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Last Updated: 10/10/18



Principal Investigator
Samuel Denmeade, M.D.


Samuel Denmeade, MD
Professor of Oncology
Johns Hopkins University School of Medicine
The Bunting-Blaustein Cancer Research Building
1650 Orleans Street
Baltimore, MD 21287
Tel: (410) 955-8875
Fax: (410) 614-8397


Prostate cancer has become one of the most frequently diagnosed cancers in men in the United States (US) and a major cause of cancer morbidity and mortality. Over the past decade and a half, dedicated prostate cancer research, accomplished by Johns Hopkins Prostate Cancer SPORE investigators and other researchers, has led to a remarkable accumulation of knowledge about the molecular mechanisms by which human prostate cancers arise and progress to threaten life. To improve screening, early detection, diagnosis, prevention, and treatment of prostate cancer, these new insights into prostate cancer molecular biology need to be translated into new hypotheses for testing in population studies and in clinical trials. The transcendent objective of the Johns Hopkins Prostate Cancer SPORE is to reduce prostate cancer incidence and mortality via the focused pursuit of translational research in prostate cancer.

The National Cancer Institute (NCI) has defined translational research for the SPORE program as “[using] the knowledge of human biology to develop and test the feasibility of cancer-relevant interventions in humans and/or [determining] the biological basis for observations made in individuals with cancer or in populations at risk for cancer.” During its initial funding period under the leadership of Donald S. Coffey, Ph.D., and in the most recent funding period under the leadership of William G. Nelson, M.D., Ph.D., the Johns Hopkins Prostate Cancer SPORE Program has emerged as a major center for translational research in prostate cancer, successfully promoting (i) the identification of new methods for prostate cancer risk assessment, (ii) the application of new strategies for prostate cancer screening, (iii) the discovery of new molecular biomarkers for prostate cancer diagnosis, detection, and prognosis, (iv) the development of new opportunities for prostate cancer prevention, and (v) the introduction of new approaches to prostate cancer treatment, including the use of endothelin receptor antagonists, replication-restricted adenoviruses, and genetically-modified prostate cancer cell vaccines. Since the last competitive renewal application, the Johns Hopkins Prostate Cancer SPORE Program Investigators and other Prostate Cancer Program researchers have produced some 566 published manuscripts. To accomplish its translational research mission, the Johns Hopkins Prostate Cancer SPORE Program established a productive research team by recruiting a diverse collection of dedicated prostate cancer researchers from the Departments of Urology, Oncology, Pathology, Radiation Oncology, and Radiology in the Johns Hopkins University School of Medicine and its Sidney Kimmel Comprehensive Cancer Center (SKCCC), as well as from the Departments of Environmental Health Sciences and Epidemiology in the Johns Hopkins Bloomberg School of Public Health, and by identifying and mentoring talented new prostate cancer researchers through Career Development initiatives. The SPORE Program has also succeeded in creating critical Core Resources, which, along with other dedicated institutional resources, have been exploited to support the critical mass of translational researchers, and in establishing productive interactions with other funded Prostate Cancer SPORE Programs at other institutions.

For the future, the Johns Hopkins Prostate Cancer SPORE Program aims to build on track record of success to further its translational research agenda. With support from the Patrick C. Walsh Prostate Cancer Research Fund, a $1,000,000 institutional commitment to the SPORE Program goals, and from the SPORE Program Career Development and Developmental Research Programs, the SPORE Program leadership team, William G. Nelson, M.D., Ph.D., serving as Principal Investigator, and Kenneth J. Pienta, M.D., serving as Co-Principal Investigator, has assembled a vibrant pipeline of new prostate cancer translational research opportunities. This ample pipeline has enabled the Johns Hopkins SPORE Program to remain true to the SPORE goal of “…capitalizing on research opportunities that have the potential to change the current paradigm in the prevention, detection, diagnosis, and/or treatment of human cancer…[leading] to a human application within the 5-year term of the grant…”: each of the current SPORE Projects will have achieved this goal by the spring of 2008. For this SPORE Program renewal application, a collection of six translational Research Projects, two Projects evolving from the currently funded SPORE and four new Projects emerging from the discovery pipeline, three Core Resources, two Developmental Research Projects, and two Career Development Projects, has been assembled to best exploit the most recent advances in the understanding of prostate cancer molecular biology, to best apply the most modern research technology to human prostate cancer, and to best accelerate the introduction of innovative new approaches for prostate cancer screening, early detection, diagnosis, prevention, and treatment.

