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Last Updated: 10/10/18

Vanderbilt University Breast SPORE

Principal Investigators:
Jennifer A. Pietenpol, PhD and Ingrid A. Mayer, MD, MSCI


Jennifer Pietenpol, PhD
Director, Vanderbilt-Ingram Cancer Center
Executive Vice President for Research, VUMC
Vanderbilt University Medical Center
652 Preston Research Building
Nashville, TN 37232
Tel: 615-936-1512
Fax: 615-936-1790

Ingrid A. Mayer, MD, MSCI
Ingram Associate Professor of Cancer Research
Associate Professor of Medicine
Division of Hematology/ Oncology
Vanderbilt University Medical Center/ Vanderbilt-Ingram Cancer Center
2220 Pierce Ave. 777 PRB
Nashville, TN 37232
Tel: 615-936-2033
Fax: 615-343-7602


This Breast Cancer SPORE renewal application was submitted by the VICCC and VUMC. It is comprised of investigators with expertise in cellular signaling and molecular biology, breast pathology, medical, surgical, and radiation oncology, clinical trial design, epidemiology and population studies, mass spectrometry, biostatistics, and biomedical informatics. The SPORE application is built on established and newer Institutional strengths. The investigators in the SPORE are truly committed to reducing the incidence, morbidity and mortality of breast cancer. All four projects are translational and multidisciplinary as discussed below. They are led by co-investigators from multiple Departments in the School of Medicine and with complementary basic science and translational/clinical expertise.

Project Title Clinical/Translational Basic/Translational
Inhibition of PI3 kinase as a strategy to abrogate antiestrogen resistance in breast cancer Ingrid A. Mayer, MD, MSCI
Carlos L. Arteaga, MD
(Hematology/Oncology, Cancer Biology)
Strategies to improve outcomes for triple negative breast cancer patients involving subtype-specific targeted therapies and genomic discovery Vandana Abramson, MD
Jennifer A. Pietenpol, PhD
McI-1 inhibitors for the treatment of breast cancer Melinda E. Sanders, MD
Rebecca S. Cook, PhD
(Cancer Biology)

Stephen W. Fesik, PhD
The obesity-metabolic biomarker axis and breast cancer risk William J. Blot, PhD

Loren Lipworth, ScD
Wei Zheng, MD, PhD, MPH


Carlos L. Arteaga, MD, Project Leader
Ingrid A, Mayer, MD, MSCI, Project Co-Leader

Antiestrogen therapies have changed the natural history of hormone-dependent, estrogen receptor-positive (ER+) human breast cancer. However, many ER+ tumors develop drug resistance and progress, with more patients still dying from ER+ breast cancer than all other breast cancer types combined. For the majority of these cancers, mechanisms of escape from antiestrogens remain to be discovered. During the previous award period, we have shown that activation of the phosphatidylinositol-3 kinase (PI3K) pathway can promote resistance to endocrine therapy, though demonstration of this mechanism awaits further confirmation in the clinic. The PI3K pathway is overall the most frequently altered oncogenic pathway in cancer. Mutations in PIK3CA, the gene encoding the p110a catalytic subunit of PI3K, are the most common somatic alterations of this pathway in breast cancer, where =80% occur within the helical (E542K, E545K) and kinase (H1047R) domains of p110a. These mutations confer increased PIP3-forming catalytic activity and induce a transformed phenotype including growth factor- and anchorage-independent growth, resistance to anoikis, and drug resistance. Small molecule pan-PI3K inhibitors that bind reversibly to the ATP pocket of p110 have completed phase I trials. Preclinical and few clinical studies have already suggested that ER+/PI3K mutant tumors exhibit a lower response to antiestrogens compared to ER+/PI3K wild-type tumors. Thus, we hypothesized that antiestrogens in combination with a PI3K inhibitor will be more effective against ER+/PI3K mutant breast cancers compared to the antiestrogen alone. In addition, breast cancers that do not respond to the combination will contain somatic alterations causally associated with drug resistance. To test these hypotheses, for the current funding period we proposed the following specific aims:

