CURRICULUM VITAE
THOMAS RUSSELL HUNDLEY
Home Phone : 301-***-****. Email address: *********@***.***
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