GI SPORE

The goal of the University of Arizona Cancer Center's Specialized Program of Research Excellence (SPORE) is to prevent and cure gastrointestinal (GI) cancers. The SPORE approaches this goal through studies in prevention, genetics and therapeutics.

The esophagus, pancreas and colon are some of the organs that make up the body's gastrointestinal tract. Cancers of these organs often carry a poor prognosis, and as a result, these cancers are responsible for more than 17 percent of cancer deaths in the United States. Laboratory and clinical research associated with the University of Arizona Cancer Center's GI SPORE focuses on addressing this poor survivability (which is linked to delayed detection of the cancers) and ultimately reducing the incidence and mortality of GI cancers.

What is SPORE? • GI SPORE Goals • Project Descriptions •
Core Descriptions • Developmental Research Program • Advocacy Programs • Supplements • Career Development • Faculty •
 

What is SPORE?

In 1992, the National Cancer Institute (NCI) established the Specialized Programs of Research Excellence (SPOREs) to promote cooperative research and to speed the information exchange between basic and clinical science. Through the SPORE program, laboratory and clinical scientists work together to plan, design and implement research programs that impact on cancer prevention, detection, diagnosis, treatment and control. This cooperative exchange supports translational research. In other words, it helps to move basic research discoveries-new ideas that have the potential to reduce cancer incidence and mortality, improve survival, and to improve the quality of life-from the laboratory bench to the patient's bedside. The SPORE program also includes a career development aspect that recruits scientists from within and outside the SPORE institution to enlarge the cadre of laboratory and clinical scientists dedicated to translational research on human cancer. Institutions united by the SPORE program meet annually to share data, assess research progress, identify new research opportunities and establish priorities for research most likely to reduce incidence and mortality and to increase survival. 

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GI SPORE Goals

Gastrointestinal (GI) cancers account for nearly 20 percent of cancer deaths, and colorectal cancer (CRC) continues to be the second leading cause of such deaths, in the USA in 2006. The long-term objective of our SPORE in GI Cancers is to decrease mortality due to GI cancers by developing novel approaches for risk assessment, screening, chemoprevention and therapeutics. The GI SPORE includes four projects, three cores and developmental research and career development programs are proposed.

Project 1 is entitled Genetic Variability as Prognostic or Predictive Factors in Colorectal Intraepithelial Neoplasia (IEN). The translational goal of this project is to demonstrate that tailoring prevention therapy in high-risk individuals, based on host and adenoma characteristics, will reduce the development of clinically significant colonic IEN.

Project 2 is entitled Barrett’s Esophagus and Oxidative Stress: Role of Gastric Acid and Bile Acids. The translational goal of this project is to determine if ursodeoxycholic acid can modify markers of oxidative stress and/or cancer risk in patients with Barrett’s esophagus.

Project 3 is entitled Mechanistic Translational Studies of the Stress Response in Gastrointestinal Cancer. The translational goal of this project is to exploit processes associated with altered blood perfusion in tumors for therapeutic benefit.

Project 4 is entitled Drug Targeting of G-Quadraplex-NM23-H2 Complex in the c-MYC Promoter, and targets an important oncogene in GI cancer development.

The goals of both Projects 3 and 4 are to conduct translation studies with novel target-directed drugs for treatment of GI cancers.

The projects are supported by an extensive Human GI Tissue Resource, which includes access to existing normal and neoplastic tissue specimens, which have been gathered from approximately 6,000 participants in colon polyp prevention trials, over 600 patients with Barrett’s esophagus, and over 500 surgical patients who were treated for various GI malignancies. A Statistics and Informatics Core provides state-of-the-art statistical, computational and informatics support for all projects in our efforts to discover new prognostic markers and drug targets. The Evaluation and Administration Core is the critical feedback loop necessary for a productive SPORE. The Developmental Research Program ensures that the most promising translational ideas are nurtured and funded. The complementary Career Development Program will support and mentor physicians and scientists in translational research. 

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Project Descriptions

Project 1: Genetic variability as prognostic or predictive factors in colorectal interaepithelial neoplasia (IEN)

Project Co-Leaders:
Eugene W. Gerner, PhD (Basic Scientist)
Patricia Thompson, PhD (Applied Scientist)

The translational goal of this project is to identify host characteristics that can be used to individually tailor colon cancer prevention therapy in order to reduce the development of clinically significant colorectal intraepithelial neoplasia (IEN) in humans with elevated risk for colon cancer.