Aim 1: To determine the rate of clinical response and pathological complete response (pCR) at the time of definitive surgery at 24 weeks in patients with operable ER+/HER2– breast cancer treated with the aromatase inhibitor letrozole and a PI3K inhibitor (BKM120, a pan-PI3K inhibitor, or BYL719, an a-specific PI3K inhibitor). Patients with stage II-III ER+/HER2– (with wild-type or mutant PIK3CA) breast cancer were randomized to letrozole + placebo vs. letrozole + BKM120 vs. letrozole + BYL719 for 24 weeks. An ultrasound-guided biopsy was performed at two weeks to determine if the PI3K inhibitor increases letrozole action as measured by cellular, molecular and metabolic markers of tumor growth. Final results of this trial are expected in December 2017.

Aim 2: To identify molecular alterations potentially associated with drug resistance in breast cancers after neoadjuvant therapy with letrozole plus PI3K inhibitor. DNA was harvested from pre-treatment and surgical (post therapy) biopsies and will be subjected to whole exome sequencing. To validate copy-number variations, somatic single-nucleotide variants and insertion-deletions, and for tumors with scarce tissue, low cellularity and/or high heterogeneity, a (275) gene-targeted capture assay will be used.

Aim 3: To determine whether molecular alterations identified in post-treatment residual cancers are causally associated with resistance to the combination of letrozole and the PI3K inhibitor. Higher frequency mutations/amplifications identified in Aim 2 will be tested using conventional shRNA-based and overexpression approaches in human breast cancer cells and xenografts to determine a causal association with drug resistance. As a complementary approach and using a kinase-open reading frame (ORF) expression system, finally we will interrogate actionable mediators of resistance to antiestrogen therapy plus PI3K inhibitor in the human kinome.


Jennifer A. Pietenpol, PhD., Project Leader
Vandana Abramson, MD, Project Co-Leader

The term "triple negative breast cancer" (TNBC) is used to classify 10% - 20% of all breast cancers that lack estrogen receptor (ER) and progesterone receptor expression as well as amplification of the human epidermal growth factor receptor 2 (HER2). TNBC is biologically more aggressive than ER+ disease, with higher rates of relapse in the early stage and decreased overall survival in the metastatic setting. Disease heterogeneity and the absence of well-defined molecular targets have made treatment of TNBC challenging. There is a major need to better understand the molecular basis of this type of breast cancer as well as to develop effective therapeutic strategies against it.

We leveraged TNBC specimens collected from previous and ongoing Vanderbilt-Ingram Cancer Center (VICC) Breast SPORE-funded clinical trials (VICC: BRE9936, BRE0368, BRE0904) as well as 21 publicly available datasets from eight countries to perform a comprehensive analysis of gene expression (GE) data from 3247 breast cancer tumors. This compilation of worldwide data resulted in a data set of 587 TNBCs and classification of the disease into six subtypes with differing biologies [two basal-like, two mesenchymal-like, an immunomodulatory, and a luminal subtype expressing androgen receptor (LAR)]. We have since validated these using The Cancer Genome Atlas (TCGA) data. In addition, we identified 25 TNBC cell line models representative of these subtypes. Predicted ‘driver’ signaling pathways were pharmacologically targeted in these preclinical models as proof of concept that analysis of distinct GE signatures can inform therapy selection. Cell lines representative of the basal-like subtypes have higher expression of proliferation and DNA Damage Response (DDR) genes and preferentially respond to cisplatin. Mesenchymal subtype cell lines are enriched in growth factor pathway signaling and are sensitive to PI3K/mTOR inhibitors. Cell lines representative of a luminal subtype expressing androgen receptor (LAR) are uniquely sensitive to bicalutamide (an AR antagonist), and we discovered that LAR tumors and cells lines have high frequency of PIK3CA mutations.

