Innovative Treatments: Search for a Cure

To stimulate the development of more effective treatments, we fund a variety of research approaches. These include alternative medicines, novel clinical approaches, testing promising leads in animal models of breast cancer, and rational drug design, which is a methodical approach based on understanding the molecule-level interactions between a potential drug and the disease process. For many of our investigators, research under this priority subject area is an extension of their research previously funded under our priority subject area of Pathogenesis.

We have divided the innovative treatment priority issue into four broad areas of research:

Research Conclusions
Immune Therapy: Mobilizing the Body's Defenses
New Drug Design: Creative Science Hormone and Chemotherapy Targets: Improving Today's Arsenal Gene Therapy and Other Treatments: New Frontiers

Research in Progress
Immune Therapy: Mobilizing the Body's Defenses
New Drug Design: Creative Science 108 Hormone and Chemotherapy Targets: Improving Today's Arsenal Gene Therapy and Other Treatments: New Frontiers

Research Initiated in 2000
Immune Therapy: Mobilizing the Body's Defenses
New Drug Design: Creative Science Hormone and Chemotherapy Targets: Improving Today's Arsenal Gene Therapy and Other Treatments: New Frontiers

Research Conclusions

Immune Therapy: Mobilizing the Body's Defenses

Receptor Antibody-Enhanced Chemotherapy for Breast Cancer

In order to grow, tumor cells require a substance produced in the body, insulin-like growth factor. Insulin-like growth factor-I receptor (IGFIR) is a substance on tumor cells that allows them to take up insulin-like growth factor. Yoko Fujita-Yamaguchi, Ph.D., of the Beckman Research Institute - City of Hope, Duarte designed a therapeutic approach that blocked tumors' IGFIR as a means of stopping tumor growth. She successfully constructed an anti-IGFIR antibody that blocked the receptor and inhibited the growth of human tumors that were transplanted into mice. She tested whether the inhibitory effects of the antibody could enhance the effects of the chemotherapy drugs doxorubicin and tamoxifen. Anti-IGFIR did not enhance doxorubicin, but therapy with anti-IGFIR and tamoxifen was more effective than either component alone. Results from this project were published in Cancer Immunology and Immunotherapy 49: 243-252 (2000).

Peptide-Pulsed Dendritic Cell Therapy for Breast Cancer

Dendritic cells are white blood cells that enable the immune system to identify foreign proteins more effectively. CEA (carcino-embryonic antigen) is a protein that is present on the surface of some tumor cells but is not generally found on normal cells. Jeffrey Weber, M.D., Ph.D., of the University of California, Los Angeles completed an early clinical trial to determine (1) whether patients who had tumors with CEA could be treated with their own dendritic cells that had been taught to recognize CEA, and (2) whether this treatment caused side effects. He found that, since the patients had been heavily pre-treated with chemotherapy, the function of the dendritic cells was impaired and the treatment did not stimulate the immune system or cause tumors to shrink. However, dendritic cell therapy has succeeded in melanoma patients whose cancer has spread to other parts of the body, but who have not had chemotherapy. So Dr. Weber believes breast cancer patients with minimal disease who have not had chemotherapy would be ideal for future dendritic cell therapy trials.

New Drug Design: Creative Science

A New System for Breast Cancer Drug Delivery

Daryl Drummond, Ph.D., from the California Pacific Medical Center, San Francisco finished a project to modify liposomes (microscopic fat particles) that contain a chemotherapy drug, to target them more specifically and effectively toward breast tumors. This should reduce the toxicity of the drug to the rest of the body. The critical need was to administer these liposomes in the blood, then have them 'home in' on breast tumors. Using human breast tumors grown in mice, they targeted the liposomes to the breast cells by placing an antibody (anti-Her2) on the liposome surface. Overcoming a major technical hurdle, they formulated liposomes that did not release the chemotherapy drug they contained, doxorubicin, until after the breast cancer cells took up the liposomes. The initial success in cells and animal models indicted that this approach could greatly reduce systemic toxicity associated with chemotherapy. Dr. Drummond published his results in Pharmacological Reviews 51: 691 (1999) and Biochem. Biophys. Acta 1463: 383 (2000).

Novel Drugs to Inhibit Breast Cancer Metastasis

Joseph Konopelski, Ph.D., from the University of California, Santa Cruz targeted for drug development (1) a protein (laminin), which is needed by both normal and tumor cells and found in their immediate micro-environment and (2) its molecular interaction with a surface receptor on breast cancer cells (Laminin Binding Protein-LBP). The drug design involved only a small region of laminin, called peptide 11, which is responsible for this process. Dr. Konopelski's collaborators at Montana State University determined the amino acid side-chain and backbone molecular structure of peptide 11. Then, his team developed a chemical synthesis for a potential inhibitor of the laminin peptide 11-LBP interaction. They were unable to complete the complex synthesis in the time frame of BCRP's funding. However, the National Institutes of Health and the Congressionally Directed Research Program at the Department of Defense are funding the continuation of this work.