PROJECT 1: PEG-Prom Mediated Theranostics for Prostate Cancer

Martin Pomper, M.D., Ph.D.
Paul B. Fisher, Ph.D.

Robert Hobbs, Ph.D.
George Sgouros, Ph.D.
Steve Yoon-Ho Cho, M.D.

The goal of this proposal is to develop a platform technology for detection and therapy of prostate cancer (PCa) based on induced cancer-specific expression of target proteins. A variety of treatment options are available for PCa at various stages of the illness. In the US active surveillance is being reconsidered as an option for local disease due to the increasing recognition that many men undergo unnecessary prostatectomies. The idea behind active surveillance is that there is an indolent form of PCa that will never metastasize and will therefore not pose a major threat to the patient in the short or long term. There is currently no way to differentiate between indolent or aggressive disease — no marker or panel of markers, no imaging agent to follow the course of the disease in vivo reliably. One approach is that since it is nearly impossible to determine which tumors will progress, they should all be treated, and preferably when they are small, before they further de-differentiate and begin to metastasize. But they should not all be treated surgically, due to the well-known co-morbidities for resection of PCa, even with modern, nerve-sparing techniques. Last year the US Preventive Services Task Force issued a draft recommendation statement against prostate-specific antigen (PSA) screening for all age groups. The recommendation specifically states that “prostate-specific antigen-based screening results in small or no reduction in prostate cancer-specific mortality and is associated with harms related to subsequent evaluation and treatments, some of which may be unnecessary.” That statement underscores the need for new, sensitive biomarkers for PCa, which can be used along with PSA history to provide suitable, tailored therapy. We are proposing a radical new method for detecting and treating PCa, whether it is localized, just beyond the capsule or widespread and metastatic to bone. The method relies on the discovery of the progression elevated gene-3 promoter (PEG-Prom), which is up-regulated in cancer and only cancer, i.e., it remains quiescent within normal or even immortalized normal tissue. It is by virtue of the concurrent expression of the transcription factors AP-1 and PEA-3 that PEG-Prom becomes activated. When cloned in front of an imaging reporter gene, such as firefly luciferase (Luc) or the herpes simplex type 1 virus thymidine kinase (HSV1-tk) or a therapeutic gene, such as melanoma differentiation associated gene-7/interleukin-24 (mda-7/IL-24), these latter genes become activated only in the presence of malignancy — including PCa. Furthermore, we have shown that the PEG-Prom can be delivered systemically using a non-viral, nanoparticle vector. Activated only within malignant tissues, the PEG-Prom system can seek out and become activated specifically within PCa to delineate and concurrently eradicate it. PCa is among the cancers that have demonstrated PEG-Prom activity in vitro and has proved highly susceptible to the activity of mda-7/IL-24. The goal of this proposal is to move these promising in vitro and limited (direct injection) in vivo results to relevant rodent models en route to clinical translation.

Specific Aim 1:
Development and optimization of vector constructs for PEG-Prom mediated imaging and therapy for PCa.

Specific Aim 2:
Quantitative imaging of relevant PCa metastatic model systems in vivo via bioluminescence and single photon emission computed tomography (SPECT).

Specific Aim 3:
Therapy of metastatic PCa through use of therapeutic analogs of the HSV1-TK substrates (a) ganciclovir (GCV) and (b) [131I] FIAU. Development and testing of the theranostic agent (Luc + mda-7/IL-24).

Specific Aim 4:
First-in-man PEG-Prom mediated imaging in metastatic PCa.