Preclinical and clinical findings showing high frequency alterations in p53 and PI3K/mTOR signaling pathways lead to the proposed studies that translate preclinical findings to targeted therapies for TNBC patients. We leveraged cell-based models and our ever-growing, clinically annotated and integrative TNBC data set to determine mechanisms of drug response and resistance and to define biomarkers for patient selection. We proposed three specific aims to test the following interrelated hypotheses:

In TNBC patients with the LAR subtype (~10%), AR and PI3K signaling synergistically drive tumor growth, and treatment of these patients with an AR antagonist (enzalutamide) in combination with a PI3K pathway inhibitor will be an effective therapy. In the remaining 90% of TNBC patients, the high frequency of p53 mutations and PI3K signaling pathway alterations in their tumors will result in therapeutic vulnerability to the genotoxic agent cisplatin given in combination with a PI3K inhibitor. Comprehensive analysis of well-characterized tumors from patients on hypothesis-driven clinical trials will allow discovery of mechanisms of sensitivity and resistance as well as biomarkers that can be used in the development of new treatment regimens and selection of patients for future trials.

Aim 1: a) To evaluate the efficacy, as measured by clinical benefit rate (CBR) of enzalutamide + the Β-sparing PI3K inhibitor taselisib in patients with AR+ metastatic TNBC. b) To evaluate the efficacy, as measured by overall response rate (ORR) of cisplatin + pan-PI3K inhibitor pictilisib versus cisplatin alone in patients with metastatic AR-negative TNBC. We will determine if a set of genomic markers can predict sensitivity or resistance to the regimens tested in this phase II clinical trial.

Aim 2: To determine mechanisms of inherent and acquired resistance to cisplatin and PI3K inhibitors in the TNBC setting. Integrating data from synthetic lethal and forward genetic screens with genomic analyses of clinical specimens from our SPORE-related TNBC clinical trials, we will identify pathways leading to resistance.

Aim 3: To develop validated clinical biomarkers for TNBC subtyping and use in selection of patients for future clinical trials or new standard treatments. We will leverage comprehensive genomic information from our ever-growing data set of TNBC tumors and additional sets of TNBC tumors for validation of biomarkers.


Rebecca Cook, PhD, Project Co-Leader
Stephen Fesik, PhD, Project Co-Leader
Melinda Sanders, MD, Project Co-Leader

During breast tumorigenesis, deregulation of apoptotic signaling promotes tumor cell survival and limits cell death processes required to maintain normal tissue metabolism and function. Defects in apoptotic signaling are central to tumor initiation and maintenance of breast cancer cells, particularly in the context of unregulated tumor cell proliferation. Therefore, neutralizing the function of anti-apoptotic proteins may offer an effective strategy to arrest or eliminate breast cancer cells.

Amplification of the gene encoding the anti-apoptotic protein myeloid cell leukemia-1 (Mcl-1) is a common genetic aberration in human cancer. Mcl-1 overexpression in human breast cancer has been associated with high tumor grade and poor patient survival. Preclinical evidence suggests that Mcl-1 is a promising target for the treatment of breast cancers including the highly aggressive triple negative breast cancer (TNBC) subtype, which lacks molecularly targeted therapies. Further, Mcl-1 activity has been implicated in resistance to multiple therapies used in patients with breast cancer including microtubule-targeting agents. Therefore, we proposed that targeted inhibition of Mcl-1 will result in restoration of apoptotic signaling and increased sensitivity to chemotherapy in Mcl-1-dependent breast tumors.