The hypothesis to be tested in this proposal is that individual responses to certain colon cancer preventive agents, including specific non-steroidal anti-inflammatory drugs (NSAIDS) and agents that target features of polyamine metabolism, are influenced by host factors, including genetic background, and diet.

Three specific aims are proposed to test this hypothesis. First, we will determine if genetic variability in the host gene encoding ornithine decarboxylase (ODC) can explain individual variability in colorectal mucosal polyamine contents. We will also determine if variability in the ODC and/or the flavin monooxygenase 3 (FMO3) genes modulate the action and/or bioavailability of the chemopreventive agents sulindac and difluoromethylornithine (DFMO) when given in combination for the reduction of colon polyp recurrence. Second, we will determine if the association between the ODC G316A promoter variant alleles and adenoma recurrence in aspirin users involves other genes, which affect polyamine metabolism. This aim will focus on the spermidine/spermine N1-acetyltransferase (SSAT), and determine if acetylated polyamines, which are substrates for polyamine export, may be a useful biomarker of NSAID action. Third, we will assess the independent and joint effects of aspirin use, dietary sources of polyamines, and gene modifiers of polyamine synthesis (ODC) on risk of colorectal adenoma recurrence. We will pool data from three adenoma recurrence studies, including the Polyp Prevention Trial (PPT), Wheat Bran Fiber (WBF) and Ursodeoxycholic Acid (UDCA) colon polyp prevention trials to assess these effects on overall adenoma recurrence and recurrence of advanced lesions.

The long-term goal of this project is to determine the influence of host and adenoma factors as predictors of efficacy for the chemoprevention of colorectal adenomas, particularly advanced, clinically significant lesions, and to use this information to reduce the incidence of colorectal cancer in individuals with high risk of developing this disease.
 

Project 2: Barrett's esophagus and oxidative stress: Role of gastric acid and bile acids

Project Co-Leaders:
Katerina Dvorak, PhD (Basic Scientist)
Richard Sampliner, MD (Applied Scientist)

Our major translational goal is to develop a chemopreventive strategy for inhibiting progression of Barrett’s esophagus to esophageal adenocarcinoma. We hypothesize that the deleterious effects of hydrophobic bile acids and low pH may be inhibited by the cytoprotective bile acid, ursodeoxycholic acid (UDCA), that was shown to protect cells against oxidative injury.

The central hypothesis to be tested in this proposal is that bile acids in combination with low pH induce oxidative stress that leads to DNA damage, genomic instability and apoptosis resistance in Barrett’s esophagus. Therefore, an alteration of bile acid composition by ursodeoxycholic acid treatment may be beneficial to Barrett’s esophagus patients in the prevention of neoplastic progression.

Three specific aims are proposed to test this hypothesis. First, we will evaluate the effect of a bile acid cocktail and/or low pH on the generation of reactive oxygen species (ROS), oxidative DNA damage, expression of DNA repair proteins, anti-oxidant and anti-apoptotic proteins in vitro in esophageal cell lines and ex vivo in BE biopsies. We will determine the effect of acute, repeated and chronic exposure to bile acids and/or low pH (1) on the induction of superoxide, (2) formation of 8-OH-dG, a marker of oxidative DNA damage, (3) expression of DNA repair proteins (i.e. Mlh1, Pms2 and PARP), anti-oxidant (i.e. superoxide dismutases and catalase) and anti-apoptotic proteins (i.e. Mcl-1, survivin, Bcl-xL). Furthermore, we plan to identify patterns of DNA alterations using microarray-based comparative genomic hybridization (CGH) in novel esophageal cell lines developed for resistance to bile acids and/or low pH. In specific aim #2 we plan to evaluate the effects of UDCA and its conjugated forms [(tauro-ursodeoxycholic acid (TUDCA), glyco-ursodeoxycholic acid (GUDCA)] on ROS production, oxidative DNA damage, genomic instability and the expression of DNA repair proteins, anti-oxidant and anti-apoptotic proteins induced by low pH and cytotoxic bile acids in vitro. Since UDCA is an excellent scavenger of ROS we anticipate that UDCA will reduce damage caused by bile acids and low pH. Finally, in specific aim #3 we propose to conduct a pilot clinical trial to evaluate UDCA as a potential preventive agent that changes the composition of bile acids in the refluxate so that less toxic bile acids are refluxed to the esophagus. Thus, bile acid composition at the baseline and post UDCA treatment will be determined. Furthermore, markers of oxidative stress (8-OH-dG) and proliferation (Ki-67) will be assessed in BE biopsies at the baseline, 6 months on UDCA and 6 months after discontinuation of UDCA using immunohistochemistry in conjunction with image analysis.

