The Cancer Research Foundation: Newsletters

Each year, the Cancer Research Foundation accepts grant requests from young men andwomen engaged in first-projectlaboratory and/or clinical cancer research. These proposals come to the Foundation already reviewed and
ranked by afaculty awards committee, using the National Institutes of Health peer review process. Only the innovative and bold proposals with practicable research plans are considered for funding.

After receipt by the Foundation, our medical consultants, Dr. Joseph B.Kirsner and Dr. Richard L. Schilsky, interpret the complex science to the trustees. Cancer Research Foundation trustees make all funding decisions.

Last November, five young scientists from the University of Chicago Medical Center were awarded young investigator grants:

These awards are for one year. At the end of the year, if the hypotheses have proven worthy of further study, this early research will be used as a basis for application for major outside funding.

Philippe Cluzel, Ph.D.
Assistant Professor
Department of Physics, Institute for
Biophysical Dynamics, and
the James Franck Institute
$50,000.

NON-GENETIC INDIVIDUALITY IN BACTERIAL CHEMOTAXIS

Cancer may be caused by minute changes in a single cell embedded within a population of healthy cells. Since this single cell may proliferate and develop cancer, it is clear that population measurements provide an incomplete
understanding of how the disease is triggered. The goal of this proposal is to develop a new technology. We will measure simultaneously changes at the molecular level and behavioral characteristics of individual living cells.

Philip P. Connell, M.D.
Instructor
Department of Radiation and Cellular Oncology
$50,000.

SENSITIZING CANCER CELLS TO CHEMOTHERAPY AND RADIATION USING PEPTIDEBASED INHIBITORS OF DNA REPAIR

Radiation and most chemotherapeutic drugs kill cancercells by damaging their DNA. However, tumor cells can become resistant to treatments if they can repair this DNA damage. This research project will develop new drugs that interfere with the DNA repair machinery in cancer cells. If successful, these new agents will improve the effectiveness of present cancer treatments.

Kay F. Macleod, Ph.D.
Assistant Professor
The Ben May Institute for Cancer
Research
$50,000.

MOLECULAR DISSECTION OF RB TUMOR SUPPRESSOR GENE FUNCTION IN VIVO

The function of a gene called retinoblastoma tumor suppressor gene (Rb) is disrupted in most human cancers. Kay has isolated a protein encoded by Rb – delta Rb –that plays a role in human breast,lung, and gastric cancers. She would like to generate experimental mice inwhich this gene is not expressed (i.e., it is “knocked out”) in order to compare the tumor incidence of these mice to other mutant mice. This will allow her to analyze both groups to determine exactly how this gene influences cell behavior in response to genetic or environmental stress.

RECOGNITION OF CEAEXPRESSING
TUMORS BY T CELL
RECEPTOR GENE- MODIFIED
PERIPHERAL BLOOD
LYMPHOCYTES

A small group of T cells within the body’s immune system can recognize and kill cancer cells, but this rarely results in the natural destruction of an entire tumor. Mark will identifythe T cells that recognize a tumor protein called CEA and isolate thereceptor genes in these cells that are responsible for tumor recognition. He will then test whether T cells that do not normally recognize tumors become cancer-killing T cells when he transfers receptor genes to them inthe laboratory. In the future, Mark hopes to use this strategy to generate large numbers ofcancer- killing T cells, so that transfusions ofthese cells can be used to cause tumor destruction in patients.

Olatoyosi M. Odenike, M.D.
Instructor
Department of Medicine, Section of
Hematology/Oncology
$50,000.

A NOVEL THERAPY BASED ON INHIBITION OF PDGFR SIGNALING IN MYELOID METAPLASIA WITH MYELOFIBROSIS

This project is designed to test the efficacy of inhibition of the protein PDGF (platelet derived growth factor) in patients with myeloid metaplasia with myelofibrosis (MMM). MMM is a form of chronic leukemia in which there is excessive fibrosis (scar tissue) in the bone marrow leading ultimately to low blood counts and problems with infections and bleeding. The cause of the marrow fibrosis has been linked to high levels of the protein PDGF(platelet derived growth factor) in patients with this disease. The drug Gleevec works to block the action of this protein, and Olatoyosi will be evaluating its effects in patients with MMM by examing patients' blood and bone marrow samples in the laboratory.