Shawn Lupold, Ph.D.
Theodore DeWeese, M.D.

Radiation therapy is one of two primary treatments for clinically-localized prostate cancer (PCa) and is the principal therapy for locally-advanced disease associated with a higher grade, stage and/or PSA. While the success rate for both radiation and surgery is high for low-risk, organ-confined disease, the estimated ten-year disease-free survival for advanced PCa is less than 50%. Therefore, a means to improve the treatment of patients with clinically-localized high stage and/or grade prostate cancer would significantly decrease the morbidity and mortality of this disease.

In the previous funding cycle, we hypothesized that the therapeutic index for local treatment of PCa would be improved by selectively sensitizing prostate cancer cells to ionizing radiation (IR). To address this, we developed prostate-targeted RNA interference (RNAi) agents that selectively inhibit DNA repair pathways (Fig 1). Tissuespecific targeting was achieved through an RNA aptamer, A10-3, which binds to the Prostate Specific Membrane Antigen (PSMA) on the cellular surface and is then internalized into cells. The conjugated short hairpin RNAs (shRNAs) are then processed by cellular RNAi machinery, leading to knock-down of specific DNA repair mRNA and proteins. Aptamer-targeted knock down of DNA Protein Kinase (DNA-PKcs) prior to IR therapy significantly enhanced IR therapeutic response, resulting in a dramatic extension of tumor quadrupling time from one week with IR alone to ten weeks with aptamer-sensitized IR [31]. Here we are now proposing two translational aims to bring these agents into the clinic and to develop them as systemic agents for the enhanced treatment of high risk localized and metastatic PCa.

Prostate cancer cells, like normal prostate secretory-luminal epithelial cells, produce very high levels of the PSA. PSA is aptly named, in that it is produced at high levels exclusively by prostate cells and is not produced in significant amounts by any other normal tissue in the human male. PSA is a chymotrypsin-like serine protease that is used extensively as a biomarker to screen for prostate cancer, to detect recurrence following local therapies and to follow response to systemic therapies for metastatic disease. PSA, however, is also a well credentialed therapeutic target for prostate cancer. The focus on PSA’s role as a biomarker has made perhaps made “PSA” synonymous with “biomarker” and this may explain why PSA has not been given consideration as a therapeutic target. However, a significant number of studies have also implicated a role for PSA in the pathobiology of prostate cancer. These studies emphasize the importance of PSA as a therapeutic target for prostate cancer. Therefore, the hypothesis of this project is that small molecule inhibitors of PSA’s enzymatic activity will have therapeutic efficacy against prostate cancer local growth, progression and/or metastases. The goal of this project, therefore is to identify and develop novel small molecule inhibitors of PSA. To achieve this goal, we propose the following Specific Aims:

Specific Aim 1:
Clinical evaluation of A10-3-DNA-PK.

Specific Aim 2:
Systemically delivered aptamer-siRNA radiation sensitizing agents


William G. Nelson, M.D., Ph.D.
Srinivasan Yegnasubramanian, M.D., Ph.D.

Michael Carducci, M.D.
Sarah Wheelan, M.D., Ph.D.

Somatic epigenetic defects are present in all human prostate cancers, leading to silencing of critical genes and pathways (1). However, unlike genetic deletions and mutations, the epigenetic alterations are potentially reversible. For this reason, reactivation of epigenetically silenced genes offers a rational approach to prostate cancer treatment. Small molecule inhibitors of DNA methyltransferases (DNMTs) and histone deacetylases (HDACs) have already secured US Food and Drug Administration (FDA) approval, as single agents, for myelodysplasia and cutaneous T-cell lymphoma, respectively; however, these agents have shown only limited activity thus far when used as single agents to treat advanced prostate cancer (2-4). Nonetheless, epigenetic drugs trigger the reactivation of ~400 genes or more in cancer cells, altering various signaling and stress response pathways and effectively reprogramming the cancer cells. As a result, the epigenetic drugs expose new vulnerabilities to agents targeting products of genes critical to cell survival in the reprogrammed state. To explore this possibility for prostate cancer, a discovery research program, supported by a Mazzone Challenge Award from the Prostate Cancer Foundation (PCF), screened for promising combinations of epigenetic drugs and targeted drugs that exhibit synthetic lethality, a phenomenon where at concentrations for which neither drug is toxic to prostate cancer cells when given as a single agent, combined treatment proves profoundly effective at cancer cell killing. This treatment paradigm has been referred to as Induced Synthetic Lethality with Epigenetic Treatment (ISLET). The screen yielded 41 candidate molecular targets showing properties of synthetic lethality, at least 7 of which are actionable using existing approved or investigational targeted drugs. One of the targets, Aurora kinase A, has available inhibitors that have been introduced in early clinical trials for cancer (5). The goal of this new Project is to translate a new combination of a DNMT inhibitor (decitabine) and a targeted drug (the Aurora kinase inhibitor alisertib) into human clinical studies for advanced prostate cancer.