Our long-term goal is to evaluate factors and molecular mechanisms leading to BE development and/or progression to esophageal adenocarcinoma and to inhibit these processes.
 

Project 3: Mechanistic translational studies of the stress response in gastrointestinal cancer

Project Co-Leaders:
Garth Powis, D.Phil, PhD (Basic Scientist)
James Abbruzzese, MD (Applied Scientist)

The translational goal of this project is to develop new target-directed drugs for the treatment of colorectal cancer. Colorectal tumors exist in a stressed environment. As they grow, they outstrip new blood vessel formation leading to poor perfusion, nutrient deprivation and hypoxia. Cancer cells adapt to this stress by changes in key cell survival signaling pathways leading to resistance to cell death, increased anaerobic metabolism, new blood vessel formation and increased metastasis. Although the changes give aggressive, resistant tumors they also provide an Achilles heel for selectively attacking the tumor because without the changes the cancer cells will die.

The hypothesis upon which our studies are based is that the signaling pathways that regulate the growing tumor’s response to inadequate blood perfusion, nutrient deprivation and hypoxia provide novel targets for the development of agents to selectively treat cancer. We will study two pathways and conduct two clinical trials in colorectal cancer of agents developed by us that inhibit the pathways. The first pathway is the thioredoxin-1 (Trx-1) redox signaling pathway and its inhibitor PX-12 that has already shown antitumor activity in patients with colorectal cancer in a Phase I trial. We have show that PX-12 inhibits the hypoxia inducible factor-1 and the Sp1 mediated increase in tumor VEGF formation, EGFR and IGF-1R expression and increases the activity of the Nrf2 transcription factor that plays a dual role in regulating polyamine metabolism through the polyamine response element (PRE) and the antioxidant defense through the antioxidant response element (ARE) in cancer cells. The second pathway is the phosphatidylinositol-3-kinase (PI-3-K) stress signaling pathway, the most frequent signaling abnormality in human cancer. PI-3-K is mutated and activated in many colorectal cancers. We have developed PX-866 a potent inhibitor of PI-3-K and identified a potential biomarker for predicting response.

The specific aims are:1) to investigate the mechanisms for the redox regulation of transcription factors by Trx-1 and its reversal by PX-12; 2) to conduct a Phase I/II clinical trial of PX-12 in colorectal cancer with mechanistic molecular marker and imaging; 3) to investigate mechanisms mediating the response to PI-3-K inhibition in colorectal cancer; and 4) to conduct a PhaseI/II clinical trail of PX-866 in colorectal cancer with mechanistic marker and imaging studies.
The long-term goal of our work is to conduct translational studies of the mechanisms of stress induced gene expression that will lead to the development of novel agents for colorectal cancer treatment.

Project 4: Drug targeting of G-quadraplex-NM23-H2 complex in the c-MYC promoter

Project Co-Leaders:
Laurence Hurley, PhD, DSc (Basic Scientist)
Daniel D. Von Hoff, MD, FACP (Applied Scientist)

The translational goal in Project 4 is to identify and bring forward into clinical trials one or two lead compounds that will suppress c-Myc transcription by targeting the NM23-H2–DNA complex.

This proposal builds upon progress from the last grant period and will further test hypothesis that the NM23-H2–DNA complex is critically involved in transcriptional activation of c-Myc and c-Myc is a critical factor in colon cancer.
The specific aims of the proposal are (1) structural characterization of the G-quadruplex–drug complexes in the c-Myc promoter, (2) to establish in vitro biochemical and cell-based screens to identify small molecules that inhibit binding of NM23-H2 to the G-quadruplex in the silencer element of the c-Myc promoter, (3) to discover and optimize G-quadruplex- and NM23-H2-interactive compounds using computer-aided drug design and structure-based and virtual-screening approaches, (4) In vivo evaluation and subsequent preclinical development, and (5) to file an IND for Phase I clinical trial and overall clinical development program. High-field NMR will be used to characterize the drug–G-quadruplex complex, molecular modeling will be used to identify new lead compounds, and fluorescence resonance energy transfer (FRET) and double-filter methods will be used for identification of in vitro biochemical hits. A luciferase-based high-throughput screen has already been used to identify hits, and subsequent assays will be carried out in matched cell lines genetically engineered to provide proof of principle that the mechanism of action is as proposed. Structure-based approaches will be used to aid in lead optimization. Following lead optimization, an IND will be filed and the clinical development program will be based upon discoveries from specific aims 1–4. Immunohistochemistry will be used to guide patient selection and phase I and II clinical trial plans will be designed to determine whether the new agents will help patients with advanced colorectal cancer.