Mcl-1 mediates its effects primarily through protein-protein interactions and is therefore considered difficult to target with small molecules. Although attempts to target Mcl-1 have been reported, compounds specifically targeting Mcl-1 have not entered the clinic. Using a combination of fragment-based methods and structure-based design, we have discovered novel small molecules that bind to Mcl-1 with high affinity (KD = 35nM) for the BH3-binding pocket, the motif used by Mcl-1 to bind to and sequester pro-apoptotic proteins. A similar strategy led to the successful development of ABT-263 (Navitoclax), a Bcl-2/Bcl-xL inhibitor currently in clinical trials (discovery led by Stephen Fesik, PhD, co-Leader of this Project). We proposed to further refine the current lead compounds to generate potent Mcl-1 inhibitors with sub-nanomolar binding affinities, robust cellular efficacies and desirable drug metabolism and pharmacokinetics (DMPK) profiles. We will use these compounds to evaluate a therapeutic strategy in breast cancer models. Our goal is to discover a small molecule Mcl-1 inhibitor that will be suitable for early clinical trials focused in patients with the triple negative subtype of breast cancer upon completion of the proposed Aims.

Aim 1: Discover potent (sub-nanomolar) and specific Mcl-1 inhibitors using fragment-based methods and structure-based design. Compounds binding tightly to Mcl-1 will be optimized using structure-based design and an iterative medicinal chemistry approach. Binding to Mcl-1 will be analyzed and the results will be incorporated into future analog design.

Aim 2: Optimize potent Mcl-1 inhibitors for their cell-based activities, pharmaceutical properties and in vivo efficacy in breast cancer models. A panel of TNBC cell lines will be analyzed using RNAi methodology to assess relative sensitivity to Mcl-1 loss of function. Sensitive cells will be used to test our lead Mcl-1 compounds in culture and in xenograft in vivo. In a genetically engineered mouse model of TNBC that develops mammary tumors overexpressing human Mcl-1, we will determine the antitumor effect of the lead Mcl-1 compounds in the context of an intact immune system and tumor microenvironment.

Aim 3: Identify genetic and molecular biomarkers of sensitivity to Mcl-1 inhibition, alone or in combination with other anticancer agents. The lead Mcl-1 inhibitory compounds will be tested in combination with chemotherapeutic drugs, including microtubule inhibitors and other Bcl-2 family inhibitors that have a different binding profile (ABT-263, ABT-199). Gene expression profiles and genomic aberrations in Mcl-1 inhibitor sensitive vs. resistant TNBC cell lines will be analyzed to identify molecular markers that predict response to the inhibitors as single agents and in combination with taxanes, Bcl-2 family inhibitors and other chemotherapeutic agents. As part of these analyses, we will determine the relevance of Mcl-1 gene copy number and/or protein overexpression to sensitivity to Mcl-1 inhibitors.


William Blot, PhD, Project Co-Leader
Loren Lipworth, ScD, Project Co-Leader
Wei Zheng, MD, PhD, MPH, Project Co-Leader

Existing epidemiologic studies suggest a complex relationship between obesity and breast cancer, with obesity generally associated with increased risk among postmenopausal women but reduced risk among premenopausal women, although results have been noted to vary by cancer subtype and race. Limited information exists on the obesity-breast cancer association for black women, the group with the highest prevalence of obesity, higher incidence of triple negative (and basal-like breast cancer), but lower incidence of the luminal subtype. It is possible that inconsistent associations between obesity and breast cancer risk in blacks and whites are explained in part by their differences in underlying mechanisms through which obesity is related to postmenopausal breast cancer risk. Although these mechanisms are not entirely clear, it is in general believed that obesity acts primarily by inducing insulin signaling and resistance, increased estrogen biosynthesis and inflammation to increase the risk of breast cancer. The relative contribution of these mechanisms to the pathogenesis of breast cancer may differ between blacks and whites, which may contribute to racial difference in risk of breast cancer by subtype. We propose a study to directly evaluate the relationship of these mechanisms to breast cancer risk and, further, to investigate through which pathway(s) obesity is related to breast cancer risk. The proposed research builds upon substantial published and preliminary analyses, in which we have demonstrated striking variation between black and white women in mean serum levels of adiponectin and leptin, anti- and pro-inflammatory cytokines, respectively, produced in adipose tissue, insulin-like growth factor 1 (IGF1) and C-reactive protein (CRP) and their associations with obesity. Our data support the hypothesis that these biomarkers act differently in their association with obesity and risk of breast cancer between racial groups.