Specific Aim 1:
To estimate the therapeutic index of DNMT inhibitor/Aurora kinase inhibitor combinations using human prostate cancer cell lines propagated as xenograft tumors in immunodeficient mice.

Specific Aim 2:
To explore molecular determinants of response to DNMT inhibitor/Aurora kinase inhibitor combinations.

Specific Aim 3:
To introduce a DNMT inhibitor/Aurora kinase inhibitor combination into human clinical trials for men with castration-resistant prostate cancer.


John T. Isaacs, Ph.D.
Samuel Denmeade, M.D.

Presently, there is no effective treatment for either preventing the initial development of prostate cancer or curing a man once he develops prostate cancer throughout the body (i.e., metastatic disease). While intensive research efforts have yielded several new agents with modest effects on survival, the standard therapy for prostate cancer once it has spread throughout the body has remained nearly the same for the last 70 years. The standard approach is to block the body’s ability to produce androgens. This is termed androgen ablation or more commonly hormonal therapy. In men with prostate cancer spread throughout the body, such androgen ablation does produce an initial positive relief from clinical symptoms. Unfortunately, however, after a variable period of symptom relief, symptoms return eventually killing the patient. Thus, prostate cancer will kill more than 32,000 US males this year alone (1).

Based upon substantial published literature from multiple groups, as well as unpublished studies to be presented from the applicants’ laboratories, there is strong documentation that bone marrow- derived Mesenchymal Stem Cells are released into the blood stream and home to sites of primary and metastatic prostate cancer driven by the inflammatory microenvironment characteristically present within prostate cancer’s stromal compartment. Thus, the hypothesis of this application is that allogeneic human bone marrow-derived MSCs (hbMSCs) can be used as a cell-based targeting vehicle to selectively deliver (i.e., home) therapeutic agents to sites of prostate cancer, thus sparing host toxicity. In this application, data will be presented validating the rationale for this “Trojan Horse” approach in which allogeneic hbMSCs are genetically-engineered to express a recombinant pro-aerolysin protein protoxin. While initially inactive, this protoxin is engineered to be selectively hydrolyzed to a picoMolar killing molecule by the enzymatic activity of a protease [i.e., Prostate Specific Antigen (PSA)] which is only enzymatically active in high levels within the stroma at sites of prostate cancer. In support of this approach, since the original submission, we have received Prostate Cancer Foundation/Movember Challenge Funding to perform a Phase 0 clinical trial testing the homing hbMSCs to sites of prostate cancer following intravenous infusion in men with localized prostate cancer prior to undergoing prostatectomy. Dr. Denmeade is the PI of this study that will be performed under an IND that was FDA-approved in May of 2013. This support is paying for cost of GMP production of hbMSCs by the Johns Hopkins Cell Therapeutics Lab. Dr. Denmeade has prepared a protocol that includes a detailed data safety monitoring plan and after review of protocol (NA_00083720), design and ethical issues associated with the approach he has received approval from the Johns Hopkins University School of Medicine IRB to infuse these hbMSCs into patients pre-prostatectomy. Tissue from harvested prostates will undergo digital PCR-based BEAMing analysis for the cell proportions in sites of prostate cancer. The expenses for these BEAMing analyses are provided by a DOD Synergistic Award to Dr. Isaacs. It is anticipated that the first patient will receive treatment early in November. The results from this trial will support the design of in vivo infusion protocols described in this proposal. Furthermore, since hbMSCs are being tested in clinical trials for regenerative medicine and recombinant PSA-activated pro-aerolysin is in clinical testing as local therapy for prostate diseases, the proposed use of PSA-activated pro-aerolysin (PSA-PA) expressing hbMSCs could rapidly enter clinical development as systemic therapy for lethal metastatic prostate cancer based upon the successful completion of the following specific aims:

Specific Aim 1:
Is to genetically modify hbMSCs to endogenously express and secrete biologically active recombinant PSA activated pro-aerolysin (PSA-PA)

Specific Aim 2:
Is to develop a “standardized infusion protocol” for allogeneic hbMSCs in xenograft studies which mimics the homing efficiency to sites of prostate cancer in humans.

Specific Aim 3:
Is to use this “standardized infusion protocol” to evaluate the therapeutic efficacy vs. host toxicity of PSA-PA expressing allogeneic hbMSCs against a series of human prostate cancer xenografts growing subcutaneously, orthotopically in the prostate, or in the bone.


Elizabeth Platz, Sc.D., M.P.H.
Alan K. Meeker, Ph.D.

Toby Cornish, M.D., Ph.D.
H. Ballentin Carter, M.D.
Christopher M. Heaphy, Ph.D.
Corinne Joshu, Ph.D.

For Project 5, the population science project, we assembled an interdisciplinary prostate cancer research team, co-led by an applied (epidemiologist) and a basic (telomere biologist) scientist, to address an unmet clinical need for prostate cancer patients: improved risk stratification. Specifically, we will verify a novel tissue biomarker of prognosis in men with clinically-localized prostate cancer that we discovered — telomere length variability in prostate cancer cells combined with short telomere length in cancer-associated stromal cells (“telomere biomarker”). In the prospective cohort — Health Professionals Follow-up Study (HPFS), the telomere biomarker was strongly associated with prostate cancer death after prostatectomy, including in Gleason 7 disease. Men without the biomarker rarely died of their cancer over 15 years. Because current prognostic factors inadequately distinguish between aggressive and nonaggressive disease, new markers that inform beyond the current factors are needed for clinical management decision-making. While our findings point to the telomere biomarker’s prognostic utility, we have completed only the discovery phase.

Project 6 is responsive to the prostate cancer SPORE population science project requirement in that we focus on risk for disease lethality and we use populations of men at risk for prostate cancer death, epidemiologic designs and methods, and population-level inferences. Further, Project 6 is responsive to the overall SPORE requirements because it is co-led by applied and basic scientists, includes a clinical investigator and other scientists, who have a track record of productive, interdisciplinary prostate cancer team science, will heavily use the Pathology and Biostatistics Cores and be supported by the Administrative Core. We expect that in 5 years the telomere biomarker will be tested for prognostic utility in a clinical trial.

Specific Aim 1:
Demonstrate the validity and reproducibility of automated “TELI-FISH”, our FISH-based telomere length measurement tool, and re-estimate the association between the telomere biomarker and prostate cancer death in the same prospective HPFS cohort study.

Specific Aim 2:
Conduct a nested case-control study to verify the association between the telomere biomarker, assessed using automated TELI-FISH, and lethal prostate cancer, including in men with Gleason 7 disease, a group for whom clinical management decisions are not always clear.

Specific Aim 3:
Determine optimal cutpoints to refine the telomere biomarker model for risk stratification using the prospective cohort and nested case-control studies of lethal prostate cancer from Aims 1 and 2.

Specific Aim 4:
Evaluate whether the prevalence of the refined telomere biomarker from Aim 3 differs by age, race, and body mass index (BMI) in cross-sectional and nested case-control studies.