The long-term goal of this research is to develop novel target-directed drugs for treatment of colorectal cancer.
 

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Core Descriptions

Core A: Human GI Tissue Resource

Core Director: Achyut Bhattacharyya, MD

The GI Human Tissue Resource coordinates histopathological assessment of all GI tissues collected from two local Tucson-area hospitals and existing banks of normal and neoplastic GI tissues. Approximately 400 colorectal, esophageal and pancreatic cancer patients are seen annually at the University of Arizona Cancer Center (AZCC) and the Southern Arizona Veterans Administration Medical Center (SAVAMC). During the past funding period, we collected over 2,000 surgical specimens prospectively. Existing tissue banks contain over 5000 frozen and fixed samples of normal and neoplastic intestinal and pancreaticobiliary tissues. More than 1500 colon adenomas and over 800 specimens from patients with Barrett's esophagus have been collected and stored during the course of cancer prevention studies conducted at the AZCC and SAVAMC. Standard methods of preservation and storing tissues are employed to facilitate measurement of desired endpoints. Special services, such as laser capture microdissection, tissue arrays, and digitized virtual slides of the specimens are available to SPORE investigators.

The activities of Core A-GI Tissue Resource are coordinated with other resources, to ensure collection of tissues from patients participating in the clinical trials, standards of marker measurement in tissues, adequacy of statistical input into design of trials and evaluation of results from patient studies. With the assistance of Core B -Informatics, a comprehensive database for all samples within the GI Tissue Resource has been established. This database is designed so that it can be interrogated for patient related information, including outcome data, and specific prognostic and/or predictive factors obtained during the course of this research effort. The GI Tissue Resource is essential for translational aspects of all the GI SPORE projects. We have a significant resource for our GI SPORE and outside SPORE investigators.

Core B: Statistical and Informatics Resource

Core Co-Leaders:
Bonnie LaFleur, PhD
David Mount, PhD

Core B provides essential statistical, computational, and informatics expertise that is necessary for all GI SPORE projects and investigators to achieve the translational goals of the SPORE grant in a timely and efficient manner. Core B personnel are expertly qualified for this task and represent a broad spectrum of capability in biostatistics and computational analysis. They contribute significantly to the GI SPORE projects through extensive interactions with SPORE investigators and have been actively involved with experimental design and analysis for each project. Core B contributions fall into two main areas, biostatistics and informatics.

Biostatistical analysis includes descriptive analysis of data, hypothesis testing, group comparisons using t-tests or analysis of variance, linear and logistic regression, zero-inflated Poisson regression, Generalized Estimating Equations, and assessment of relationships between time and potential clinical, laboratory, and treatment covariates. Transformations are used as needed to meet statistical assumptions and, when such transformations are not available, nonparametric procedures are used. False discovery rates are estimated to compensate for multiple comparisons common in high throughput data analysis. Biostatistical input also includes an essential role in planning of projects, study design, and protocol development.

Informatics includes web sites for data storage and information sharing, data management support, bioinformatics support for sequence and genome analysis, software methods for finding and validating predictive markers and drug targets, haplotype analysis, advanced computational modeling of large data sets, and biological interpretation of microarray and high-throughput data. Core B personnel are expert data managers and perl/java/R programmers prepared to meet the computational needs of the SPORE grant.

The combined biostatistical and informatics expertise of Core B offers a full range of data analysis and exploratory methods that are of enormous importance to each SPORE project. 
 

Core C: Evaluation and Administration 

Core Leader: Eugene W. Gerner, PhD

SPORE grants have several unique features that require added attention to evaluation and administration. The Evaluation and Administration Core provides a framework for supporting the unique features of the SPORE as well as the more routine administrative tasks associated with a large, diverse, multiple project grant. The essential services provided by this core are listed below.