Mechanism of Novel Anti-Angiogenic Therapy for Breast Cancer

Continuing research BCRP funded from 1995-98, Francis Markland, Ph.D., from the University of Southern California, Los Angeles completed a project to develop the therapeutic potential of a protein from snake venom, called contortrostatin (CN). The net effect of CN is to block both blood vessel formation and the spread of breast cancer cells. Integrin adhesion receptors are found on all types of cells; they attach individual proteins found in the cells' micro-environment to the cells. Dr. Markland's team succeeded in identifying the specific breast cancer and blood vessel integrin adhesion receptors that CN blocks, and they moved towards defining how CN does this. In addition, Dr. Markland's group made important strides in developing a method for delivering CN to the body, and they studied small peptide compounds derived from CN. Several publications resulted from this support, including articles in Biochemistry & Biophysics Research Communications 267: 350 (2000), and Breast Cancer Research & Treatment 61: 249 (2000). BCRP is continuing to fund this project.

Novel Enzyme Inhibitors for Estrogen-Dependent Breast Cancer

Masato Tanabe, Ph.D., of SRI International, Menlo Park designed orally-administered drugs that inhibit estrone sulfatase, an enzyme responsible for producing estrogen. The drugs cut off the estrogen supply for estrogen-dependent breast tumors. He was able to develop three new estrone sulfatase inhibitors (ESIs) that have strong activity against human breast tumors grown in mice. An advantage of these ESIs over most estrogen inhibitors is that the ESIs do not themselves have estrogenic activity, and therefore cause fewer side effects. At least one of the new ESIs is effective enough to undergo further pre-clinical and clinical testing and may ultimately provide a viable, less toxic alternative to anti-estrogens currently in use.

Blocking Stromelysin-3 to Inhibit Breast Cancer Metastasis

Nurulain Zaveri, Ph.D., also at SRI International, Menlo Park investigated Stromelysin-3 (ST-3), one of a class of enzymes called proteases that tumor cells release to digest their immediate micro-environment and allow tumor cell movement. However, ST-3 does not actually act as a protease. Rather, it counteracts inhibitors of this process and permits other, more potent proteases to function. Dr. Zaveri synthesized inhibitors of ST-3. She first designed protein-like inhibitors, and then worked on synthetic, non-protein inhibitors. These were tested though a collaboration with Dr. Stephen Weiss at the University of Michigan. This research validated ST-3 as an attractive target for therapy to prevent the spread of breast cancer to other parts of the body. Dr. Zaveri's efforts advanced two approaches against ST-3 that are part of rational drug design: (1) using solid support, a quicker type of chemical synthesis useful with low yields; and (2) combinatorial chemistry, where the researcher produces and tests all types of a specific molecule.

Hormone and Chemotherapy Targets: Improving Today's Arsenal

Enhancing Breast Cancer Sensitivity to Chemotherapy

Daniel Mercola, M.D., Ph.D, from the Sidney Kimmel Cancer Center, San Diego explored whether blocking a series of protein interactions inside cells (called the JNK pathway) will overcome cell resistance to chemotherapy. Dr. Mercola inhibited JNK by using special "antisense" molecules in order to make breast cancer cells and tumors sensitive to a chemotherapeutic drug, cisplatin. This approach had promise specifically in one type of breast tumor (Her-2/neu-positive), but did not appear effective in another type, estrogen-receptor-positive tumors. Dr. Mercola performed these experiments on human tumor cell lines grown in mice. Several publications resulted from this funding, including a report in Cell Growth & Differentiation 10:545-554 (1999). Matching appropriate therapies to subgroups of breast cancer patients whose tumors interact with specific hormones or other bodily substances is a topic of intense research interest. Also, new approaches are needed to tackle Her-2/neu-positive breast cancer, since the current drug, Herceptin, is successful in only about 30% of patients.

How Indole-3 Carbinol Inhibits Breast Cancer Cell Growth

Liqun Zhang, Ph.D., at the University of California, Berkeley investigated how indole-3-carbinol (I3C), a compound found in cruciferous vegetables such as cabbage and broccoli, inhibits growth in breast cancer cells. She exhaustively studied a series of protein interactions that take place inside cells, the MAPK (mitogen-activated protein kinase) pathway. In a variety of experiments, it appeared that MAPK is not connected with I3C, and her team plans to look at other protein interactions inside cells to understand I3C's growth-inhibiting effect on breast cancer.

