Ride Cincinnati Grants Help Fund Influential Research
The importance of medical research is monumental, as it leads newer and better therapies that can change disease outcomes and improve public health as a whole.
However, this research takes funding, and with federal sources decreasing, the need for independent support or seed grants from professional and academic organizations is essential now more than ever.
Additionally, this type of funding allows for more experimental concepts to be investigated, whereas federal agencies may not choose to support these high-risk, high-reward studies.
This is where the Marlene Harris-Ride Cincinnati event and efforts come into play, providing UC Cancer Institute researchers with the financial support needed to continue promising breast cancer research.
Ride Cincinnati has funded 19 projects since its inception, and in seven years has raised over $1.5 million for breast cancer research pilot grants.
"It’s partners like this that help make the UC Cancer Institute a success,” says William Barrett, MD, director and associate director of education and community outreach at the institute, chair of the department of radiation oncology at the UC College of Medicine and medical director for UC Health’s Barrett Center. "Without this important funding, which is used for everything from hiring lab staff to purchasing supplies to actually running the experiments, some of these important findings would never be discovered.”
In 2013, Ride Cincinnati is funding seven influential projects by researchers at the institute which include:
"Targeting Metabolic Vulnerabilites of ERB2-Driven Breast Cancers,”being led by Kakajan Komurov, PhD, an assistant professor in the department of pediatrics at the UC College of Medicine; Cincinnati Children’s Hospital Medical Center.
"Defining the Role of the DEK Oncogene in Breast Cancer Stem Cell Tumorigenicity and Pre-Clinical Testing of Therapeutic DEK Targeting Strategies,”being led by Lisa Privette Vinnedge, PhD, a research instructor in the department of pediatrics at the UC College of Medicine; Cincinnati Children’s Hospital Medical Center—"Previous research has shown that DEK, a unique protein that organizes the DNA within a cell, is increased in many types of breast cancer. DEK promotes tumor growth, the spread of the disease throughout the body (metastasis), and increases the size of the breast cancer stem cell population. Breast cancer stem cells are typically drug resistant, which promotes tumor recurrence, and they have been associated with metastasis. Our research project aims to test whether DEK is important for breast cancer metastasis and chemotherapy drug resistance in the breast cancer stem cell population—we’ll do this by regulating key stem cell-related molecular pathways—and to test if DEK is a potential therapeutic target in breast cancer.”"Prognostic Evaluations of Serotonin and PTHrP in Individual Human Breast Tumor Specimens,” being led by Nelson Horseman PhD, professor in the department of molecular and cellular physiology at the UC College of Medicine—"This project is based on the discovery in our lab that serotonin is the primary signal for parathyroid hormone-related protein, or PTHrP—a protein member of the parathyroid hormone family. PTHrP, in turn, causes breast cancers to spread to bones and cause their breakdown. We determined that the serotonin receptor that is responsible for stimulating PTHrP is the type 2B receptor, abbreviated 5-HT2B.We identified 5-HT2B to be strongly correlated with ‘claudin-low’—meaning low levels of the major cell adhesion protein claudin and hormone receptor negative (challenging to treat)—tumors. These results may provide a new way of thinking about treatments for these ‘claudin-low’ tumors. Since they do not have estrogen receptors, they cannot be treated with anti-estrogen therapies. However, targeting 5-HT2B may prove to be a possible treatment.”
"Regulation and Function of LM07 in Metastatic Breast Cancer,”being led by Jinsong Zhang, PhD, former faculty member in the department of cancer biology at the UC College of Medicine—"We have previously shown that LMO7 (a protein) is highly expressed in metastatic but not non-metastatic breast cancer cells. To explain the function of LMO7 in metastatic breast cancer cells, we performed RNA-sequencing analyses in MDA-MB-231 cells, which are metastatic breast cancer cells. These cells were treated with either control or LMO7-specific shRNAs. shRNAs are used to target and silence gene expression by interfering with their RNA levels. A total of 3,760 genes showed strong reduction in RNA expression, meaning that these were LMO7-dependent genes in metastatic cancer cells. Previously, we have identified a set of LMO7-regulated genes with increased expression in human breast cancer patients with aggressive cancer. To reveal the common set of genes that are dependent on LMO7 for expression in both cultured cells and initial tumors, we compared both gene sets which led to the identification of 61 common LMO7-dependent genes whose biological function was uncovered by functional gene enrichment analysis. This set of genes regulate various functions of the cells that are related to cell migration. They are also controlled by the serum response factor (SRF) transcription factor, which has been shown to be activated by LMO7 in invasive breast cancer cells. Importantly, these genes are strongly linked to the development of invasive breast cancers. Our finding of the specific set of LMO7-dependent genes not only gives hope for therapeutic and diagnostic targets but also sets the stage for further investigation of the role and mechanism of LMO7 in the regulation of the SRF gene network. We have also performed studies aimed at understanding the mechanism by which LMO7 expression is enhanced in MDA-MB-231 cells as compared to non-metastatic cells.”
