Chairperson
Health Science Policy Analyst, Office of Scientific Program and Policy Analysis
National Institute of Diabetes and Digestive and Kidney Diseases
Bethesda, MD
Prior to coming to NCI, I completed my Ph.D. in tumor biology at the
Mayo Clinic College of Medicine in Rochester, MN where my thesis
research focused on characterization of an epidermal growth factor
receptor (EGFR) isoform. During my training at Mayo, I also became
interested in translational research that combines the techniques of
both epidemiology and basic science. I joined the CPF program at NCI
because it provided me with amazing resources to pursue my interests.
Through support from the CPF program, I also attained a Master of
Public Health degree in epidemiology and biostatistics from The George
Washington University in Washington, D.C. My research at NCI focuses on
the prolactin pathway and its role in human breast cancer. I also am
interested in early life events that may affect breast cancer
susceptibility.
Chairperson-Elect
Postdoctoral Fellow, Oncology and Pathogenesis Program
Memorial Sloan-Kettering Cancer Center, New York, NY
In 2007, it is estimated that about 219,000 men will be diagnosed with
prostate cancer and over 27,000 men will die from the disease.
Anti-androgen therapies are often effective in slowing prostate cancer
cell growth, but after prolonged treatment with anti-androgens, many
prostate cancers become insensitive to these anti-androgens and
progress. In some cases this conversion to a hormone-refractory state
is accompanied by amplification of or mutation in the androgen
receptor, but these changes in the androgen receptor are not found in
all cases of hormone-refractory prostate cancer and, therefore, cannot
solely explain the progression of the disease. The contribution of
androgen receptor signaling in prostate cancer is not fully understood
and it is my interest to further investigate and dissect modulators of
androgen receptor signaling and the transition from androgen sensitive
prostate cancer to hormone-refractory disease.
Past Chairperson
Scientific Investigator, Laboratory of Systems Biology
Van Andel Institute, Grand Rapids, MI
The primary focus of my laboratory is aimed at identifying and
understanding the genes and signaling pathways that control cell
survival, specifically those that when mutated contribute to the
pathophysiology of cancer. We take advantage of RNA interference (RNAi)
and novel proteomic approaches to identify the kinases and phosphatases
in the genome that control cell growth, cell proliferation, and cell
survival. For example, after screening over 600 kinases and 200
phosphatases encoded by the human genome (called the "kinome" and
"phosphatome") that cooperate with chemotherapeutic sensitization in
control of apoptosis, we identified 73 kinases (11%) and 72
phosphatases (32%) whose role in cell survival was previously
unrecognized. These studies led to several unanswered questions. How
are these novel survival kinases and phosphatases regulated at the
molecular level? What signaling pathway(s) do they regulate? Does
incubation of these genes inhibit waves of compensatory changes at the
cellular level (system level changes)? What are the system level
changes after reduction or loss of each gene?
We also take a systems biology approach to
understanding two key molecular pathways, the Ras/MAPK cascade and the
PI3K/mTOR pathways. One project in the lab involved answering the
question of whether the evolutionarily conserved MAPK pathway exhibits
a switch-like or graded response in mammalian cells. Ultrasensitive
switch-like responses control cell-fate decisions in many biological
settings, and the regulation of kinase activity is one way in which
ultrasensitive behavior can be initiated. In the case of extreme
ultrasensitive responses, signaling molecules switch between two
discontinuous, stable states with no intermediate responses; this is
referred to as a bistable response. Given the irreversible, all-or-none
nature of many cell behaviors, including cell cycle control and
apoptosis, significant effort has been focused on identifying the
cellular mechanisms underlying bistability in biological systems.
Graduate Student
University of Connecticut Health Center, Farmington, CT
(2008-2010)
My primary research interest is the role of microRNAs in cancer. This includes elucidating the mechanism by which miRNAs function, as well as how microRNAs control tumorigenesis. In my current graduate school research I have focused on microRNAs and breast cancer, which involves understanding endocrine-hormonal feedback loops, as well as the elucidation of hormonal regulation of microRNAs. I have applied for and received funding through various sources to continue my work on microRNAs in human breast tumor samples, so as to enhance the translational aspect of my research. I intend to continue this research career studying microRNAs within various tumor types. I feel that strong leadership, communication, and collaboration with other scientists are qualities that every early-career scientist must have in order to succeed.
