Research Program Six:  Cancer Risk and Prevention

Program Leaders:  Olufunmilayo (Funmi) I. Olopade, MBBS and Andrea King, PhD

Overview and Scientific Goals

This Program, formerly named Clinical Cancer Genetics and Prevention, has undergone substantial growth, and has been renamed Cancer Risk and Prevention to more accurately reflect the depth, breadth, and new areas of strength in population research. The overall goals of the Program are to harness the intellectual capacity at the University to determine the genetic, psychological, behavioral, and socio-environmental basis of cancer, and to disseminate cancer control efforts through research in our local community. Research interactions focus on elucidating the pathogenesis of cancer, with the ultimate goal of developing new and improved methods for risk assessment, early detection, and prevention of cancer. Thematically, the research is focused on high-risk individuals defined by genetics, exposure (behavior, environmental), and/or other vulnerabilities (e.g., older age) or disparities based on race/ethnicity or access to health care. The Program has grown to 33 members from 12 departments and two University Divisions (Biological Sciences, Social Sciences). As a cross-cutting theme, the majority of our program members are focused on health disparities research.  The scientific goals of the programs are to:

  • elucidate the genetic and environmental basis for common cancers (breast, ovarian, colorectal, prostate, lung, and skin), and to translate this new knowledge into clinical and public health practice;
  • develop animal models for chemoprevention studies and identify biomarkers for early detection of cancer;
  • identify the psychological and bio-behavioral basis of cancer risk and prevention; and 4) establish an organized outreach research effort in the Southside Chicago neighborhoods to enhance and empower their participation in University research, educational and clinical services.

Program Highlights 2005 – 2007

  • Marc Bissonnette, MD, demonstrated that Gefitinib suppresses the development of overt tumors in AOM-treated rats; thus, EGFR plays an obligate role in early colon carcinogenesis. These studies suggest that chemopreventive strategies involving agents that block EGFR could offer promising new approaches for individuals at high-risk for colon cancer (Cohen et al. Cancer Res 66:5656, 2006).
  • In seminal work describing the association of BRCA1 promoter methylation in sporadic breast cancer with reduced BRCA1 copy number and chromosome 17 aneusomy, Olufunmilayo Olopade, MBBS, provided further support for a model of breast carcinogenesis in which BRCA1 promoter methylation serves as a “first hit”, much like an inherited germline mutation, and promotes tumor progression down a restricted set of molecular pathways (Wei et al. Cancer Res 65:10692, 2005).
  • Using data from the NSABP, James Dignam, PhD and Blasé Polite, MD, MPP, reported that obesity was a risk factor for poor outcomes in colorectal cancer treatment as a BMI greater than 35.0 kg/m2 at diagnosis was associated with an increased risk for recurrence of, and death from, colon cancer (Dignam et al. J. Natl Cancer Inst 98:1647, 2006).
  • In research that crosses two continents (Africa and North America), Dr. Olopade demonstrated that breast tumors with the most aggressive phenotype may be overrepresented in women of African ancestry. Contrary to previous work that focused on lack of access, this work suggests that these tumors might be more deadly because they typically do not express surface receptors, such as ER, PR, and HER2, that are the targets of current therapies (Ikpatt et al. AACR Meeting Abstracts 598-599, 2005).
  • Harriet de Wit, PhD, made a seminal observation that responses to acute stress among beginning smokers are predictive of progression to regular daily smoking (de Wit et al. Pharmacol, Biochem Behav 86:312, 2007).
  • Andrea King, PhD, determined that the opioid antagonist, naltrexone, improved smoking cessation quit rates particularly in women smokers and decreased cessation-related weight gain (King et al. Nicotine Tobacco Research 8:671, 2006).
  • Paul Vezina, PhD, Daniel McGehee, PhD, and William Green, PhD, have developed a model relating enhanced nicotine intake to neuronal acetylcholine upregulation, long-term potentiation, and sensitization in the ventral segmental area (Progress in Neuropsychopharmacology and Biological Psychiatry, in press, 2007).
  • Martha McClintock, PhD, and colleagues demonstrated a plausible link between vulnerability to cancer and other diseases, and social neglect in socially-isolated male and female Sprague-Dawley rats, a naturally gregarious species (Hermes et al. Am J Physiol Regul Integr Comp Physiol  290:R273-R282, 2006)

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Links

Program 1
Cell Signaling and Gene Regulation
Program Leaders: Marsha Rosner, PhD and Suzanne Conzen, MD

Program 2
Molecular Genetics and Hematopoiesis
Program Leaders: Wendy Stock, MD and Michael Thirman, MD

Program 3
Immunology and Cancer
Program Leader: Thomas F. Gajewski, MD, PhD

Program 4
Clinical and Experimental Therapeutics
Program Leaders: Everett E. Vokes, MD and M. Eileen Dolan, PhD

Program 5
Advanced Imaging
Program Leaders: Maryellen L. Giger, PhD and Heber MacMahon, MD

Program 6
Cancer Risk and Prevention
Program Leaders: Olufunmilayo (Funmi) I. Olopade, MBBS and Andrea King, PhD