticoids:

Mechanisms and consequences

In International Sendai Histamine Symposium, Excerpta Medica

International Congress Series. 2001 Yanai, K. and Watanabe, T. eds.

Elsevier Science, Amsterdam, Netherlands.

Abstracts:

1) Thomas Hundley, Dhanrajan Tiruchinapalli, Malathi Sathyamoorthy, Anna

Solomon, Cheryl Horton, Alexei Miagkov, and Hao Chen.

Characterizing cellular signal transduction cross-talk using kinase

screen and cell imaging. AACR, 2012

2) Alexei Miagkov, Rajneesh Uzgare, Shaobin Zhong, Lisa Leary, Janine

Ondrus, Thomas Hundley, Malathi Sathyamoorthy, Dhanrajan Tiruchinapalli,

Nicole Todaro, Christina Griffin, Rao Mulpuri, Damon Hostin, Jeffery

Otto, and Hao Chen.

Establishment and characterization of primary human lung

squamous carcinoma implant.

AACR, 2012

3) Malathi Sathyamoorthy, Rajneesh Uzgare, Julia Guzova, Anna Solomon,

Cheryl Horton, Thomas Hundley, Janine Ondrus, Alexei Miagkov, Ming Liu,

Victoria Wong, Hao Chen, and Karen Leach.

Development of a Cellular Kinase Assay Panel for use in Kinase Inhibitor

Selectivity Assessment.

Society of Toxicology 2012

4) Hao Chen, Ming Liu, Qi Su, Alexei Miagkov, Anna Solomon, Cheryl

Horton, Dhanrajan Tiruchinapalli, Edmond Massuda, Janine Ondrus, Lisa

Leary, Malathi Sathyamoorthy, Rajneesh Uzgare, Shaobin Zhong, Thomas R.

Hundley, and Xiaoyu Shen.

Stimulation for Discriminative Stimulus Effect of Cocaine Requires

Concurrently Attenuated Dopaminergic and Adrenergic Reuptake Activities.

Neuroscience 2011

5) Thomas R. Hundley, and Basil Rigas

Mitogen activated protein kinase (MAPK) signaling mediates the cell

growth Inhibitory effect of nitric oxide donating aspirin.

American Association for Cancer Research, 2004

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