Gene Therapy and Other Treatments: New Frontiers

Outpatient Stem Cell Transplants for Breast Cancer

High-dose chemotherapy with bone marrow or stem cell transplant is a treatment option for breast cancer that has spread to other parts of the body or for high-risk breast cancer. Traditionally, it requires prolonged inpatient hospitalization. Kathryn Hollenbach, Ph.D., of the University of California, San Diego compared two groups of women, one who had the treatment as inpatients, and another who had it as outpatients. She compared the groups for (1) cost , (2) the patient's psychological well being, (3) the psychological well being of the family member or friend who acted as caregiver, (4) toxicity associated with treatment, and (5) hospital re-admissions. There were no statistically significant differences between inpatient and outpatient groups on number of days from first date of high-dose chemotherapy to the date the patient returned to the referring oncologist. There were also no differences in toxicity, number of hospital re-admissions, or length of hospital readmission. Adjusting for age and symptom severity, on average, outpatient costs were 71% less than inpatient. No differences in well-being were seen in patients or caregivers at the beginning of treatment or 60 days after treatment. However, after adjusting for age, symptom severity and quality of well being at the beginning of treatment, outpatients had significantly poorer well-being during treatment. Similar differences were not seen for caregivers. There was no difference in well-being between the inpatient and outpatient groups at the end of treatment or at subsequent follow-up. Results demonstrate that this therapy, administered in an outpatient setting, was associated with significant cost savings and no permanent adverse effects. The significant cost savings support consideration of making this therapy widely available. Dr. Hollenbach was co-author of a publication reporting this research, Bone Marrow Transplantation 21:927-32 (1998).

Improved Delivery of Pharmaceuticals to Breast Cancer

Demetrios Papahadjopoulos, Ph.D., (deceased) and Dmitri Kirpotin, Ph.D., at the California Pacific Medical Center Research Institute, San Francisco completed a project with the goal of designing a new way to deliver chemotherapeutic drugs directly to breast tumors. They encapsulated an anti-cancer drug inside liposomes (microscopic fat particles that can enter the cell wall), and targeted the liposomes to the tumor cells through the blood. They also heated the tumor slightly above normal to enlarge tumor blood vessels and maximize the efficiency of delivering anti-cancer drugs. Drs. Papahadjopoulos and Kirpotin found that when they heated a tumor, it took up three times more liposomes. They designed specialized liposomes they called "stealth" liposomes that work especially well with heating tumors. This study has resulted in a Phase I/II clinical trial, where the drug delivery method will be tested for safety and effectiveness in humans. Additional details were published in Pharmacological Reviews 51: 691-743 (1999).

Targeted Gene Therapy Using Anti-p185Her2 Immunoliposomes

John Park, M.D., of the University of California, San Francisco developed a way to use liposomes (microscopic fat particles) to deliver genes to breast tumors. The formulation he developed, called anti-Her2 immunoliposomes, contains liposomes, genes or DNA, and an antibody that targets the treatment to breast cancer cells. Dr. Park was able to deliver test genes to breast cancer cells in test tubes and to human breast tumors grown in mice. Most of the targeting systems developed for delivering gene therapy to breast tumors are based on technologies that use viruses. Dr. Park's study has shown the promise of using a non-viral system for delivering gene therapy to breast tumors. This study is discussed in numerous publications, including one in the Annals of the New York Academy of Sciences 886:293-6 (1999).

Mechanism of Radiosensitivity in Breast Cancer Cells

Xiaofei Wang, Ph.D., of The Scripps Research Institute, La Jolla investigated how cells become resistant to radiation and attempted to determine the best way to enhance radiation-induced cell killing. He found evidence that two macromolecules, ATM and Cds1, are required for establishing resistance to radiation in breast cancer. By designing inhibitors to these molecules, it may be possible to develop treatments that will increase the effectiveness of radiation therapy.

Research in Progress

Immune Therapy

New Drug Design

Hormone and Chemotherapy Targets

Gene Therapy and Other Treatments

Research Initiated in 2000

Immune Therapy

Cell-Based Immunotherapy for Breast Cancer. Nabila Jabrane-Ferrat, Ph.D., of the University of California, San Francisco will incorporate 'danger signals' (HER-2/neu with CIITA, CD80 or interferon gamma) into vaccines. These danger signals are proteins present in tumor cells at higher levels than in normal cells or with a structure slightly different from the protein in normal cells. The goal is to stimulate the immune system to produce a type of white blood cell that will recognize the danger signal and attack the tumor as a foreign body.

New Drug Design

Hormone and Chemotherapy Targets

Gene Therapy and Other Treatments