We proposed herein a case-control study of postmenopausal breast cancer nested within the prospective Southern Community Cohort Study (SCCS) that is tracking over 50,000 women, two-thirds of whom are black, for breast and other cancer incidence. The SCCS is the largest ongoing prospective cohort study of black women with stored pre-diagnostic blood samples. Adding to this project’s novelty is the availability of tumor tissue for breast cancer cases, enabling one of the first prospective joint examinations of blood and tissue markers of risk. Further, the SCCS is uniquely positioned to assess obesity-related biomarkers as this cohort was recruited from a low-income population where obesity is common (58% of SCCS black women have a BMI>30 kg/m2). Diabetes also is a prevalent co-morbidity in this cohort. The specific aims are:

Aim 1: To determine whether circulating levels of IGF1, IGF-binding protein 3, adiponectin, leptin, CRP and sex hormones [estradiol, estrone, testosterone and sex hormone-binding globulin (SHBG)] are associated with risk of postmenopausal breast cancer, and whether they differ by race and/or tumor estrogen/progesterone receptor status. We hypothesize that risk will increase with all of these biomarker indices, except for a decrease with SHBG, and that the association will be modified by race and/or ER/PR status. We will test these hypotheses using a nested case-control approach and pre-diagnostic blood for 400 postmenopausal cases (~65% black) and 800 controls.

Aim 2: To determine whether the obese state upregulates tumor IGF1 signaling, estrogen receptor (ER) signaling and inflammation gene expression signatures to increase breast cancer risk, and if the extent of upregulation differs by race. We hypothesize that obesity upregulates these pathways in breast tissue to increase risk of breast cancer, but that the extent of the upregulation by obesity differs by race. We will test these hypotheses using tumor samples from 500 postmenopausal breast cancer cases (~65% black) and adjacent normal tissue samples from a subset of 100 cases.

Aim 3: To determine whether pre-diagnostic circulating levels of IGF1, sex hormones and inflammation markers are associated with IGF1 signaling, ER signaling and inflammation gene expression signatures, respectively, in breast cancer tissues. We hypothesize that circulating levels of IGF1, sex hormones and inflammation markers (leptin, adiponectin and CRP) will correlate with markers of IGF1, ER and inflammation signaling, respectively, in breast cancer tissues. We will test these hypotheses in the subgroup of 240 breast cancer cases that have both pre-diagnostic serum and tumor biopsies available.


Core Directors: Jennifer A. Pietenpol, PhD and Ingrid A. Mayer, MD, MSCI

The Administration & Outreach Core supports SPORE projects and investigators by managing SPORE resources, quality control, and communication and outreach, including fostering interaction among SPORE components and collaborators, other SPORES, the patient and advocate community, and the NCI. This management and support is accomplished through a series of oversight committees and organized administrative and scientific meetings of SPORE investigators, institutional representatives and external advisors. Specific functions of the Core include:

  • To administratively manage and coordinate all SPORE-related research
  • To monitor and manage financial resources
  • To create and prepare documents and reports to ensure compliance with federal regulations and reporting requirements
  • To administer the Developmental Research (pilot project) and Career Development Programs
  • To organize all meetings, seminars, and travel related to Breast Cancer SPORE activities
  • To serve as a point of contact to all VICC fundraising activities focused in breast cancer
  • To support and coordinate all internal and external collaborations
  • To serve as a main point of contact to biotechnology and pharmaceutical companies

Carlos L. Arteaga, MD, will serve as Director of the Core. Arteaga reports directly to Jennifer Pietenpol, PhD, Director of VICC, and has input and assistance from the Deputy Director (Daniel Beauchamp, MD) and the Associate Directors for Basic Science (Scott Hiebert, PhD) and Cancer Epidemiology, Prevention & Control (William Blot, PhD). Arteaga provides advice to Dr. Pietenpol on programmatic directions and allocation of VICC resources for research in breast cancer. Since 2006, Ms. Jane Kennedy has served as Manager of Patient Advocacy in the VICC Office of Patient & Community Education (OPACE). Ms. Kennedy’s role includes recruiting, training and coordinating the survivors and caregivers who contribute to and support the Research Advocacy Program of VICC, including the Breast SPORE.