"Imaging Breast Tumors by their Dopamine Receptor Signature,” led by Nira Ben-Jonathan PhD, professor in the department of cancer biology at the UC College of Medicine—"This proposal was developed as a collaboration between radiation oncologist Michelle Mierzwa, MD, in the UC Cancer Institute’s Comprehensive Head and Neck Cancer Center, and me. The overall objective was to develop a non-invasive method for the detection of breast tumors by their unique dopamine receptor type 1 (D1R) mark. We proposed to use animal models without immune systems that were implanted with human breast cancer that express D1R and undergo whole body imaging using positron-emission tomography (PET). D1R detection will be done using two complementary approaches that are well suited for clinical imaging—labeled antibodies against D1R and radioactive D1R-selective ligands, which are molecules that bind to a central particle. Immunofluorescence, a test used to light biological samples, was used in initial tests, as it is it less expensive than PET. Animal models were injected with either the labeled antibodies or the ligand compounds and were imaged after three, six and 24 hours. Primary tumors and in some cases metastases were found after 24 hours. We have also contracted with a chemical company in Russia to create unique D1R ligands that can be suitable for PET imaging, as fluorescence imaging is impractical for human breast tumors or metastases. We have already made an excellent progress and are hoping to bring this project to fruition in the near future.”
"Study Investigating the In Vitro and In Vivo Effects of Cellcept on the Growth of Neoplastic Breast Adenocarcinoma Cells,”led by Atsuo Sasaki, PhD, assistant professor of medicine in the division of hematology oncology at the UC College of Medicine—"Recently developed hormone and drug therapy targeting tyrosine kinases, which function as ‘on’ or ‘off’ switches in many cellular functions, have contributed to improved long term survival of estrogen receptor positive, progesterone receptor positive, Her 2 Neu positive breast cancer patients. Triple negative breast cancer, in which none of the previously mentioned receptors is present, accounts for 15 to 20 percent of all breast cancer in the United States. This type of breast cancer lacks the expression of target molecules of hormonal therapy and tyrosine kinase inhibitors. To increase survival rates, a new approach for eliminating this type of cancer is needed. Our projects aims to clarify the effects of cellcept (mycophenolate mofetil), a medication that suppresses the immune system and is used in organ rejection, on breast adenocarcinoma and triple negative breast cancer. We’re hypothesizing that cellcept will increase tumor cell death and increase efficacy of standard chemotherapeutics.”
"Assessment of Adjuvant ‘Hormone-Therapy Fatigue’ in Breast Cancer,”led by Elyse Lower, MD, director of the UC Cancer Institute’s Comprehensive Breast Cancer Center and professor in the division of hematology oncology at the UC College of Medicine—"The diagnosis and treatment of breast cancer may alter a patient’s mental and physical quality of life. Estrogen’s effects on the brain may be neuro-protective or may be detrimental, and other endocrine therapies that could modify the effect of other therapeutic agents (adjuvant therapies) may influence cognitive functions, including fatigue. We previously reported that three months of adjuvant hormone therapy was not associated with change in fatigue. We want to determine the incidence of fatigue in early breast cancer patients and assess if hormone therapy with tamoxifen or an aromatase inhibitor worsens fatigue.”
Annual Ride Cincinnati Cycling Event June 8
The 2014 Ride Cincinnati cycling event is scheduled for June 8, 2014, at Sawyer Point in downtown Cincinnati. More than 2,000 people participated in the 2013 event, which raised more than $285,000 for local breast cancer research at the UC Cancer Institute and its affiliated adult cancer care facility, the UC Health Barrett Center. Learn more about Ride Cincinnati at ridecincinnati.org.