• Provide essential administrative support to all the projects and cores
• Maintain scientific oversight of each project and for the program as a whole
• Coordinate all activities related to the Developmental Research Program
• Coordinate all activities related to the Career Development Program
• Oversee accounting and budget administration for all components of the SPORE, including Career Development and Pilot Project awards
• Facilitate interactions with other GI SPOREs and coordinate InterSPORE collaborations
• Coordinate patient advocate activities including interactions with the national SPORE Patient Advocacy Research Team (PART) program.
• Coordinate data sharing and activities of the Data Sharing Committee (see Data Sharing Plan in Supporting Materials).
• Coordinate monthly meetings of the SPORE and GI Cancer Program to cover a wide variety of scientific developments in the GI cancer field
• Coordinate monthly and as needed Executive Committee meetings
• Coordinate annual SPORE retreat and review with External Advisory Committee
• Assist with IRB-related submissions/IND and regulatory affairs
• Maintain detailed records on SPORE activities, including meeting minutes and programmatic changes
• Publish quarterly SPORE/GI Cancer Program newsletter
• Coordinate SPORE activities with the other departments and divisions of the UA as necessary
• Sponsor events to increase interest in interdisciplinary, translational research teams

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Developmental Research Program

The goal of the SPORE in GI Cancers Developmental Research Program is to provide short-term support for promising research opportunities with a high probability for impact on GI cancers. The career development award provides support for investigators to develop successful independent research programs in the area of GI cancer. Awards are determined through a three-tier review process.

Latest Developmental Research Program Awards:

Lipid Microbubbles for Receptor Targeted Detection of Pancreatic Cancer
Bhaskar Banerjee, MD

SPECIFIC AIMS:

1. Assess the attachment of targeted lipid microbubbles to MIA-PaCa-2 pancreatic tumor cells in vitro.
2. Evaluate the specificity of intraductally injected microbubbles in targeting bioluminescent pancreatic neoplasia in mice.

Effect of TGFbeta and KRAS mutations on 5-Fluorouracil (5-FU) responsiveness in Colon Cancer
Thomas Doetschman, PhD

SPECIFIC AIMS:

1. Test the functional consequences of increased expression of uridine phosphorylase (UPP1 or UP) in the absence of TGFβ signaling on 5-FU-induced growth inhibition and host-toxicity.
2. Determine whether the KRASG13D mutation increases sensitivity of human colon cancer cells to 5-FU-induced growth inhibition by downregulating UP expression.
3. Investigate dysregulation of UP expression in human MSI-H CRCs harboring TGFBR2 mutations.

TAM signaling in gastrointestinal inflammation and cancer
Sourav Ghosh, PhD

SPECIFIC AIMS:

1. To determine whether the TAM receptors and ligands function as biological anti-inflammatory agents that prevent colitis-associated tumorigenesis in vivo using a mouse model of CAC.
2. To evaluate if the plasma expression levels of TAM ligands can function as translational biomarkers of active inflammation in inflammatory gastrointestinal diseases.

Slit/ Robo Signaling in Pancreatic Cancer Perineural Invasion
Ronald Heimark, PhD

SPECIFIC AIMS:

1. Characterize the association of Robo1/Slit2 expression levels in pancreatic ductal adenocarcinoma and perineural Invasion with tumor stage and differentiation.
2. Determine the role of the Robo1/Slit2 pathway in neural invasion of pancreatic cancer and recurrence using in vitro and in vivo model systems.

Pilot Project awards are made twice a year. For more information on the program and how to apply, contact Kim Nicolini, Research Administrator, at knicolini@azcc.arizona.edu 

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Career Development

The University of Arizona Cancer Center and the University of Arizona College of Medicine recognize the need for hypothesis-based translational research as central to development of effective strategies for treatment and prevention of gastrointestinal cancer. Recruiting and developing translational researchers with promise is clearly critical. Candidates for such career development have two sources: clinicians with research interest and basic scientists who have interest in the application and extension of their work into the clinical setting where GI cancer risk is elevated, or where treatment of GI cancer is taking place.

The objective of career development for basic scientists as a part of the GI SPORE is to help selected basic scientists see the opportunities for application of their work to GI cancer, and how that work can be translated to clinical care and prevention. The basic scientist must learn to work with also opportunities to gather samples and data from patients in the clinic. He or she must learn to recognize the problems of sample variability and limited experimental options present in the clinic.

Latest Career Development Awards:

The effect of gene copy number variation on colorectal cancer risk. Christina M.Laukaitis, MD, PhD, FACP.