Core Directors:
Samuel Denmeade, M.D.
Kenneth J. Pienta, M.D.
Bruce Trock, Ph.D.

The Administrative Core Resource is responsible for the managerial oversight of the Prostate Cancer SPORE Program, for the integration of SPORE Program translational research activities into basic and clinical research activities at the Sidney Kimmel Comprehensive Cancer Center (SKCCC) and Johns Hopkins University Schools of Medicine and Public Health, for stimulating new research opportunities through distribution of SPORE Developmental Research funds, for the identification of talented young translational researchers to be supported with SPORE Career Development funds, for facilitating and managing interactions/collaborations between the Johns Hopkins Prostate Cancer SPORE Program and Prostate Cancer SPORE Programs at other institutions, and for orchestrating productive responses to new National Cancer Institute (NCI) initiatives. Managerial coordination of the Johns Hopkins Prostate Cancer SPORE portfolio of Research Projects and Core Resources is critically needed to promote the effectiveness of the SPORE Program for translational research in prostate cancer. SPORE Investigators from several academic Departments at the Johns Hopkins School of Medicine have been assembled into multi-disciplinary Research Project teams, with expertise in prostate cancer molecular biology (“basic” investigators) and in population studies or in clinical trials (“applied” investigators). The Administrative Core aims to manage the SPORE research activities in such a way as to eliminate any boundaries between academic Departments, between “basic” and “applied” investigators, and between SPORE Research Projects and Core Resources.


Core Directors:
Angelo DeMarzo, M.D., Ph.D.
William B. Isaacs, Ph.D.

Core Co-Directors:
Georges Netto, M.D.
Jonathan Epstein, M.D.

The primary goal of the Biospecimen/Pathology core is to facilitate translational research related to prostate tissue-based studies. The major functions of the core are to collect, annotate, provide quality control/quality assurance measures, develop standard operating procedures, catalog specimens within databases, improve operations, and test and implement new technologies for interrogating biomarkers in tissue-based studies. The CORE functions to facilitate translational research endeavors by SPORE members as well as non-SPORE members at JHU and those from outside institutions. The biospecimen Core has in place appropriate informatics capabilities for tracking, as well as linkage to clinical follow-up data sets. Essential pathological, clinical, and family history information is available for most specimens in our repository. In addition, we have developed enhanced technologies for producing cell line tissue microarray’s (TMAs), and these serve as standardized reference specimens for biomarker validation studies. Being at the crucial interface of clinical pathology and translational research, the Core has a long history of performing these functions including supplying tissues and their derivatives to multiple investigators, performing immunohistochemical workups and staining protocols, testing and implementing new immunohistochemical and in situ hybridization technologies, performing research on biospecimens to determine optimal methods for preparations of DNA, RNA and protein, and development of a large number of tissue microarrays as well as a TMA database with build-in image analysis tools (TMAJ and FrIDA). The core has also collaborated and shared tools and biospecimens with other SPORES within our institution and across the country. The Specific Aims of the Tissue Archive Core are the following:

Specific Aim 1:
To maintain and enhance a repository of prostate tissues containing a wide range of neoplastic and non-neoplastic samples from both fresh frozen and paraffin tissues, prostatic fluids, DNA, RNA, and protein, and, to distribute these samples to SPORE and other investigators as needed.

Specific Aim 2:
To provide high quality histopathologic diagnoses of tissue specimens and tissue microarrays.

Specific Aim 3:
To continue to perform as a tissue-based technology development lab to test and develop state of the art protocols for IHC, immunofluorescence, FISH, and in situ hybridization for mRNA and microRNAs.

Specific Aim 4:
To continue to design, produce and distribute tissue microarrays using human prostate tissues, cell lines, and xenografts.

Specific Aim 5:
To aid in the interpretation and quantitative analyses of IHC, FISH, and in situ hybridization slides and TMA stained slides to facilitate the achievement of the specific aims of the individual research projects.

Specific Aim 6:
To work with other SPOREs to develop standardized reference materials and processes to translate tissue biomarkers into the clinic.