Core Director: Ingrid Mayer, MD, MSCI

The Clinical Core is designed to support all VICC breast cancer clinical trials conducted in the SPORE. Its main goals are: a) translate the latest insights of disease biology into rigorously designed SPORE clinical trials; b) streamline biologic sample collection in these clinical trials; c) minimize delays in the activation and promote timely completion of SPORE clinical trials; d) ensure safety of research subjects, adherence to institutional and federal regulatory requirements, and compliance with protocol-specified activities; and e) provide the expertise and manpower to develop, implement, manage and monitor all Breast Cancer SPORE clinical trials (internally and externally - multicentric trials). Over the course of this grant, the Clinical Core will support translational clinical trials coming from: two of the four main projects described in this grant application (projects 1 and 2), future pilot and career development projects, Inter-SPORE and inter-institutional collaborations, aligned with our SPORE. The Clinical Core will work closely with other SPORE Cores and the Clinical Trials Shared Resource of VICC to coordinate all aspects of clinical research, including imaging data extraction, biostatistics support, and biospecimen collection/ processing. The intensive nature of the clinical trials conducted by the SPORE (in terms of precisely timed interventions, the need for coordination of clinical intervention, radiological evaluation, specimen procurement, stabilization, and transport to the Pathology & Tissue Informatics Core, and the need to ensure protection of patients safety and privacy while linking clinical and specimen databases) must be tightly coordinated so that they are done on a consistent schedule, in a consistent fashion, to ensure that information obtained from one patient is comparable to data collected from all the others. Close coordination of clinical, administrative, and research staff activities are required to ensure that the responsibilities and costs for every element of the clinical trial are clearly defined and delineated. In summary, a Clinical Core focused on SPORE related clinical trials is essential for the success of the SPORE, and it has all resources available to achieve the aims outlined in the proposal.


Core Co-Director: Mia Levy, MD, PhD
Core Co-Director: Melinda E. Sanders, MD

The Pathology and Tissue Informatics Core (PTIC) is essential for the success of the Vanderbilt Breast Cancer SPORE. The goal of the PTIC is to facilitate the clinical and translational research aims of this renewal application via three primary missions: 1) To provide human tissue and body fluid collection, processing and quality control according to standardized protocols by trained personnel; 2) To provide specialized technical and diagnostic histo-pathology services in human and mouse tumors including expertise in performance and interpretation of immunohistochemistry (IHC), immunofluorescence (IF), and fluorescence in situ hybridization (FISH) assays, diagnostic and cellularity assessments on all procured tissue used for correlative studies, and construction of tissue microarrays; and 3) To provide high-quality and efficient informatics support for collection, pathological and clinical annotation, tracking and distribution of breast tissues for translational research. The core is co-directed by an expert breast pathologist and the Vanderbilt Ingram Cancer Center (VICC) Director of Clinical Informatics who oversees the development and maintenance of the clinical research information systems. All tissue is collected from patients with breast cancer consented for enrollment into SPORE and VICC protocols or under the auspices of the Vanderbilt Breast Tissue and Body Fluids Repository. The Repository, established in the initial funding period of this Breast SPORE, is now a robust collection of over 25,000 tissue, blood and urine samples, available to Breast SPORE investigators, which are linked to clinical data through the Breast SPORE Database. The core provides best practices oversight of optimal tissue utilization for each tissue specimen enabling numerous correlative studies such as gene arrays, sequencing and IHC to be performed on small tumor samples. The core will be directly involved in the analysis of these studies and will interact extensively with all the projects.