SPECIFIC AIMS

1. To test for copy number variation (CNV) in candidate genes and other cancer-influencing genes from genomic samples collected for the wheat bran fiber (WBF), ursodeoxycholic acid (UDCA), and selenium interventional trials.
2. To calculate the risk/protection conferred by copy number variant genes on metachronous adenoma development using data collected from completed trials.
3. To assess the frequency of gene duplication in the Colon Family Registry, testing the hypothesis that both deletions and duplications will occur in a CNV-prone family

Visit the Laukaitis Laboratory site to learn more.

Mechanisms of regulating centrosome duplication
Gregory C. Rogers, PhD

SPECIFIC AIMS

1. Identification of kinases that phosphorylate and promote Plk4 down-regulation.
2. Reconstitution of Plk4 phosphorylation and ubiquitination in vitro.
    

Genetic features of primary colorectal cancers predict their metastatic potential and the first sites of disease recurrence
Vassiliki LianaTsikitis, M.D.

SPECIFIC AIMS

1. To determine how the genetic makeup of colon cancers that have metastasized to different sites (namely, liver and lung) differs from each other and from cancers that did not metastasize.
2. To determine whether or not characteristic somatic genetic profiles of primary colorectal cancers can distinguish between non-metastasizing and metastasizing tumors and to determine genomic profiles that identify the specific sites of metastasis (liver and lung).
3. To collect tissue from primary tumors and from the metastatic sites of stage IV colon cancer, in order to examine whether or not genetic markers with predictive metastatic capacity are expressed in the metastatic sites and to study the acquisition of chromosomal gains or losses not seen in the primary tumors.

Career Development awards are made once a year. For more information on the program and how to apply, contact Kim Nicolini, Research Administrator, at knicolini@azcc.arizona.edu 

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Arizona Cancer Center SPORE in GI Cancer Research Advocacy Program (RAP)

What is the GI SPORE RAP?

The University of Arizona Cancer Center Specialized Program of Research Excellence (SPORE) in Gastrointestinal (GI) Cancer is one of four GI SPORE research programs funded by the National Cancer Institute (NCI). The GI SPORE is charged to translate gastrointestinal cancer research into better diagnosis, care, treatment, and prevention. The immediate goal of the UA Cancer Center GI SPORE is to prevent and cure cancers of the colon, esophagus and pancreas through studies in prevention, genetics and therapeutics.

The GI SPORE Research Advocacy Program (RAP) brings patient perspectives into SPORE research to help scientists focus on results and move the science more effectively from the lab to the clinic. RAP helps identify barriers that block advances in cancer prevention, diagnosis and treatment and helps take action to resolve issues.

Who are SPORE research advocates?

GI SPORE research advocates are individuals with a personal history or relationship with cancer, especially (but not exclusive to) cancers of the colon, esophagus and pancreas. Patient advocates include cancer survivors, caregivers, and those at risk who are willing to make a personal commitment to work directly with GI SPORE cancer researchers to help bring the best science to those who are affected by GI cancers.

What do SPORE research advocates do?

GI SPORE research advocates can be active in many ways:

• Participate in local SPORE meetings
• Monthly research meetings
• Annual retreats
• Scientific review panels
• Hold education sessions for patients and the public
• Hold education sessions for scientists and staff
• Participate in clinical trial development
• Review informed consent forms
• Develop patient-oriented tools for SPORE clinical trials
• Distribute trial information to communities
• Review tissue collection and follow-up procedures
• Give input on surveys and other tools in research
• Facilitate collaborations between the Arizona Cancer Center GI SPORE investigators, institutions, companies, and government entities

RAP Contact Information: For more information on the University of Arizona Cancer Center GI SPORE RAP program, contact:
Tamara Burkhead
GI SPORE Clinical Coordinator
Phone: (520) 626-0213
E-mail: tburkhead@azcc.arizona.edu 

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Supplement Descriptions

The GI SPORE has two funded supplements to the parent grant.

Supplement 1: Exploring the Relationship Between Arsenic and Cancer

Supplement 2: Predictive Biomarkers for Esophageal Adenocarcinoma in Patients with Barrett's Esophagus 

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Faculty Listings

The following is a list of all GI Spore faculty members, including physicians and researchers. For more information on a specific member, please click on Member Directory to be redirected to a searchable database for the member's biography and research activities.