Postdoctoral Fellow, Department of Biological Sciences
University of Maryland, Baltimore County, Baltimore, MD
(2007-2010)
My research is focused on uveal
melanoma which is the most common cancer of the eye and metastasizes in
approximately 50% of patients. Metastatic disease occurs predominantly
in the liver and is universally fatal. I am developing cell-based
vaccines that activate tumor-specific CD4+ and CD8+ T lymphocytes that
eliminate primary and metastatic uveal melanoma cells. The vaccines
(called MHC II vaccines) consist of tumor cells that are genetically
modified to express MHC Class II alleles and the costimulatory molecule
CD80. Uveal melanoma may be particularly appropriate for immunotherapy
because primary tumors arise in an immune privileged site.
FIRST Postdoctoral Fellow, Winship Cancer Institute
Emory University, Atlanta, GA
(2007-2010)
My research interest is in triple negative breast cancers that affect African-American women under the age of 45. Currently, I am working on the effects of Nitric Oxide and Galectin-3, a carbohydrate-binding molecule, and their possible roles in the induction of metastatic breast cancer. Through this project, I have found that increased expression of Galectin-3 increases the migratory rate of a non-invasive cancer cell line. As much as I enjoyed working in glycobiology, I am excited to move on to explore my own questions concerning cancer.
Research Fellow
Memorial Sloan-Kettering Cancer Center, New York, NY
(2008-2011)
My doctoral work focused on microbial-induced carcinogenesis investigating the role of H. pylori in gastric carcinogenesis. I investigated both host and microbial factors that were important to cancer development. I am continuing to investigate carcinogenesis, but am now investigating oncogene-induced carcinogenesis utilizing mouse genetic models of thyroid cancer to investigate the cooperative roles of PTEN and Ras signaling in thyroid tumorigenesis. I hope to establish a model of follicular thyroid cancer to begin pre-clinical testing of targeted therapies, including pharmacological inhibition of the MAP kinase signaling pathway. I served on several committees to act as a liaison between the student-trainee population and faculty, and want to continue this role within the Associate Member Council, serving as a voice for early-career scientists, especially female scientists. I feel very strongly that researchers in the cancer field need to give back to the community and those affected by cancer.
Assistant Member, Department of Epidemiology
Roswell Park Cancer Institute, Buffalo, NY
(2006-2009)
I was bitten by the research bug during my fourth year undergraduate research project in Dr. Edmund Li's laboratory at the University of Toronto, which examined serotonin levels in obese and normal weight rats using HPLC. Under the terrific mentorship of Dr. Li, who gave me a lot of scientific freedom to design (and negotiate) my M.Sc. project, I continued my studies in the area of serotonin metabolism and obesity. After developing a terrible allergy to rats, I left animal work and decided to study people. For my Ph.D., I delved into breast cancer research because it affected so many women, but maintained my interests on the role of lifestyle factors on disease etiology and progression, particularly the role of obesity, and decided to add genetic susceptibility to the mix. Under the mentorship of Dr. Norman Boyd, I examined the role of genetic polymorphisms in sex hormone metabolism genes on sex and IGF hormone levels, body size, and mammographic density levels, a strong independent risk factor for breast cancer. I also examined how these polymorphisms interacted with oxidative stress exposure, diet, and body size to affect breast density levels. After completing my Ph.D., I began a postdoctoral fellowship at Roswell Park Cancer Institute in Buffalo, NY with Dr. Christine Ambrosone and became interested in the determinants of weight gain in women with breast cancer. We designed and initiated a study to comprehensively examine genetic, physiologic, lifestyle, and psychosocial factors on weight gain among a prospective cohort of women being treated for breast cancer.