The PTIC provides a centralized mechanism for performance of specialized technical and diagnostic histopathology services, critical to the success of the Breast SPORE, preventing the inefficiencies of tissue acquisition by individual projects and the performance of tissue-based assays by inexperienced hands.


Core Director: Yu Shyr, PhD

The purpose of the Biostatistics Core is to provide professional expertise in biostatistics and bioinformatics for all Breast Cancer SPORE projects, investigators, and participants. Functions provided by this core include development of experimental designs, power analysis, and sample size estimation; data quality control statistical/bioinformatic analysis and interpretation of findings; and collaboration on presentation of results. To achieve these functions, the core director and core members are constantly available to investigators, and are in regular contact with project and core leaders.

The primary objectives of the Biostatistics Core are:

  1. To provide study design and review all laboratory, animal, and clinical studies including feasibility assessment, power analysis, and sample size estimation
  2. To collaborate in project data analysis, interpretation of results, and the writing of final study reports and manuscripts
  3. To work with the Pathology & Tissue Informatics Core and Imaging Core in the development of research project databases, to maintain data quality control and to ensure timely data capture
  4. To develop and evaluate statistical/bioinformatic methods for experimental design and data analysis Biostatistics Core support is required in all Breast Cancer SPORE studies. Core personnel have worked and will continue to work closely with project leaders to ensure the core provides state-of-the-art statistical/bioinformatic support.


Core Co-Director: H. Charles Manning, PhD

The overall goal of the Imaging Core is to develop, optimize, implement, and validate quantitative, surrogate predictive biomarkers of: 1) drug target engagement, 2) the type of antitumor effect induced by a particular treatment, and 3) the response of breast cancer to treatment. The Imaging Core will offer a full range of small animal functional, anatomical, and molecular imaging techniques, including magnetic resonance, computed tomography, ultrasound, fluorescence, single photon emission computed tomography (SPECT) and positron emission tomography (PET) imaging. Breast SPORE investigators will also have access to novel probe development resources, including high-throughput, diversity-oriented synthesis capabilities suitable for identifying novel imaging compounds, as well as the resources of the state-of-the-art Vanderbilt University Research Radiochemistry Core. Novel and established molecular imaging techniques will be offered which are specifically tailored for assessing quantitative metrics of cellular metabolism and proliferation, apoptosis, angiogenesis, receptor expression and inflammation. As in the previous funding cycle, the Imaging Core will continue to partner with other Cores in the SPORE and forge new connections with the VUIIS such that services are highly cost-effective. To provide this support to the projects, the Imaging Core has identified the following three specific alms:

  1. Foster collaborations between experts in advanced, quantitative non-invasive imaging and breast cancer research. In particular, the Core will support experts in all major imaging modalities, with particular emphasis on positron emission tomography (PET) and magnetic resonance imaging (MRI).
  2. Develop, validate, and provide non-invasive imaging metrics of drug distribution, drug target engagement, tumor initiation, progression and treatment response for Breast SPORE investigators.
  3. Provide support for analysis of quantitative imaging data, development of customized imaging protocols, including the co-registration and integration of multiple imaging modalities, histology and other in situ assays, and the development of novel imaging biomarkers.
Investigator Degree Department
Arteaga, Carlos L. MD Hematology/Oncology, Cancer Biology
Lehmann, Brian D. PhD Biochemistry
Blot, William J. PhD Epidemiology
Cook, Rebecca S. PhD Cancer Biology
Fesik, Stephen W. PhD Biochemistry
Abramson, Vandana MD Hematology/Oncology
Pietenpol, Jennifer A. PhD Biochemistry
Lipworth, Loren ScD Epidemiology
Manning, H. Charles PhD Radiology
Mayer, Ingrid A. MD, MSCI Hematology/Oncology
Sanders, Melinda E. MD Pathology
Levy, Mia MD, PhD Hematology/Oncology, Bioinformatics
Shyr, Yu PhD Cancer Biostatistics