Specific Aim 7:
To re-assimilate Johns Hopkins Rapid Autopsy patient biospecimen materials back into the SPORE Biospecimen Core.


Core Directors:
Bruce Trock, Ph.D.
Hao Wang, Ph.D.

Core Co-Directors:
Sarah Wheelan, M.D., Ph.D.

The purpose of the Biostatistics Core is to provide consultation and support to all projects in the program, by assisting with study design, and collection, management, visualization, analysis, quantitative modeling, interpretation and reporting of data arising from program activities. By contributing to multiple projects, biostatisticians also promote interdisciplinary interactions among projects. A major responsibility of the Biostatistics Core is to ensure appropriate design, treatment assignment, monitoring, data management and analysis of clinical trials. This includes evaluating accruals, compliance, toxicity, and adherence to protocol. The Core also facilitates interaction and communication between the trials, other investigators, and the other Cores, i.e. transfer of data, specimens, data analysis. Project-specific databases are critical to this process; the Core works with investigators to design databases that will meet the specific needs of individual trials, particularly with quality control and data security issues. In this manner, the Biostatistics Core helps to ensure that human subjects issues related to confidentiality are appropriately addressed, while providing the necessary data required to meet potential audit needs. The Biostatistics Core works closely with the Clinical Research Office to achieve these goals. Finally, the Core works closely with investigators to ensure that requisite data are obtained to answer critical trial questions, and to inform the design of subsequent higher phase trials. In addition to the pre-specified input into project design and analysis, biostatisticians have equally important informal interactions that are critical to meaningful involvement in the research process. Biostatistics core personnel take a direct interest in the substantive issues being investigated. They participate in regular project and program meetings, provide input on all quantitative matters arising in the projects and are always available for informal consultations. Many members of the Biostatistics Core participate in other SPOREs, the Cancer Center Support Grant, program projects, N01 and U01 projects involving cancer translational research, making this Core a critical point of continuity for history, study design and analysis, data systems, and the methodology of translational clinical trials. In addition, Core members play a central role in the Institution’s efforts in bioinformatics, assuring that methodologic developments in this rapidly changing discipline are available to all SPORE investigators.


The Developmental Research Program (DRP) is a special feature of the SPORE grant which allows sponsored institutions to fund important new pilot projects with promising translational potential but would have difficulty in providing sufficient preliminary data for an independently funded NIH grant. This is a crucial part of our SPORE program as it provides a pipeline and testing ground for novel substrates for translational impact. These projects are intended to last one year with the possibility of a second year of support with the demonstration of sufficient progress and are budgeted with the intention that most the funds be spent on supplies, rather than salary support. Pilot projects which make significant progress and are deemed to be capable of high translational impact will be considered for promotion to full SPORE projects. To be eligible, the applicant must have a current academic appointment at any of the Johns Hopkins Medical Institutions, Howard University or University of Maryland. Applicants must hold a M.D. or Ph.D. degree or both. The applicants are expected to provide evidence of a significant research commitment (at least 15% effort commitment) to ensure that the proposal can in fact be addressed in an effective and productive way. As many as 10 developmental research projects will be funded annually, two by funds budgeted within the SPORE and the remainder through funds available through The Patrick C. Walsh Prostate Cancer Research Fund. The Developmental Research Program will be maintained throughout the grant period.


The field of prostate cancer research has been tremendously aided by the recruitment of both new and established investigators into the area. The primary goal of the Prostate SPORE Career Enhancement Program (CEP) is to provide adequate funding to promising young investigators to facilitate their early career development and to evolve into independent investigators in translational prostate cancer research. A secondary goal of this program is to fund established investigators who wish to direct their efforts to the area of translational prostate cancer research. To be eligible, the applicant must have a current academic appointment at any of the Johns Hopkins Medical Institutions, Howard University or University of Maryland. Applicants must hold an M.D. or Ph.D. degree or both. The Prostate SPORE Career Development Program will fund two positions per year at the level of $50,000. The process of selection places special emphasis on recruiting qualified women and minorities.