Odyssey Scholar, Department of Cancer Genetics
UT M.D. Anderson Cancer Center, Houston, TX
(2008-2011)
I am investigating the role of p53
induced cellular senescence in tumor suppression and response to
chemotherapy in a mouse model system. The laboratory of Gigi Lozano,
Ph.D., where I am a postdoctoral fellow, has created knockin mouse
models of different p53 point mutants that retain varying degrees of
function. For one of our projects, I am examining the molecular
response and outcome of breast tumors bearing these different p53 point
mutations to chemotherapy drugs, with a particular interest in p53
mutants that are capable of inducing arrest but not apoptosis. I look forward to contributing the knowledge garnered as a
graduate student, postdoctoral fellow, and experiences from having
served a leadership role in comparable organizations to the Associate
Member Council.
Resident, Department of Urology
UT Southwestern Medical Center, Dallas, T
(2008-2011)
In basic research, I am investigating the role of epigenetic control in
the pathogenesis of bladder, prostate, and kidney cancer. Moreover, I
have investigated several epigenetic-modifying drugs in preclinical
models of prostate and bladder cancer. In translational research, I am
investigating the role of apoptotic and signal transduction biomarkers
for prediction of clinical outcomes after radical cystectomy for
bladder cancer. In addition, I am studying novel blood-based biomarkers
to improve the preoperative prediction of lymph node metastases and
clinical outcomes after radical prostatectomy for prostate cancer. In
clinical research, I am working on a Phase II clinical trial using DES
for treatment of patients with advanced prostate cancer. As a resident
in a surgical program with the background of a foreign medical
graduate, I want to provide representation of a vital part of the AACR
membership.
Clinical Fellow/Resident, Division of Oncology
University Hospital of Basel, Basel, Switzerland
(2006-2009)
Since my first residency in Internal Medicine at the University Hospital of Basel, Switzerland, I have focused my interests on clinical and preclinical projects in oncology. A subsequent two-and-a-half-year postdoctoral fellowship at the University of California at San Francisco fostered my interests in drug delivery systems, such as liposomal and immunoliposomal approaches. In late 2003 I returned to Basel, Switzerland and since then I have pursued basic and translational research here. Our goal is to further optimize immunoliposomal drug delivery systems, in particular anti-EGFR immunoliposomes, and transfer this promising approach from bench to bedside. In addition to this project, we are currently interested in expanding immunoliposomal techniques to different targets and other anticancer drugs.
Graduate Student, Department of Experimental Medicine
McGill University, Montréal, CANADA
(2008-2011)
My research interests focus on understanding the molecular mechanisms that govern organ-specific metastasis of breast cancer. In an effort to identify novel mediators of breast cancer metastasis, we have paired gene expression-profiling with in vivo models of aggressive breast cancer, each harboring distinct, organ-specific metastatic potential. Using this approach, we have identified a gene known as GPNMB or Osteoactivin as being a novel mediator of breast cancer metastasis to bone. GPNMB is a cell surface protein that is highly expressed in metastatic human breast cancer; as such, it represents a promising target for therapeutic intervention. Currently, the majority of my research efforts concentrate on uncovering the mechanisms of action of GPNMB and characterizing the functional domains required for its pro-metastatic effects. My interest in serving on the Associate Member Council is propelled by my desire to assist in the design and implementation of novel programs and opportunities that will encourage young female scientists to follow through with their career aspirations. Ultimately, I hope that these kinds of initiatives will promote the proportional representation of male and female scientists at the upper echelon of the scientific community.
Research Fellow, Laboratory of Human Carcinogenesis, Center for Cancer Research
National Cancer Institute, Bethesda, MD
(2007-2010)
My research interests focus on the
molecular epidemiology of colon cancer, which allows me to merge my
expertise in epidemiology and biostatistics with my strong basic
science background. Currently, I am investigating the association of
mannose-binding lectin 2 (MBL2) single nucleotide polymorphisms (SNPs)
with risk of colon cancer in African-Americans utilizing a case-control
study from the greater Baltimore, MD area. I am currently conducting a
series of functional studies in our laboratory to ascertain the
phenotypes directly related to the SNP associations we have observed.
The ability to conduct well-outlined genotype-phenotype studies is
critical in identifying individuals with increased cancer risk.